pituitrin and Ischemia

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.

Topics: Animals; Chemical and Drug Induced Liver Injury; Humans; Ischemia; Kidney Diseases; Lypressin; Shock; Skin; Terlipressin; Thrombosis; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Infusions, Intravenous; Ischemia; Prevalence; Shock; Skin; Vasoconstrictor Agents; Vasopressins

Topics: Acute Kidney Injury; Animals; Disease Models, Animal; Female; Furosemide; In Vitro Techniques; Ischemia; Kidney; Kidney Tubules; Mannitol; Perfusion; Rabbits; Ureteral Obstruction; Vasopressins

A model to study the effect of vasopressin V1a antagonist in dysmenorrhea.. A double-blind, randomized, placebo-controlled, cross-over trial was performed. Eight patients with primary dysmenorrhea and eight tuballigated, healthy subjects participated on days 1-2 of two consecutive menstruations. At each menstruation a bolus injection of 10 pmol/kg of vasopressin was administered before and during infusion of either 300 microg/min of atosiban or placebo. Intrauterine pressure was measured as area under the curve throughout the experiments. Ischemia markers in plasma and pain recorded by a visual analog scale were measured before and after each vasopressin injection as well as before and after the start of either atosiban or placebo infusion.. Vasopressin injections elevated area under the curve in both healthy volunteers and dysmenorrhea subjects. The vasopressin-induced rise in area under the curve was lower during atosiban administration than during infusion of placebo in both groups. None of the ischemia markers differed between or within groups at vasopressin injections or atosiban/placebo infusions. In subjects with dysmenorrhea the increase in pain following the administration of vasopressin was significantly lower during atosiban than during placebo infusion. Healthy volunteers experienced only slight discomfort after the vasopressin injections.. Atosiban reduces vasopressin-induced intrauterine pressure in both healthy volunteers and dysmenorrheics, and reported pain in subjects with dysmenorrhea. The ischemia markers are not a useful biomarker index in women with dysmenorrhea. The dysmenorrhea pain evoked by vasopressin correlated poorly with area under the curve, which may suggest that the effect is mediated by more than one V1a-like receptor. We conclude that this model with recordings in healthy women is useful in the evaluation of drug candidates for primary dysmenorrhea.

Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Area Under Curve; Biomarkers; Cross-Over Studies; Double-Blind Method; Dysmenorrhea; Female; Hormone Antagonists; Humans; Ischemia; Pain Measurement; Prospective Studies; Receptors, Vasopressin; Treatment Outcome; Uterine Contraction; Vasopressins; Vasotocin

Assessment of plasma renin activity (PRA) in renal vein blood is used in the diagnosis of unilateral renovascular hypertension (URVH). Recently also other markers of renal ischaemia (atrial natriuretic peptide, adrenalin, nonadrenaline and dopamine) have been described. The present study aimed to assess renal handling of vasopressin (AVP) by the ischaemic kidney in patients with URVH. In 16 patients with URVH, PRA and AVP were estimated in renal vein blood of the ischemic (IK) and non-ischemic kidney (NK), in arterial blood (A) and in blood samples withdrawn from the inferior vena cava (VCI) below the orifices of the renal veins. In contrast to PRA no significant difference between plasma levels of AVP in renal vein blood of the ischaemic and non-ischaemic kidney was noticed (4.8 +/- 0.9 pg/ml vs 5.1 +/- 0.8 pg/ml respectively).. Chronic hypoperfusion of the kidney does not influence renal handling of AVP in patients with URVH. Thus assessment of AVP in renal vein blood in these patients is deprived of diagnostic value.

Topics: Adult; Biomarkers; Female; Humans; Hypertension, Renal; Ischemia; Kidney; Male; Middle Aged; Renal Artery Obstruction; Vasopressins

Topics: Adult; Anesthesia, Dental; Clinical Trials as Topic; Epinephrine; Female; Humans; Ischemia; Male; Mepivacaine; Microcirculation; Middle Aged; Ornithine; Pain; Regional Blood Flow; Time Factors; Vasopressins

Topics: Anesthesia, General; Anesthesia, Local; Blood Pressure; Epinephrine; Frontal Sinus; Humans; Ischemia; Ornithine; Otosclerosis; Paranasal Sinuses; Pulse; Stapes Surgery; Tonsillectomy; Tympanoplasty; Vasoconstrictor Agents; Vasopressins

Goal-directed blood pressure management in the intensive care unit can improve trauma outcomes but is labor-intensive. Automated critical care systems can deliver scaled interventions to avoid excessive fluid or vasopressor administration. We compared a first-generation automated drug and fluid delivery platform, Precision Automated Critical Care Management (PACC-MAN), to a more refined algorithm, incorporating additional physiologic inputs and therapeutics. We hypothesized that the enhanced algorithm would achieve equivalent resuscitation endpoints with less crystalloid utilization in the setting of distributive shock.. Twelve swine underwent 30% hemorrhage and 30 minutes of aortic occlusion to induce an ischemia-reperfusion injury and distributive shock state. Next, animals were transfused to euvolemia and randomized into a standardized critical care (SCC) of PACC-MAN or an enhanced version (SCC+) for 4.25 hours. SCC+ incorporated lactate and urine output to assess global response to resuscitation and added vasopressin as an adjunct to norepinephrine at certain thresholds. Primary and secondary outcomes were decreased crystalloid administration and time at goal blood pressure, respectively.. Weight-based fluid bolus volume was lower in SCC+ compared with SCC (26.9 mL/kg vs. 67.5 mL/kg, p = 0.02). Cumulative norepinephrine dose required was not significantly different (SCC+: 26.9 μg/kg vs. SCC: 13.76 μg/kg, p = 0.24). Three of 6 animals (50%) in SCC+ triggered vasopressin as an adjunct. Percent time spent between 60 mm Hg and 70 mm Hg, terminal creatinine and lactate, and weight-adjusted cumulative urine output were equivalent.. Refinement of the PACC-MAN algorithm decreased crystalloid administration without sacrificing time in normotension, reducing urine output, increasing vasopressor support, or elevating biomarkers of organ damage. Iterative improvements in automated critical care systems to achieve target hemodynamics in a distributive-shock model are feasible.

Topics: Animals; Critical Care; Humans; Ischemia; Lactic Acid; Norepinephrine; Reperfusion; Resuscitation; Swine; Vasoconstrictor Agents; Vasopressins

Topics: Adrenergic beta-Antagonists; Amputation, Surgical; Cefepime; Child; Clindamycin; Debridement; Diagnosis, Differential; Epinephrine; Fasciotomy; Female; Fluid Therapy; Humans; Hypertension; Ischemia; Leg; Norepinephrine; Propranolol; Shock, Septic; Tachycardia; Therapeutic Irrigation; Treatment Outcome; Vasopressins

Women with a history of preeclampsia exhibit increased salt sensitivity of blood pressure at postpartum, which might be responsible for their increased risk of future cardiovascular diseases. However, it is unclear whether preeclampsia can cause increased salt sensitivity at postpartum. Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. Therefore, the aim of this study was to determine whether the exposure to preeclampsia, as elicited by placental ischemia, causes increased salt sensitivity at postpartum, and if so, whether vasopressin is involved in its process.. We used a reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. Pregnant Sprague-Dawley rats were categorized into the following two groups: RUPP-operated and sham-operated (SHAM) control groups. A 1-week-long high-salt diet was initiated at 3 weeks postpartum. The high-salt diet-induced increase in mean arterial pressure was significantly greater in the RUPP group than in the SHAM group. In addition, the plasma levels of copeptin, a substitute for plasma vasopressin, increased and serum osmolality decreased in the RUPP group. Double immunostaining revealed that the expression of c-Fos, a marker of neural activity, in vasopressin-producing neurons and presympathetic neurons in the hypothalamic paraventricular nucleus was significantly elevated in the RUPP group. The oral administration of conivaptan, the dual V1a/V2 vasopressin receptor antagonist, during high-salt diet abolished the enhanced increase in mean arterial pressure in RUPP rats.. Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure at postpartum probably due to enhanced vasopressin production and secretion.

Topics: Animals; Blood Pressure; Female; Ischemia; Placenta; Postpartum Period; Pre-Eclampsia; Pregnancy; Rats; Sodium Chloride, Dietary; Vasopressins

Upper gastrointestinal bleeding (UGIB) is one of the most frequent gastrointestinal complications after cardiac surgery with cardiopulmonary bypass (CPB). Endothelin expression and microcirculatory dysfunction have been shown to be involved in UGIB. The aim of this study was to analyze the effect of vasopressin during CPB on the gastric mucosal microcirculation and the involvement of the endothelin system.. Eighteen pigs were randomized into three groups (n = 6 each): group I = sham, group II = CPB (1-hour CPB) and group III = CPB + vasopressin (1-hour CPB and vasopressin administration during CPB to maintain baseline arterial pressure). All animals were observed for a further 90 min after termination of CPB. Systemic hemodynamics as well as blood flow and oxygen saturation of the gastric mucosa were measured continuously. At the end of the experiment, the gastric mucosal expressions of endothelin-1 (ET-1) and its receptor subtypes A (ET(A)) and B (ET(B)) were determined by polymerase chain reaction. Gastric mucosal injury, apoptotic cell death and leukocytic infiltration were determined by histology and immunohistochemical analyses of cleaved caspase-3 and myeloperoxidase.. CPB decreased gastric microvascular perfusion, which was associated with an increased expression of ET-1 and ET(A). Vasopressin aggravated the CPB-associated malperfusion, whereas it completely abrogated the upregulation of ET-1 and ET(A). Interestingly, vasopressin did not induce gastric mucosal morphologic injury, leukocytic infiltration or apoptotic cell death.. Vasopressin aggravates CPB-associated microvascular malperfusion of the gastric mucosa but does not induce gastric mucosal injury.

Topics: Animals; Cardiopulmonary Bypass; Endothelins; Gastric Mucosa; Hemodynamics; Ischemia; Microcirculation; Random Allocation; Swine; Vasoconstrictor Agents; Vasopressins

Lower gastrointestinal complications are rare after cardiac surgery with cardiopulmonary bypass (CPB). However, if they occur, they are associated with a high mortality. Endothelin (ET) expression and microcirculatory dysfunction have been shown to be involved in a variety of diseases of the lower gastrointestinal tract. The aim of this study was to analyze whether CPB with or without additional vasopressin administration affects the rectosigmoidal mucosal microcirculation and whether this involves the ET system.. Pigs were randomized in three groups (n = 6 each): I Sham, II CPB: 1 hour CPB, III CPB + vasopressin: 1 hour CPB and vasopressin (0.006 U/min kg) administration maintaining baseline arterial pressure. All animals were reperfused for 90 minutes. During the experiment hemodynamics and rectosigmoidal mucosal microcirculation were measured continuously. The rectosigmoidal mucosal expression of endothelin-1 (ET-1) and its receptor subtypes A (ETA ) and B (ETB ) were determined using PCR and Western blot analysis.. CPB did not change rectosigmoidal microvascular blood flow compared to baseline (68.1 ± 4.0 vs. 75.5 ± 6.6 AU; p = 0.4), but increased ET-1 (gene, 7.8 ± 1.5 vs. 2.3 ± 0.6 RQ; p = 0.002 and protein, 12.0 ± 0.5 vs. 6.9 ± 0.3 OD mm(2) ; p < 0.001), ETA (gene, 2.3 ± 0.6 vs. 0.6 ± 0.1 RQ; p < 0.001 and protein, 11.0 ± 0.3 vs. 6.2 ± 1.1 OD mm(2) ; p = 0.006) and ETB (gene, 6.7 ± 1.2 vs. 1.9 ± 0.3 RQ; p < 0.001 and protein, 25.6 ± 1.4 vs. 14.9 ± 1.5 OD mm(2) ; p = 0.002) expression compared to Sham. Vasopressin during CPB reduced the rectosigmoidal blood flow compared to baseline (26.5 ± 4.9 vs. 75.5 ± 6.6 AU, p < 0.001), and blunted the CPB-induced increase of ET-1 (gene, 1.2 ± 0.4 RQ, p = 0.1 and protein, 8.1 ± 1.6 OD mm(2) , p = 0.5 vs. Sham), ETA (gene, 0.6 ± 0.1 RQ, p = 1.0 and protein, 7.0 ± 0.6 OD mm(2) , p = 0.6 vs. Sham) and ETB (gene, 1.3 ± 0.3 RQ, p = 0.1 and protein, 19.4 ± 2.1 OD mm(2) , p = 0.1 vs. Sham).. CPB does not significantly affect rectosigmoidal mucosal microcirculation; however, it upregulates ET-1, ETA , and ETB . Vasopressin blunts the CPB-induced elevation of ET-1, ETA , and ETB and induces rectosigmoidal mucosal ischemia during CPB.

Topics: Animals; Blood Flow Velocity; Cardiopulmonary Bypass; Colon, Sigmoid; Endothelin-1; Hemodynamics; Intestinal Mucosa; Ischemia; Microcirculation; Receptors, Endothelin; Rectum; Swine; Up-Regulation; Vasopressins

Gastrointestinal blood flow can be compromised during and after cardiopulmonary bypass. Endothelin has been shown to be involved in the intestinal microcirculatory disturbance of sepsis. The aim of the present study was to analyze the involvement of the endothelin system on intestinal blood flow regulation during cardiopulmonary bypass and the effect of vasopressin given during cardiopulmonary bypass.. A total of 24 pigs were studied in 4 groups (n = 6): group I, sham; group II, ischemia/reperfusion with 1 hour of superior mesenteric artery occlusion; group III, cardiopulmonary bypass for 1 hour; and group IV, 1 hour of cardiopulmonary bypass plus vasopressin administration, maintaining the baseline arterial pressure. All the pigs were reperfused for 90 minutes. During the experiment, the hemodynamics and jejunal microcirculation were measured continuously. The jejunal mucosal expression of endothelin-1 and its receptor subtypes A and B were determined using polymerase chain reaction.. During cardiopulmonary bypass, superior mesenteric artery flow was preserved but marked jejunal microvascular impairment occurred compared with baseline (mucosal capillary density, 192.2 ± 5.4 vs 150.8 ± 5.1 cm/cm(2); P = .005; tissue blood flow, 501.7 ± 39.3 vs 332.3 ± 27.9 AU; P = .025). The expression of endothelin-1 after cardiopulmonary bypass (3.2 ± 0.4 vs 12.2 ± 0.8 RQ, P = .006) and endothelin subtype A (0.7 ± 0.2 vs 2.4 ± 0.6 RQ; P = .01) was significantly increased compared to the sham group. Vasopressin administration during cardiopulmonary bypass led to normal capillary density (189.9 ± 3.9 vs 178.0 ± 6.3; P = .1) and tissue blood flow (501.7 ± 39.3 vs 494.7 ± 44.4 AU; P = .4) compared with baseline. The expression of endothelin-1 (3.2 ± 0.4 vs 1.8 ± 0.3 RQ; P = .3) and endothelin subtype A (0.7 ± 0.2 vs 0.9 ± 0.2 RQ; P = .5) was not different from the sham group.. Cardiopulmonary bypass leads to microvascular impairment of jejunal microcirculation, which is associated with the upregulation of endothelin-1 and endothelin subtype A. The administration of vasopressin minimizes these cardiopulmonary bypass-associated alterations.

Topics: Animals; Biopsy; Blood Flow Velocity; Capillaries; Cardiopulmonary Bypass; Endothelin-1; Ischemia; Jejunum; Mesenteric Artery, Superior; Mesenteric Ischemia; Microcirculation; Models, Animal; Real-Time Polymerase Chain Reaction; Receptor, Endothelin A; Receptor, Endothelin B; Regional Blood Flow; RNA, Messenger; Splanchnic Circulation; Sus scrofa; Time Factors; Vascular Diseases; Vasopressins

Histamine in the rat stomach resides in enterochromaffin-like (ECL) cells and mast cells. The ECL cells are peptide-hormone-producing endocrine cells known to release histamine and chromogranin-A-derived peptides (such as pancreastatin) in response to gastrin. Ischemia (induced by clamping of the celiac artery or by gastric submucosal microinfusion of the vasoconstrictor endothelin) mobilizes large amounts of ECL-cell histamine in a burst-like manner. This report examines the ECL-cell response to ischemia and compares it with that induced by gastrin in rats. Arterial clamping (30 min) and gastric submucosal microinfusion (3 h) of endothelin, vasopressin, or adrenaline caused ischemia, manifested as a raised lactate/pyruvate ratio and mucosal damage. Whereas microinfusion of gastrin released both histamine and pancreastatin, ischemia mobilized histamine only. The mucosal concentrations of histamine and pancreastatin, the number and immunostaining intensity of the ECL cells, and the ultrastructure of the ECL cells were unchanged following ischemia. The long-term effects of ischemia and reperfusion (60-90 min) on gastric mucosa were examined in rats treated with the proton pump inhibitor omeprazole for 4 days. The activity of the ECL cells was suppressed (reflected in low histamine-forming capacity) but returned to normal within 1 week, illustrating the ability of the ECL cells to recover. We suggest that ischemia mobilizes cytosolic ECL-cell histamine without affecting the storage of histamine (and pancreastatin) in the secretory organelles and without causing lasting ECL-cell impairment.

Topics: Animals; Cell Compartmentation; Chromogranin A; Cytosol; Endothelins; Enterochromaffin-like Cells; Epinephrine; Female; Gastric Mucosa; Gastrins; Histamine; Histamine Release; Ischemia; Pancreatic Hormones; Rats; Rats, Sprague-Dawley; Secretory Vesicles; Vasopressins

Topics: Aged, 80 and over; Humans; Ischemia; Microcirculation; Regional Blood Flow; Skin; Vasoconstrictor Agents; Vasopressins

Survival after prolonged cardiopulmonary resuscitation (CPR) is often associated with neurological and other sequelae. We describe a patient who survived prolonged cardiac arrest due to ventricular fibrillation neurologically intact but suffered colon ischaemia and necrosis in the post-resuscitation period. Subtotal colectomy was performed. We wonder whether this complication was related to the use of vasopressin.

Topics: Adrenergic Agonists; Adult; Amiodarone; Anti-Arrhythmia Agents; Cardiopulmonary Resuscitation; Colectomy; Colon; Electric Countershock; Epinephrine; Female; Heart Arrest; Humans; Ischemia; Necrosis; Time Factors; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

To examine the coronary effects of arginine-vasopressin during reperfusion after a short ischemia, left circumflex coronary artery flow was electromagnetically measured, and 15 min total occlusion of this artery followed by reperfusion was induced in anesthetized goats (five nontreated, five treated with the inhibitor of nitric oxide synthesis Nomega-nitro-L-arginine methyl ester (L-NAME) and five treated with the inhibitor of cyclooxygenase meclofenamate). The vasoactive drugs and L-NAME were intracoronarily injected, and meclofenamate by i.v. route. At 60 min of reperfusion, coronary vascular conductance was not changed significantly in nontreated and was decreased by 35% (P<0.01) in L-NAME-treated and by 30% (P<0.01) in meclofenamate-treated animals. During reperfusion, the coronary vasodilatation with acetylcholine (3-100 ng) and sodium nitroprusside (1-10 microg) was not altered in nontreated animals, and the vasodilatation with acetylcholine but not with sodium nitroprusside was partially decreased in L-NAME--but not in meclofenamate-treated animals. The vasoconstriction in response to arginine-vasopressin (0.03-0.3 microg) was increased during reperfusion in nontreated, was not changed in L-NAME-treated and was decreased in meclofenamate-treated animals. Therefore, it is suggested that during reperfusion after a short ischemia: (1) the coronary vasodilator reserve is preserved; (2) the coronary vasodilatation with acetylcholine is also preserved, but in this vasodilatation, the role of nitric oxide may be attenuated and prostanoids may be not involved; and (3) the coronary vasoconstriction with arginine-vasopressin is increased, probably due to both attenuation of the modulatory role of nitric oxide and the release of vasoconstrictor prostanoids.

Topics: Acetylcholine; Anesthesia; Animals; Blood Pressure; Coronary Circulation; Coronary Disease; Enzyme Inhibitors; Female; Goats; Heart Rate; Hemodynamics; Ischemia; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Nitroprusside; Prostaglandins; Reperfusion; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Abnormal gastric tonometric variables, a surrogate for splanchnic ischemia, occur in approximately 50% of patients at the end of routine cardiac operations and are associated with postoperative morbidity. We sought to determine whether gastric tonometric variables deteriorate after left ventricular assist device insertion and to explore the association between abnormal gastric tonometric variables and vasoconstrictor use.. Nineteen patients who had insertion of a left ventricular assist device were enrolled in a prospective, observational study. Automated air tonometry was used to determine the difference between gastric and arterial partial pressure of carbon dioxide (CO2 gap) at five time points perioperatively.. Compared with baseline, systemic blood flow was significantly increased at the end of operation (1.9 +/- 0.6 versus 2.9 +/- 0.7 L x min(-1) x m(-2), p < 0.0001). Tonometric variables, which were normal at baseline, became abnormal in 90% of patients (baseline CO2 gap 4 +/- 2 mm Hg versus end of operation CO2 gap 24 +/- 15 mm Hg, p < 0.0001). Elevated CO2 gaps correlated with larger doses of norepinephrine (r = 0.69, p = 0.001) and vasopressin (r = 0.88, p < 0.0001). Abnormal gastric tonometric variables at the end of operation correlated with postoperative intensive care unit length of stay (r = 0.70, p = 0.0009) and multiple organ dysfunction score (r = 0.64, p = 0.0033).. Despite a significant increase in systemic blood flow after left ventricular assist device implantation, abnormal gastric tonometric variables developed and were associated with larger vasoconstrictor dose. These data provide evidence that gastric ischemia can develop independently of changes in systemic blood flow and support the potential role of vasoconstrictors as a cause of splanchnic ischemia.

Topics: Acid-Base Equilibrium; Adult; Aged; Carbon Dioxide; Catheters, Indwelling; Critical Care; Dose-Response Relationship, Drug; Female; Gastric Mucosa; Heart Failure; Heart-Assist Devices; Humans; Ischemia; Male; Manometry; Middle Aged; Monitoring, Physiologic; Norepinephrine; Postoperative Complications; Prospective Studies; Splanchnic Circulation; Vasoconstrictor Agents; Vasopressins

The use of vasopressin instead of adrenaline/epinephrine during resuscitation improves vital organ perfusion, but the effects on mesenteric perfusion following successful resuscitation are not fully evaluated. The present study was designed to compare the effects of vasopressin and adrenaline/epinephrine, given to rats during resuscitation from ventricular fibrillation, on to mesenteric ischaemia, as determined by intestinal mucosal tonometer pCO(2) during the postresuscitation period.. Male Sprague-Dawley rats (n=28) were allocated randomly to receive vasopressin (0.8 U/kg) or adrenaline/epinephrine (90 microg/kg) after 5 min of ventricular fibrillation. Precordial chest compression was initiated 4 min after the start of ventricular fibrillation, continued for 4 min, and followed by defibrillation. Seven of 14 (vasopressin) and 12 of 14 (adrenaline/epinephrine) rats were successfully defibrillated (P=0.10, Fisher's exact test) and observed for 60 min. Intestinal mucosal tonometer pCO(2) measurements before cardiac arrest and 15, 30, and 60 min following return of spontaneous circulation were 47+/-3, 73+/-8, 63+/-7, and 56+/-6 mmHg in the vasopressin group and 48+/-5, 78+/-7, 67+/-6, and 62+/-6 mmHg in the adrenaline/epinephrine group (P<0.05 at 60 min between vasopressin and adrenaline/epinephrine). Right atrial hemoglobin oxygen saturations at these time points were 73+/-5, 51+/-12, 58+/-11, and 63+/-5% in the vasopressin group and 76+/-7, 44+/-10, 52+/-10 and 54+/-8% in the adrenaline/epinephrine group (P<0.05 at 60 min between vasopressin and adrenaline/epinephrine).. We conclude that in this rat model the administration of vasopressin instead of adrenaline/epinephrine for CPR tends to be associated with lower resuscitation success, but less mesenteric ischaemia during the postresuscitation period in successfully resuscitated rats.

Topics: Adrenergic Agonists; Animals; Blood Gas Analysis; Carbon Dioxide; Epinephrine; Heart Arrest; Ischemia; Male; Manometry; Mesentery; Models, Animal; Rats; Rats, Sprague-Dawley; Resuscitation; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

Topics: Animals; Blood Pressure; Chemoreceptor Cells; Denervation; Heart Rate; Ischemia; Kidney; Ligation; Male; Rabbits; Renal Artery; Renin; Vasopressins

Topics: Adult; Atrial Natriuretic Factor; Female; Humans; Ischemia; Kidney; Kidney Transplantation; Male; Renin-Angiotensin System; Time Factors; Tissue Donors; Vasopressins

Topics: Aged; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Intravenous; Ischemia; Male; Scrotum; Vasopressins

We evaluated the effects of common vasoactive agents on collateral blood flow to an ischemic segment of small intestine and on the hemodynamic determinants of that flow. Two adjacent canine jejunal segments were isolated together, and the artery to each was cannulated for autoperfusion from a femoral and a carotid artery, respectively. Arterial pressure, arterial blood flow into, and venous outflow from each segment was measured separately. Venous pressure was zero. Vascular resistances were calculated. After clamping the arterial circuit to one segment, designated "ischemic," its steady-state venous outflow was taken as the collateral blood flow from the nonischemic into the ischemic segment. Without drugs, collateral blood flow was equal to 29 +/- 4 ml/min X 100 gm or, 56% +/- 8% of normal, well above the level needed to sustain oxygen consumption and thereby prevent ischemic injury. Local intra-arterial infusion of the vasodilators isoproterenol and papaverine not only failed to increase collateral flow but actually caused a small but (with isoproterenol) significant reduction, caused by vasodilation in the nonischemic bed, and a resulting drop in arterial pressure distal to the occlusion in the ischemic segment (i.e., a steal phenomenon). The vasoconstrictors levarterenol and vasopressin also reduced collateral flow but by direct and preferential vasoconstriction of the dilated ischemic bed. These findings suggest that collateral blood flow may be optimal without drugs and is decreased only by vasoactive agents, including vasodilators. This contradicts the rationale for vasodilator therapy for the direct augmentation of collateral blood flow in acute occlusive intestinal ischemia.

Topics: Animals; Blood Pressure; Collateral Circulation; Dogs; Female; Ischemia; Isoproterenol; Jejunum; Male; Norepinephrine; Papaverine; Regional Blood Flow; Vascular Resistance; Vasopressins

Myoglobinuria and acute renal failure were observed in two patients with vasopressin-treated gastrointestinal hemorrhage. Because there were no other obvious causes of renal failure in either patient, we propose that skeletal muscle ischemia developed during vasopressin infusion, followed by release of myoglobin and renal damage. This association should be considered in the period after vasopressin-treated gastrointestinal hemorrhage.

Topics: Acute Kidney Injury; Aged; Female; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Ischemia; Male; Middle Aged; Muscles; Myoglobinuria; Rhabdomyolysis; Vasopressins

Glomerular visceral epithelial cells (podocytes) undergo flattening and spreading of major processes detectable by scanning electron microscopy in early postischemic acute renal failure in both animals and man. The authors examined the kinetics of development of these epithelial cell changes in the renal pedicle-clamping model of ischemic renal failure in the rabbit. They found that these changes develop progressively, increasing with increasing length of ischemia, and occur while the pedicle clamp is still in place. To assess the possible role of angiotensin II and vasopressin in producing the epithelial changes, the authors compared glomerular morphology before and during pedicle clamping in hydrated rabbits and in dehydrated rabbits. Dehydration alone produced changes in glomerular epithelial cells comparable to those seen in the postischemic kidney. The angiotensin-converting enzyme inhibitor captopril did not prevent the podocyte changes in either group. In vitro incubation studies confirmed that both angiotensin II and vasopressin produce glomerular epithelial cell changes with a threshold between 10(-7) M and 10(-8) M, a concentration that may be physiologically significant for angiotensin II, which is synthesized at the glomerulus and may have local paracrine effects. Such local synthesis may not be inhibited by systemic administration of captopril. Angiotensin II may play a role in producing podocyte alterations during renal ischemia, as well as in the dehydrated state.

Topics: Angiotensin II; Animals; Constriction; Dehydration; Epithelium; Female; Ischemia; Kidney Glomerulus; Kinetics; Rabbits; Vasopressins

Topics: Colitis; Colon; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Intestinal Mucosa; Ischemia; Male; Middle Aged; Vasopressins

Topics: Animals; Dogs; Intestinal Mucosa; Intestine, Small; Ischemia; Radiation Injuries, Experimental; Radiation-Protective Agents; Regional Blood Flow; Vasopressins

Topics: Angiography; Catheterization; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Intestine, Large; Ischemia; Ischemic Attack, Transient; Thrombosis; Vasodilator Agents; Vasopressins

Topics: Acute Kidney Injury; Angiotensin II; Humans; Ischemia; Kidney; Kidney Tubular Necrosis, Acute; Kidney Tubules; Oliguria; Prostaglandins; Renin; Vasopressins

Topics: Acute Kidney Injury; Animals; Blood Volume; Ischemia; Kidney; Nephrectomy; Rats; Uremia; Vasopressins

The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension was investigated in the conscious dog. Intravenous infusion of synthetic arginine vasopressin to elevate plasma levels approximately fivefold to 31 pg/ml caused bradycardia in normal dogs, together with suppression of plasma renin activity and angiotensin II. This plasma level of vasopressin also caused elevation of mean arterial blood pressure in dogs with pharmacological total autonomic blockade. A similar degree of elevation of plasma vasopressin concentration was observed following mild nonhypotensive hemorrhage; more severe hemorrhage resulted in an approximate 100-fold increase in plasma vasopressin levels. Severe renal artery constriction in unilaterally nephrectomized dogs caused a marked rise in mean arterial blood pressure, but only a doubling of plasma vasopressin concentration. A suppressor infusion of vasopressin did not potentiate the pressor response to infused angiotensin II. It is concluded that vasopressin may play a role in normal cardiovascular homeostatic responses, but it is unlikely to have a significant direct vasoconstrictor role in the pathogenesis of this form of experimental renal hypertension.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Dogs; Heart Rate; Hypertension, Renal; Ischemia; Male; Renal Artery; Vasopressins

Experiments performed on male Wistar, Long Evans and Brattleboro rats indicate that the latter strain of animals, lacking vasopressin in their posterior pituitaries, are extremely sensitive to hemorrhagic and bowel ischemic shock. Mild forms of both hemorrhagic and bowel ischemic shock, as produced in Wistar or Long Evans rats, results in marked hypotension, hemoconcentration and blockade of the reticuloendothelial system (RES) in Brattleboro animals of similar sex, age and weight. These direct findings indicate that release of endogenous vasopressin in shock syndromes may be critical in maintenance of circulatory homeostasis and RES function.

Topics: Animals; Blood Pressure; Hematocrit; Hemorrhage; Intestines; Ischemia; Male; Mononuclear Phagocyte System; Phagocytosis; Rats; Shock; Species Specificity; Vasopressins

Clonidine, an antihypertensive drug that inhibits renin release and causes a water diuresis in normal animals, was tested for its ability to reduce the severity of post-ischemic acute renal failure produced in rabbits by clamping the left renal pedicle for 1 hour and removing the opposite kidney. Clonidine significantly lessened renal failure when given during, or 1 hours after, the ischemic insult in dehydrated rabbits. It was also effective when given during the ischemic insult in vasopressin-treated water-drinking rabbits but not in control water-drinking rabbits. In vasopressin-treated rabbits, clonidine lessened renal failure observed 2 days after the ischemic insult despite the fact that in the immediate postischemic period it lowered total renal blood flow, produced hypotension, and did not bring about lower plasma renin levels. Clonidine treatment resulted in less outer medullary microvascular damage (demonstrated by colloidal carbon staining), higher outer medullary blood flow 1 to 2 hours after unclamping, fewer casts, and higher creatinine clearance and free water clearance/creatinine clearance 4 to 6 hours after unclamping compared with controls. The effect of clonidine was unrelated to plasma renin activity. Clonidine did not alter plasma vasopressin concentration. Demeclocycline and lithium, two agents that blunt renal responsiveness to vasopressin, had a beneficial effect in dehydrated animals similar to that of clonidine, but the angiotensin II antagonist saralasin and the angiotensin converting enzyme inhibitor SQ20881 did not. Normal rabbits given a large dose of vasopressin in oil plus clonidine had significantly greater urine output and free water clearance and lower urine osmolality than did rabbits given vasopressin in oil alone. These results suggest that clonidine may be beneficial because it prevents ischemic microvascular injury in the renal outer medulla, an effect that may decrease tubular obstruction by lessening desquamation of damaged tubular cells or cell constituents into the tubular lumen. Clonidine may also decrease formation of obstructive hyaline casts in collecting ducts by blunting the kidney's response to vasopressin and increasing tubular fluid flow rate.

Topics: Acute Kidney Injury; Animals; Clonidine; Creatinine; Disease Models, Animal; Diuresis; Female; Ischemia; Kidney; Microcirculation; Nephrectomy; Rabbits; Regional Blood Flow; Vasopressins

Aggressive treatment with H(2) receptor blocking agents and/or antacids has been advocated as effective prophylaxis against and treatment for "stress ulcer," based on the logical but infrequently tested assumption that the severity of the disease is critically determined by the concentration of intraluminal acid. The present study investigated this assumption in a model which employed topical acid, topical bile acid and mucosal ischemia to induce ulcerogenesis. With vascularized, chambered ex vivo wedges of canine proximal gastric wall, groups of animals were studied during three sequential periods using topical test solutions (TS) containing either 0 mM, 100 mM or 160 mM HCI. During period 1, mucosae were exposed to TS alone; during period 2, either to TS containing 1 mM sodium taurocholate (TC) or to TS and concomitant vasopressin infusion (VP); and during period 3, to TS + TC + VP. Parameters evaluated included net H(+) flux ( big up tri, openH(+)), aminopyrine clearance (AC), a measure of mucosal blood flow, net TC flux ( big up tri, openTC) and the lesion index, graded 0-5. The data indicate that in nonischemic mucosa exposed to constant [TC], AC was significantly increased, big up tri, openH(+) ("back-diffusion") increased as a linear function of [H(+)] and no lesions were observed. Under the same circumstances in ischemic mucosa, big up tri, openH(+) increased as linear function of [H(+)]. As a consequence, lesion severity was also a linear function of [H(+)]. big up tri, openTC was enhanced at low pH but bore no relation to the degree of mucosal damage induced. Assuming applicability of the model, these studies provide support for the use of H(2) receptor blocking agents and/or antacids to prevent or ameliorate "stress ulcer" disease.

Topics: Acute Disease; Administration, Topical; Aminopyrine; Animals; Bile Acids and Salts; Disease Models, Animal; Dogs; Female; Gastric Mucosa; Humans; Hydrogen-Ion Concentration; Ischemia; Male; Stomach Ulcer; Stress, Psychological; Taurocholic Acid; Vasopressins

Topics: Adolescent; Asphyxia Neonatorum; Brain; Brain Edema; Female; Humans; Hyponatremia; Hypoxia, Brain; Infant, Newborn; Ischemia; Male; Vasopressins

Topics: Animals; Dogs; Female; Hepatic Artery; Intestine, Small; Ischemia; Liver; Male; Mesenteric Arteries; Regional Blood Flow; Vasopressins

Topics: Acute Disease; Administration, Topical; Aminopyrine; Animals; Bile Acids and Salts; Dogs; Gastric Mucosa; Hydrogen; Ischemia; Methylprednisolone; Sodium; Stomach Ulcer; Vasopressins

Topics: Animals; Blood Pressure; Dogs; Female; Gastric Mucosa; Hemodynamics; Ischemia; Male; Oxygen; Oxygen Consumption; Partial Pressure; Stomach; Vasopressins

Topics: Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Ileum; Infusions, Parenteral; Intestinal Diseases; Ischemia; Jejunum; Mesenteric Arteries; Mesenteric Vascular Occlusion; Middle Aged; Thrombosis; Vasopressins

Topics: Animals; Dogs; Female; Gastrointestinal Hemorrhage; Hemostasis, Surgical; Intestinal Mucosa; Ischemia; Jejunum; Male; Mesenteric Arteries; Radioisotope Dilution Technique; Regional Blood Flow; Vasopressins; Xenon Radioisotopes

1. Glycogen phosphorylase (a form, in rapidly freeze-clamped samples) and glucose release were measured in the perfused liver, in response to a range of concentrations of adrenaline, [8-arginine]vasopressin (anti-diuretic hormone) and angiotensin II. 2. All three hormones increased phosphorylase a activity by about 10 mumol/min per g of fresh liver, which was more than sufficient to explain concomitant glucose release (1-2mumol/min per g). 3. Minimally effective concentrations which activated phosphorylase were: adrenaline, 10nM (2ng/ml); vasopressin, 40pM (40pg/ml, 15 muunits/ml); angiotensin II, 60pM (60pg/ml). 4. Glycogen synthase activity was inhibited by adrenaline and vasopressin but not significantly by angiotensin II. 5. Vasoconstriction observed with adrenaline and angiotensin II (but not vasopressin) might explain part of the activation of phosphorylase, since equivalent vasoconstriction (in separate perfusions) activated phosphorylase, did not stimulate glucose output or inhibit synthase. 6. The potency of these effects suggests that all three hormones can stimulate hepatic glycogen degradation in vivo (by direct hepatic action). It is proposed that hormones, and ischaemia, stimulate glycogen degradation to provide glucose phosphates for disposal within the liver cell, as well as for release as free gluose.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Epinephrine; Glucose; Glycogen Synthase; In Vitro Techniques; Ischemia; Liver; Liver Glycogen; Male; Phosphorylases; Rats; Vasopressins

Pressor amine therapy in circulatory shock has been generally unfavorable, presumably because these drugs produce unselective, intense vasoconstriction and curtail rather than improve true capillary inflow, distribution and outflow in the microcirculation. The present study compares the influence of a new analog of vasopressin, [2-phenylalanine, 8-ornithine]vasopressin (POV), over wide dose ranges and Ringer's solution on: 1) survival after circulatory shock, induced by different means (e.g., hemorrhage, bowel ischemia); 2) blood pressure and hematocrit in shocked animals; and 3) various microcirculatory parameters after induction of hemorrhage and bowel ischemia shock (e.g., lumen diameters of various types of microvessels, reactivity of microvessels, microvascular flow patterns, leukocytic sticking, petechial hemorrhage formations, vasomotion, etc.). Local administration of POV, in contrast to constrictor catecholamines, induces a venular-to-arteriolar profile of constrictor activity in the normal rat mesenteric microcirculation. Systemic administration of POV to rats subjected to either lethal hemorrhage or bowel ischemia shock: 1) increases survival rates 2- to 8-fold over control rats receiving Ringer's solution; 2) produces a plateau-like effect on arterial blood pressure and returns arterial hematocrits toward normal after hemorrhage; and 3) regenerates and sustains vasomotion and venular tone, decreases microvascular hyper-reactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes toward normal, predisposes to a splanchnic microbed virtually free of stasis and petechiae, and restores capillary perfusion and outflow to near-normal. These findings indicate that it is possible to synthesize vasoactive molecules which exert selective microvascular effects and are highly beneficial in therapy of low-flow states.

Topics: Animals; Blood Pressure; Female; Intestines; Ischemia; Microcirculation; Rats; Shock, Hemorrhagic; Time Factors; Vasopressins

The present study indicates that: (a) local administration of low concentrations of an analog of vasopressin, 1-deamino-[2-phenylalanine, 8-arginine]-vasopressin (DPAVP), constricts venules in the rat splanchnic terminal vascular bed of normal animals, unlike that seen for catecholamines; (b) maximal concentrations of DPAVP narrow but do not occlude both arterioles and venules: (c) microscopic muscular venules (31-39 mu i.d.) do not narrow more than 20% in response to the vasopressin analog DPAVP; and (d) terminal arterioles (17-23 mu i.d.) do not narrow more than 50% in response to DPAVP. Systemic administration of DPAVP to rats subjected to hemorrhage or bowel ischemia shock more than doubles survival rates over control rats receiving Ringer solution. Infusion of DPAVP produces a dose-dependent effect on arterial blood pressure, microscopic capacitance vessels, large arterioles and small arteries. In addition, i.v. administration of DPAVP: (a) returns arterial hematocrit towards normal after shock; and (b) regenerates and sustains vasomotion and venular tone, decreases microvascular hyperreactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes towards normal, predisposes to a splanchnic microbed virtually free of stasis, petechiae and leukocytic sticking, and restores capillary perfusion and outflow to near-normal. Further, DPAVP effectively restores the early reticuloendothelial system (RES) phagocytic depression, characteristic of shock syndromes, to normal; the latter eventuating in RES hyper-phagocytic activity. These findings indicate it is possible to synthesize vasoactive molecules which: (a) exert selective microvascular and RES phagocytic effects; and (b) are highly beneficial in the therapy of low-flow states, at least in rats.

Topics: Animals; Blood Pressure; Female; Intestines; Ischemia; Microcirculation; Mononuclear Phagocyte System; Phagocytes; Rats; Shock; Shock, Hemorrhagic; Vasopressins

Topics: Animals; Bile; Bile Acids and Salts; Disease Models, Animal; Dogs; Gastric Juice; Gastric Mucosa; Gastritis; Gastrointestinal Hemorrhage; Humans; Hydrogen-Ion Concentration; Ischemia; Peptic Ulcer Hemorrhage; Secretory Rate; Stomach Ulcer; Vasopressins

Topics: Animals; Bile Acids and Salts; Gastric Mucosa; Haplorhini; Intubation, Gastrointestinal; Ischemia; Macaca; Membrane Potentials; Sodium; Stomach; Time Factors; Vasopressins; Water; Water-Electrolyte Balance

Topics: Animals; Aorta, Thoracic; Blood Vessels; Digestive System; Dose-Response Relationship, Drug; Epinephrine; Hemodynamics; Hydrocortisone; In Vitro Techniques; Ischemia; Male; Methylprednisolone; Microcirculation; Mononuclear Phagocyte System; Muscle, Smooth; Norepinephrine; Phagocytosis; Rats; Serotonin; Shock; Shock, Hemorrhagic; Time Factors; Vasopressins

Topics: Animals; Ischemia; Norepinephrine; Rats; Stomach; Stomach Ulcer; Stress, Physiological; Sympathetic Nervous System; Vasopressins

Topics: Adult; Angiography; Contrast Media; Foot; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Intestine, Small; Ischemia; Male; Mesenteric Arteries; Vasopressins; Wounds and Injuries

Topics: Aged; Angiography; Blood Transfusion, Autologous; Humans; Intubation, Gastrointestinal; Ischemia; Male; Necrosis; Peptic Ulcer Hemorrhage; Stomach; Stomach Diseases; Stomach Ulcer; Vasopressins

Topics: Aminopyrine; Animals; Bethanechol Compounds; Blood Pressure; Diffusion; Dogs; Gastric Mucosa; Hemorrhage; Histamine; Hydrochloric Acid; Injections, Intravenous; Ischemia; Norepinephrine; Pentagastrin; Sodium Chloride; Stomach Ulcer; Time Factors; Vasopressins

Topics: Aminopyrine; Animals; Carbon Radioisotopes; Denervation; Diffusion; Dogs; Gastric Mucosa; Glycols; Hydrochloric Acid; Injections, Intra-Arterial; Ischemia; Sodium Chloride; Stomach; Time Factors; Vasopressins

Topics: Anesthesia, Intravenous; Aneurysm; Angiography; Angiotensin II; Animals; Arteriovenous Fistula; Blood Pressure Determination; Dye Dilution Technique; Hypertension; Ischemia; Kidney; Norepinephrine; Phentolamine; Punctures; Rabbits; Spectrophotometry; Thrombosis; Trimethaphan; Urinary Catheterization; Vasopressins

Topics: Adaptation, Physiological; Angiotensin II; Animals; Blood Pressure; Catheterization; Female; Intestine, Large; Ischemia; Mononuclear Phagocyte System; Norepinephrine; Phagocytes; Phagocytosis; Rats; Shock; Shock, Hemorrhagic; Shock, Traumatic; Vasopressins

Topics: Angiography; Angiotensin II; Animals; Dogs; Ergolines; Ergonovine; Female; Graft Rejection; Hemodynamics; Ischemia; Kidney; Kidney Transplantation; Models, Biological; Norepinephrine; Phenoxybenzamine; Propranolol; Tolazoline; Transplantation Immunology; Transplantation, Autologous; Vasoconstrictor Agents; Vasopressins

1. Study of the delayed responses to lethal doses of endotoxin in cats is complicated by acute pulmonary vasoconstriction which results in hypotension, cardiac failure and pulmonary oedema. This acute response is abolished if the animal is pretreated with aspirin (10-100 mg/kg). In these cats, pretreated with aspirin, arterial pressure and right atrial pressure remain unchanged in the first 2 h after administration of endotoxin. Later, arterial pressure falls and the animals die but no haemorrhagic lung lesions are visible.2. These results confirm our previous conclusion that the delayed lethal response to endotoxin is an independent action and not a secondary consequence of the acute response. The mechanism of the action of aspirin is discussed and it is suggested that it prevents the release by endotoxin of vasoactive substances, possibly from platelets.3. In cats pretreated with aspirin, administration of endotoxin results in a marked mesenteric vasoconstriction. Although arterial pressure does not decrease significantly, superior mesenteric arterial flow decreases to 20% of control in the first hour after endotoxin and remains at this low level until the animal dies. Mesenteric ischaemia may contribute to the cat's death.4. The mesenteric vasoconstriction is not reduced by prior administration of phenoxybenzamine and is only slightly reduced after phenoxybenzamine, hypophysectomy and nephrectomy. It is concluded that catecholamines, vasopressin and angiotensin play at most a minor role in the mechanism of this vasoconstriction and that other unknown factors are predominant.

Topics: Angiotensin II; Animals; Aspirin; Blood Platelets; Blood Pressure; Cats; Endotoxins; Heart Failure; Hypophysectomy; Hypotension; Ischemia; Mesenteric Arteries; Nephrectomy; Phenoxybenzamine; Pulmonary Edema; Time Factors; Vasoconstrictor Agents; Vasopressins

Topics: Acute Kidney Injury; Angiography; Animals; Diatrizoate; Diuresis; Dogs; Female; Graft Rejection; Ischemia; Kidney; Kidney Concentrating Ability; Kidney Transplantation; Transplantation Immunology; Urography; Vasopressins

Topics: Animals; Coronary Disease; Dogs; Ischemia; Vasopressins; Vectorcardiography

Topics: Angiotensin II; Animals; Blood Pressure; Female; Intestines; Ischemia; Mononuclear Phagocyte System; Norepinephrine; Phagocytosis; Rats; Shock, Hemorrhagic; Shock, Traumatic; Sodium; Vasopressins

Topics: Adolescent; Adult; Aged; Anesthesia, Local; Anesthetics; Humans; Ischemia; Lidocaine; Middle Aged; Ornithine; Peptides; Vasopressins

Topics: Anesthetics, Local; Blood Pressure; Epinephrine; Felypressin; Hemostasis; Humans; Ischemia; Nausea; Otorhinolaryngologic Diseases; Oxytocin; Pulse; Tachycardia; Vasoconstrictor Agents; Vasopressins

Topics: Adenosine Triphosphate; Animals; Dehydration; Ischemia; Kidney; Male; Rats; Vasopressins

Topics: Animals; Coronary Vessels; Dipyridamole; Electrocardiography; Heart; Heart Ventricles; Hypertension; Ischemia; Myocardium; Norepinephrine; Perfusion; Propranolol; Radioisotopes; Rubidium; Vasopressins

Topics: Animals; Drug Synergism; Electrocardiography; Heart; Hypoxia; Ischemia; Isoproterenol; Male; Rats; Vasopressins

Topics: Adenosine Triphosphate; Animals; Epinephrine; Erythrocytes; Female; Glucagon; Humans; Hypothermia, Induced; Ischemia; Liver Transplantation; Oxygen Consumption; Perfusion; Swine; Transplantation Immunology; Transplantation, Heterologous; Transplantation, Homologous; Vascular Resistance; Vasomotor System; Vasopressins

Topics: Angiotensin II; Animals; Intestinal Diseases; Ischemia; Norepinephrine; Rats; Shock, Hemorrhagic; Vasopressins

Topics: Angiotensins; Arginine Vasopressin; Endotoxins; Felypressin; Intestinal Diseases; Ischemia; Norepinephrine; Pharmacology; Rats; Research; Shock, Septic; Shock, Traumatic; Vasoconstrictor Agents; Vasopressins

Topics: Arginine Vasopressin; Blood Flow Velocity; Carbohydrate Metabolism; Cats; Cervical Plexus; Creatine; Creatinine; Dogs; Electric Stimulation; Epinephrine; Ergotamine; Glucagon; Glucose; Ischemia; Isoproterenol; Permeability; Pharmacology; Phenoxybenzamine; Physiology; Research; Saliva; Submandibular Gland; Sucrose; Sympathetic Nervous System; Tolazoline; Vasopressins

Topics: Angiotensin Amide; Angiotensins; Arginine Vasopressin; Epinephrine; Felypressin; Guinea Pigs; Ischemia; Mice; Pharmacology; Rabbits; Rats; Research; Sympathomimetics; Vasopressins