pituitrin and Pulmonary-Edema

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Topics: Aldosterone; Altitude Sickness; Cell Membrane Permeability; Epinephrine; Humans; Hypertension, Pulmonary; Nifedipine; Norepinephrine; Pulmonary Edema; Radiography; Renin-Angiotensin System; Vasopressins

Topics: Adrenal Cortex Hormones; Arrhythmias, Cardiac; Cardiovascular Diseases; Catecholamines; Cerebrovascular Disorders; Humans; Hyperglycemia; Hypertension; Hyponatremia; Models, Biological; Pulmonary Edema; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Alkalosis, Respiratory; Anaphylaxis; Animals; Cardiovascular Diseases; Collagen Diseases; Gastrointestinal Diseases; Gonadotropins; Hematologic Diseases; Hormones, Ectopic; Humans; Hypoxia; In Vitro Techniques; Infant, Newborn; Lung; Lung Diseases; Lung Neoplasms; Microscopy, Electron; Neuromuscular Diseases; Neurotransmitter Agents; Paraneoplastic Endocrine Syndromes; Pulmonary Edema; Pulmonary Embolism; Pulmonary Emphysema; Rats; Respiratory Distress Syndrome, Newborn; Skin Diseases; Syndrome; Vasopressins

Topics: Addison Disease; Adrenal Cortex Hormones; Adrenal Glands; Adrenocorticotropic Hormone; Anti-Inflammatory Agents; Asthma; Corticotropin-Releasing Hormone; Facial Paralysis; Glucocorticoids; Granulomatosis with Polyangiitis; Hepatitis; Humans; Hypothalamus; Melanocyte-Stimulating Hormones; Myasthenia Gravis; Pituitary Gland; Pulmonary Edema; Retroperitoneal Fibrosis; Shock, Septic; Vasopressins

Topics: Adrenal Glands; Aldosterone; Diagnosis, Differential; Edema; Extracellular Space; Female; Heart Diseases; Humans; Kidney; Kidney Diseases; Liver Cirrhosis; Male; Parasitic Diseases; Pituitary Gland; Posture; Pre-Eclampsia; Pregnancy; Pulmonary Edema; Sodium; Vasopressins; Water-Electrolyte Balance

To investigate the hypotheses that activated coagulation, catecholamine release, or arginine vasopressin release are involved in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured these variables in seven subjects susceptible to HAPE and in nine control subjects at an altitude of 1,600 m, and after 6 and 12 h at a simulated altitude of 4,150 m. Each subject was studied twice, once after 3 days of placebo medication and once after 3 days of premedication with aspirin and dipyridamole. At high altitude, HAPE-susceptible subjects showed significantly exaggerated hypoxemia and a slightly higher end-tidal carbon dioxide partial pressure that did not account fully for the hypoxemia. Fibrinolytic activity was significantly accelerated in both groups at high altitude, whereas other coagulation measurements, catecholamines and arginine vasopressin levels, and pulmonary function tests were not significantly changed. Similar findings were obtained after both placebo and platelet-inhibitor premedication. The results indicate that none of the three hypothesized mechanisms, i.e., activated coagulation, excessive catecholamine release, or antidiuresis, would account for HAPE susceptibility. Instead, HAPE-susceptible subjects exhibited exaggerated hypoxemia associated with relative hypoventilation and a widened alveolar-arterial gas pressure difference.

Topics: Adolescent; Altitude; Aspirin; Blood Coagulation; Child; Dipyridamole; Fibrinolysis; Humans; Oxygen; Oxyhemoglobins; Pulmonary Edema; Respiration; Syndrome; Vasopressins

A 34-year-old patient underwent a laparoscopic myomectomy, complicated by a profound episode of bradycardia and hypotension following intramyometrial infiltration of vasopressin (20 IU), promptly corrected with intravenous ephedrine (6 mg) and glycopyrrolate (200 µg). At extubation, pink frothy fluid was noted in the endotracheal tube; she was visibly distressed, desaturated to 89% in air and was coughing up pink stained fluid. Acute pulmonary oedema secondary to vasopressin was suspected. A tight-fitting oxygen mask (100%) with positive end expiratory pressure was applied and intravenous furosemide (20 mg) and diamorphine (4 mg, 1 mg increments) were administered to facilitate diuresis and oxygenation. Chest X-ray confirmed acute pulmonary oedema. Arterial blood gas demonstrated type 2 respiratory failure. Over 12 hours, the oxygen was weaned to 1 L/min. She demonstrated excellent diuresis. Troponin and brain-natriuretic peptide were elevated, but echocardiogram was normal. The cardiology diagnosis was vasopressin-induced coronary vasospasm, precipitating acute pulmonary oedema. She was discharged home on day 5.

Topics: Adult; Airway Extubation; Bradycardia; Dose-Response Relationship, Drug; Female; Humans; Positive-Pressure Respiration; Pulmonary Edema; Uterine Myomectomy; Vasoconstrictor Agents; Vasopressins

Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013-June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 0.66 ± 1.50 μg/L; DCS: 0.0061 ± 0.0040; controls: 0.0090 ± 0.01; IPE versus DCS or controls: P < 0.01). The combined "BNP-cTnI" levels provided most discrimination: all IPE patients, but none of the DCS patients, had elevated levels of either/both of these markers.We propose that antidiuretic hormone acts together with a myocardial ischemic process to promote IPE. Thus, monitoring of antidiuretic hormone and cardiac biomarkers can help to make a quick and reliable diagnosis of IPE.

Topics: Adult; Aged; Biomarkers; Decompression Sickness; Diagnosis, Differential; Diving; Female; Heart Diseases; Humans; Male; Middle Aged; Prospective Studies; Pulmonary Edema; Vasopressins; Young Adult

Current research suggests that administration of vasopressin to patients with uncontrolled hemorrhagic shock (UHS) can avoid the detrimental effects associated with aggressive fluid resuscitation. However, vasopressin has a short half-life of 10~35 minutes in in vivo use and precludes its use in the pre-hospital setting. To increase the half-life of vasopressin, we proposed to synthesize liposome-encapsulated vasopressin and test it in a rat model of UHS.. The film hydration method was used to prepare liposomal vasopressin consisting of: Dipalmitoylphosphatidylcholine, cholesterol, and dipalmitoyl phosphatidylethanolamine (20:20:1 mole ratio). 42 rats were subjected to UHS and randomly received 5 different treatments (vasopressin, liposomal vasopressin, lactate ringer (LR), liposome only and sham). Outcome of UHS were measured using 4 common prognostic tests: mean arterial pressure (MAP), serum lactate level, inflammatory profile and pulmonary edema.. The dynamic light scattering results confirmed that we had prepared a successful liposomal vasopressin complex. Comparing the serum vasopressin concentration of liposomal vasopressin and vasopressin treated animals by ELISA, we found that the concentration of vasopressin for the liposomal vasopressin treated group is higher at 60 minutes. However, there was no significant difference between the MAP profile of rats treated with vasopressin and liposomal vasopressin in UHS. We also observed that animals treated with liposomal vasopressin performed indifferently to vasopressin treated rats in serum lactate level, inflammatory profile and edema profile. For most of our assays, the liposome only control behaves similarly to LR resuscitation in UHS rats.. We have synthesized a liposomal vasopressin complex that can prolong the serum concentration of vasopressin in a rat model of UHS. Although UHS rats treated with either liposomal vasopressin or vasopressin showed no statistical differences, it would be worthwhile to repeat the experiments with different liposomal compositions.

Topics: 1,2-Dipalmitoylphosphatidylcholine; Animals; Cholesterol; Disease Models, Animal; Fluid Therapy; Interleukin-6; Isotonic Solutions; Light; Liposomes; Male; Phosphatidylethanolamines; Pulmonary Edema; Rats; Rats, Wistar; Resuscitation; Ringer's Lactate; Scattering, Radiation; Shock, Hemorrhagic; Tumor Necrosis Factor-alpha; Vasopressins

Epithelial Na(+) transport participates in control of various body functions and conditions: e.g., homeostasis of body fluid content influencing blood pressure, control of amounts of fluids covering the apical surface of alveolar epithelial cells at appropriate levels for normal gas exchange, and prevention of bacterial/viral infection. Epithelial Na(+) transport via the transcellular pathway is mediated by the entry step of Na(+) across the apical membrane via Epithelial Na(+) Channel (ENaC) located at the apical membrane, and the extrusion step of Na(+) across the basolateral membrane via the Na(+),K(+)-ATPase located at the basolateral membrane. The rate-limiting step of the epithelial Na(+) transport via the transcellular pathway is generally recognized to be the entry step of Na(+) across the apical membrane via ENaC. Thus, up-/down-regulation of ENaC essentially participates in regulatory systems of blood pressure and normal gas exchange. Amount of ENaC-mediated Na(+) transport is determined by the number of ENaCs located at the apical membrane, activity (open probability) of individual ENaC located at the apical membrane, single channel conductance of ENaC located at the apical membrane, and driving force for the Na(+) entry via ENaCs across the apical membrane. In the present review article, I discuss the characteristics of ENaC and how these factors are regulated.

Topics: Adenosine Triphosphate; Aldosterone; Biological Transport; Catecholamines; Cell Membrane; Cyclic AMP-Dependent Protein Kinases; Cytosol; Epithelial Cells; Epithelial Sodium Channels; Homeostasis; Humans; Membrane Potentials; Osmotic Pressure; Protein Kinase C; Protein-Tyrosine Kinases; Pulmonary Edema; Sodium; Sodium-Potassium-Exchanging ATPase; Vasopressins

In the last two decades, the role of the alveolar active sodium transport was extensively studied and was found to play a crucial role in regulating alveolar fluid clearance (AFC), and thus in keeping the airspaces free of edema. The recent development of highly selective nonpeptide vasopressin-receptor antagonists gives us a rare chance to explore the role of vasopressin in the pathogenesis of lung edema. Therefore, the present study examined the involvement of vasopressin in modulating the ability of the lung to clear edema. Vasopressin enhanced the rate of lung edema clearance by 30% as compared with untreated control rats (from 0.49 ± 0.02 to 0.64 ± 0.02 ml/h), whereas V(2) receptor antagonists significantly decreased the ability of the lung to clear water (from 0.64 ± 0.02 to 0.31 ± 0.06 ml/h; P < 0.0001). In contrast, V(1) receptor antagonist did not change the rate of AFC. The administration of ouabain (a Na,K-ATPase inhibitor) and amiloride (a Na(+) channel blocker) inhibited the stimulatory effects of vasopressin (from 0.64 ± 0.02 to 0.22 ± 0.02 ml/h [P < 0.0001] and from 0.64 ± 0.017 to 0.23 ± 0.02 ml/h [P < 0.0001], respectively). Vasopressin significantly increased Na,K-ATPase protein abundance in the basolateral membranes of the alveolar epithelial cells via V(2) receptor activation. We report a novel role of the vasopressin pathway in AFC. This observation indicates a beneficial role of vasopressin in AFC by up-regulating active sodium transport.

Topics: Alveolar Epithelial Cells; Amiloride; Animals; Antidiuretic Hormone Receptor Antagonists; Cells, Cultured; Colchicine; In Vitro Techniques; Indoles; Male; Morpholines; Ouabain; Permeability; Pulmonary Alveoli; Pulmonary Edema; Pyrrolidines; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Sodium-Potassium-Exchanging ATPase; Spiro Compounds; Vasopressins

Vasopressin has been documented to effectively reduce blood loss in gynecologic practice. However, local infiltration of vasopressin may cause lethal cardiopulmonary complications in spite of rarity of reported cases. Severe bradycardia and cardiac arrest were encountered after intramyometrial injection of vasopressin in our two healthy patients undergoing open uterine myomectomy. We herewith discuss the associated complications and the anesthetic considerations.

Topics: Adult; Baroreflex; Bradycardia; Female; Heart Arrest; Hemostatics; Humans; Injections; Myometrium; Pulmonary Edema; Vasopressins

Small-dose IV vasopressin infusion may be beneficial in acute brain injury patients with unstable hemodynamics who are refractory to fluid resuscitation and catecholamine vasopressors.

Topics: Brain Injuries; Catecholamines; Humans; Hypotension; Male; Middle Aged; Myocardial Ischemia; Pulmonary Edema; Resuscitation; Vasoconstrictor Agents; Vasopressins

A 35-year-old male sustained a full-skin thickness chemical burn involving 60 per cent of TBSA when hydrochloric acid was applied to his face, trunk and extremities by his girlfriend. Debridements and skin graftings were performed smoothly and he was doing well until day 23 after injury, when massive GI tract bleeding caused a drop in blood pressure. Vasopressin was given intravenously to control the bleeding, which stopped, and the blood pressure returned to normal after transfusion. After the vasopressin infusion was tapered off acute pulmonary oedema developed abruptly, which required treatment by intubation and PEEP using a respirator. The lung condition had returned to normal by the following day. A second episode of massive GI tract bleeding recurred 10 days later, again vasopressin was given through a catheter into the inferior mesenteric artery. Again pulmonary oedema developed 38 h after the vasopressin use, the oedema disappeared within 2 days when the vasopressin infusion tapered off. It should be kept in mind that acute pulmonary oedema may develop when high doses of vasopressin are used in the treatment of Curling's ulcer or other GI tract bleeding.

Topics: Acute Disease; Adult; Burns, Chemical; Debridement; Gastrointestinal Hemorrhage; Hemostatics; Humans; Infusions, Intravenous; Male; Pulmonary Edema; Radiography, Thoracic; Skin; Skin Transplantation; Vasopressins

To report a case of pulmonary edema after local injection of vasopressin at laparoscopy.. University teaching hospital.. A 24-year-old woman who underwent a laparoscopic myomectomy.. Injection of vasopressin (10 mL of 0.5 U/mL) into the uterine wall overlying the myoma.. Bradycardia, atrioventricular block, and pulmonary edema.. The use of vasopressin can be associated with severe cardiopulmonary complications.

Topics: Adult; Blood Pressure; Bradycardia; Female; Heart Rate; Humans; Injections; Laparoscopy; Leiomyoma; Myometrium; Pulmonary Edema; Uterine Neoplasms; Vasoconstrictor Agents; Vasopressins

Topics: Bradycardia; Cervix Uteri; Female; Hemostatics; Humans; Injections; Pulmonary Edema; Vasopressins

This paper summarizes the main findings of 3 publications of our group [2-4] examining fluid balance at high altitude. Of 57 mountaineers ascending from 1170 m to 4559 m within 22 to 77 hours, 24 developed acute mountain sickness (AMS) and 16 developed high altitude pulmonary edema (HAPE). In 14 cases HAPE was preceded by symptoms of AMS. Independently of the amount of fluid intake, which varied from 2 to 4 l/24 h in these studies, subjects developing AMS showed decreased diuresis and natriuresis compared to healthy controls with similar fluid intake. Higher fluid intake resulted in greater urine output but did not prevent AMS. Higher plasma levels of aldosterone at rest and greater exercise-induced rises of plasma aldosterone and vasopressine may explain the increased water and salt retention in subjects with AMS. Whether these hormonal changes are secondary to a more severe hypoxemic stress or present a primary cause of AMS remains to be determined.

Topics: Adult; Aldosterone; Altitude Sickness; Diuresis; Drinking; Humans; Male; Middle Aged; Mountaineering; Natriuresis; Pulmonary Edema; Vasopressins; Water-Electrolyte Balance

It has been suggested that the von Willebrand factor antigen (vWF:Ag) may be a clinical marker for pulmonary endothelial cell injury. An ELISA was developed for the measurement of rat vWF:Ag. Rat lungs were isolated and perfused with a recirculating, blood-free, physiologic salt solution. Circulating levels of vWF:Ag and the eicosanoids thromboxane B2 (TXB2) and prostaglandin 6-keto F1-alpha (6-keto PGF1 alpha) were measured before and after different forms of insult. The addition of phospholipase C (PLC) or hydrogen peroxide (H2O2) to the perfusate caused lung damage as manifested by pulmonary artery pressure increase and pulmonary edema. This was paralleled by significant release of vWF:Ag, TXB2, and 6-keto PGF1 alpha. Increased hydrostatic pressure caused pulmonary edema without vWF:Ag and eicosanoid release. The addition of vasopressin to the perfusate caused vWF:Ag release but no lung injury and no release of eicosanoids. It is concluded that in the rat model, vWF:Ag release is a nonspecific marker for lung injury.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Enzyme-Linked Immunosorbent Assay; Hydrogen Peroxide; Hydrostatic Pressure; In Vitro Techniques; Lung; Male; Pulmonary Edema; Rats; Rats, Inbred Strains; Thromboxane B2; Type C Phospholipases; Vasopressins; von Willebrand Factor

In normal anaesthetized rats (pentobarbital, 40 mg/kg i.p.), intravenous injection of a bolus of vasopressin (0.3 micrograms/kg) provoked a large increase in pulmonary and in systemic blood pressures. About three minutes later, some rats (60%) developed an acute pulmonary edema (OPA), froth appearing at the trachea. Other animals presented no OPA at the 4th minute following the injection, but OPA appeared immediately when bilateral vagotomy was performed at that time. Factors explaining the appearance of OPA are mechanical ones, circulatory or respiratory, without interferences with autonomous nervous processes.

Topics: Acute Disease; Animals; Disease Models, Animal; Hemodynamics; Pulmonary Edema; Rats; Rats, Inbred Strains; Vasopressins

A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4-7 h after arrival at 4,559 m or high altitude (HA). Mean heart rates during exercise at both altitudes and during active ascent to HA were similar. Exercise-induced changes at LA did not differ significantly between the eight subjects who stayed well and the nine subjects who developed AMS during a 3-day sojourn at 4,559 m. At HA, O2 saturation before (71 +/- 2 vs. 83 +/- 2%, P less than 0.01) and during exercise (67 +/- 2 vs. 72 +/- 1%, P less than 0.025) was lower and exercise-induced increase of plasma aldosterone (617 +/- 116 vs. 233 +/- 42 pmol/l, P less than 0.025) and plasma antidiuretic hormone (23.8 +/- 14.4 vs. 3.4 +/- 1.8 pmol/l, P less than 0.05) was greater in the AMS group, whereas exercise-induced rise of plasma atrial natriuretic factor and changes of hematocrit, potassium, and osmolality in plasma were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acclimatization; Acetaminophen; Adult; Aging; Aldosterone; Altitude Sickness; Blood Proteins; Exercise; Exercise Test; Heart Rate; Hematocrit; Hormones; Humans; Male; Middle Aged; Mountaineering; Oxygen Consumption; Pulmonary Edema; Urodynamics; Vasopressins; Water-Electrolyte Balance

The experiment on white rats has revealed that water-soluble antioxidant-emoxipin, having obvious membrane modulating effect, does not influence the rate of watering and congestion of the lungs, the speed of reabsorption of fluid from lung tissue, the permeability of the capillary-alveolar barrier both in the blood-tissue direction and vice versa. Preliminary introduction of emoxipin increased the amount of edema fluid in the lungs when noradrenaline, centrogenic and especially vasopressin pulmonary edema developed, but in did not influence the development of vagotomic pulmonary edema. Stimulation of adenylcyclase or introduction of prostacyclin slowed down the development of centrogenic and vasopressin edema of the lungs. On the basis of these data it can be concluded that the intensification of pulmonary edema after emoxipin introduction is connected with its antioxidant activity.

Topics: Animals; Antioxidants; Norepinephrine; Picolines; Pulmonary Edema; Rats; Vagotomy; Vasopressins

Topics: Child; Dose-Response Relationship, Drug; Humans; Ornipressin; Pulmonary Edema; Vasopressins

Topics: Acute Kidney Injury; Diagnosis, Differential; Humans; Hypoxia; Pulmonary Edema; Urethral Obstruction; Vasopressins

Topics: Angiotensin II; Animals; Bradykinin; Epinephrine; Hemorrhage; Hexamethonium Compounds; Histamine; Hypertension, Pulmonary; Intracranial Pressure; Male; Norepinephrine; Organ Size; Pentolinium Tartrate; Phenoxybenzamine; Pulmonary Edema; Rats; Serotonin; Stereotaxic Techniques; Vagotomy; Vagus Nerve; Vasoconstrictor Agents; Vasopressins

Topics: Adult; Altitude; Catecholamines; Humans; Hydrocortisone; Male; Military Medicine; Pulmonary Edema; 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: Edema; Female; Humans; Hyponatremia; Middle Aged; Neurologic Manifestations; Polyradiculopathy; Pulmonary Edema; Vasopressins

Topics: Adolescent; Adult; Aged; Body Weight; Child; Diuretics; Edema; Female; Heart Failure; Hematocrit; Humans; Lung; Lung Compliance; Male; Middle Aged; Oxygen; Positive-Pressure Respiration; Pulmonary Edema; Radiography; Respiration, Artificial; Respiratory Function Tests; Respiratory Insufficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Blood Pressure; Capillary Permeability; Glucose; Injections, Intramuscular; Injections, Intravenous; Osmosis; Pulmonary Circulation; Pulmonary Edema; Rats; Sodium Chloride; Vasopressins

Topics: Animals; Capillary Permeability; Cell Membrane Permeability; Fatty Acids, Essential; Pulmonary Circulation; Pulmonary Edema; Rats; Vasopressins; Water