vasopressin--1-(1-mercaptocyclohexaneacetic-acid)-2-(o--methyl-l-tyrosine)-8-l-arginine- and Hemorrhage

Four groups of Sprague-Dawley rats were anaesthetized with isoflurane (ISO) (1.7% end-tidal concentration) in 40% oxygen, and mechanically ventilated. The animals were bled 15 mL kg-1 b.w. from the femoral vein over 10 min, followed by an observation period of 30 min. Ten minutes before haemorrhage each group of animals was pre-treated with intravenous injection/infusion of either: isotonic saline (Group B; CON; n=7), vasopressin V1-receptor antagonist [d(CH2)5Tyr(Me)AVP; 10 microg kg-1] (Group C; AVP-a; n=7), the non-selective angiotensin II receptor antagonist saralasin (10 microg kg-1 min-1) (Group D; SAR; n=7) or hexamethonium (10 mg kg-1) (Group E; HEX; n=7). A separate group of conscious animals were pre-treated with isotonic NaCl and subjected to the same haemorrhage protocol (Group A; AW; n=7). Mean arterial pressure (MAP), heart rate (HR) and blood gases were observed during the experiments. Only pre-treatment with SAR and HEX reduced MAP significantly. The pre-haemorrhage HR was only affected by HEX, which caused a reduction by 17%. The HR was significantly lower at the end of haemorrhage compared with pre-haemorrhage levels in all groups except that group treated with HEX. In that group the HR changed in the opposite direction. The ability to maintain MAP during haemorrhage, and the post-haemorrhage period, was significantly impaired in the groups treated with AVP-a, SAR or HEX compared with the group receiving NaCl. It is concluded that autonomic nervous activity is of major importance for the maintenance of MAP during isoflurane anaesthesia, whereas circulating angiotensin II and vasopressin levels contribute to a much smaller degree in this regard. General anaesthesia in combination with different degrees of neurohumoral blockade impairs the haemodynamic responses to blood loss, seen in conscious individuals. The impairment involves both the early and late phases during haemorrhage, as well as the post-bleeding recovery period. All three neurohumoral systems (autonomic nervous activity, angiotensin II and vasopressin) are of importance for regulating MAP during and after haemorrhage, although the autonomic nervous outflow appears to contribute to a larger extent.

Topics: Anesthesia; Anesthetics, Inhalation; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Blood Gas Analysis; Blood Pressure; Ganglionic Blockers; Heart Rate; Hemorrhage; Hexamethonium; Hydrogen-Ion Concentration; Isoflurane; Male; Neurotransmitter Agents; Rats; Rats, Sprague-Dawley; Saralasin

The aim of this study was to generate hemorrhage-triggered fluctuations in blood pressure (BP) at low frequency (LF, < 0.2 Hz) in conscious rats and investigate with spectral analysis the relative roles of hemorrhage-activated catecholamines, the renin-angiotensin system (RAS), and arginine vasopressin (AVP) on the generation of these fluctuations. The individual contribution of these factors was assessed using a combination of the selective antagonists, prazosin, losartan, and Manning compound (AVPX). At rest, systolic BP (SBP) LF fluctuations were slightly increased by losartan. The mid-frequency (MF; 0.2-0.6 Hz) oscillations of SBP and diastolic BP (DBP) were decreased by prazosin alone or associated with AVPX or losartan. The high-frequency (HF; respiratory) oscillations of SBP were increased by prazosin, prazosin plus losartan, and prazosin plus AVPX. After severe hemorrhage (20 ml/kg), the spontaneous BP recovery was characterized by the occurrence of slow fluctuations of SBP and DBP, centered approximately 0.065 Hz, and by increases of MF (89%) oscillations of SBP. The HF component of SBP variability tended to be increased by blood loss. The occurrence of the SBP LF fluctuations was prevented when alpha 1-adrenergic activity was blocked by prazosin. These oscillations were always present, despite inhibition of angiotensin II, and were increased after inhibition of the AVP activity. Pretreatment with the specific inhibitors used in these studies favored the amplifying effect of hemorrhage on HF fluctuations while they prevented the postbleeding increase in MF oscillations. In conclusion, the present results show an association between the dependence of the postbleeding blood pressure level on catecholamines and the occurrence of slow fluctuations of BP. The buffering role of AVP suggests the establishment of a hierarchy between humoral systems in the genesis of the LF oscillations of BP, with the slow oscillations being generated by the main pressor system and being dampened by the other systems. The postbleeding rise in the MF component of SBP variability could be considered a reflection of the activations of both the sympathetic vasomotor drive and the RAS. The postbleeding increase in the HF component of BP variability was dampened by the activation of the humoral systems. These effects may reflect the low preload state due to hypovolemia.

Topics: Animals; Antihypertensive Agents; Arginine Vasopressin; Biphenyl Compounds; Blood Pressure; Carbon Dioxide; Consciousness; Diastole; Heart Rate; Hemorrhage; Hormone Antagonists; Imidazoles; Losartan; Male; Oxygen; Prazosin; Rats; Rats, Wistar; Renin-Angiotensin System; Signal Transduction; Systole; Tetrazoles; Time Factors

1. Profound haemorrhage activates a number of pressor mechanisms, including the release of catecholamines, angiotensin II and arginine-vasopressin, which contribute to the subsequent cardiovascular recovery. Using specific single or combined blockade with prazosin, losartan and Manning compound (AVPX), the aim of this study was to evaluate the involvement of the three pressor systems in blood pressure recovery following severe haemorrhage (20 ml kg-1). 2. Haemorrhage of conscious, unrestrained rats resulted in a significant initial decrease in blood pressure of approximately 60 mmHg, and heart rate of approximately 70 bpm. Then, blood pressure tended to return to the control level within 10 min. The total cardiovascular recovery corresponded to increments of 52 +/- 5 mmHg (81% of the acute fall) for systolic blood pressure, and of 92 +/- 22 bpm (124%) for heart rate at 60 min post-bleeding. Significant falls in haematocrit (-10.5 +/- 1.2%, P < 0.01), in plasma concentrations of proteins (-10.3 +/- 0.9 g l-1, P < 0.01) and haemoglobin (-2.58 +/- 0.72 g 100 ml-1, P < 0.05) were observed at 60 min post-bleeding. 3. Pretreatment with one or two specific antagonists did not exaggerate the initial fall in blood pressure. The initial bradycardia was weakened only by combined blockade with losartan and AVPX. 4. The blood pressure recovery from a haemorrhage was delayed by approximately 25 min by the inhibition of vasopressin activity. The systolic blood pressure recovery in control animals (81% of the acute fall) was blunted by losartan (55% of the acute fall), prazosin (49%), combined losartan and AVPX (36%), prazosin and AVPX (36%), and also by prazosin plus losartan (13%). The diastolic blood pressure recovery was blunted only in the groups where the activity of angiotensin II was inhibited by losartan. 5. In conclusion, we have shown that neither catecholamines, angiotensin II nor vasopressin, although activated, individually compensate the acute hypotensive response to haemorrhage. The contribution of vasopressin to the blood pressure recovery post-bleeding is transient and is rapidly replaced by the pressor activity of the catecholamines and angiotensin II. The full systolic blood pressure recovery from severe haemorrhage requires the combined activity of these two pressor systems, while the diastolic blood pressure recovery seems to be only dependent upon angiotensin II activity.

Topics: Adrenergic alpha-1 Receptor Antagonists; Adrenergic alpha-Antagonists; Angiotensin II; Animals; Antihypertensive Agents; Arginine Vasopressin; Blood Pressure; Catecholamines; Diastole; Heart Rate; Hemodynamics; Hemorrhage; Hormone Antagonists; Losartan; Male; Prazosin; Rats; Rats, Wistar; Receptors, Adrenergic, alpha-1; Renin-Angiotensin System; Systole

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

Topics: Analysis of Variance; Angiotensin II; Animals; Arginine Vasopressin; Autonomic Nervous System; Blood Pressure; Captopril; Female; Heart Rate; Hemorrhage; Hindlimb; Hypertension, Renal; Mecamylamine; Muscle, Skeletal; Norepinephrine; Rabbits; Regional Blood Flow; Regression Analysis

We sought to determine whether arginine vasopressin (AVP) modulates arterial pressure (AP) by a receptor-mediated action in the nucleus reticularis rostroventrolateralis (nRVL). Immunocytochemical labeling with an antiserum against a synthetic AVP conjugate revealed a discrete although modest presumptive neuropeptidergic innervation of the nRVL. Electron microscopic analysis of vasopressinergic processes in the nRVL revealed that AVP-like immunoreactivity (AVP-LI) was primarily in axons and axon terminals. Immunoreactive terminals contained numerous small clear vesicles and large dense core vesicles and formed synapses with unlabeled dendrites. In the nRVL, retrograde transport-immunofluorescence data demonstrated close appositions between vasopressinergic beaded processes and a compact subambigual column of reticulospinal neurons labeled by deposits of cholera toxin beta-subunit into the thoracic spinal cord. Similar methods were used to define the origins of the AVP-afferent projection to nRVL. These retrograde transport-immunofluorescence studies demonstrated numerous retrogradely labeled neurons in the hypothalamus, including the paraventricular nucleus (PVN), after injections of a retrograde tracer, Fluoro-Gold into the ventrolateral medulla. However, double-labeled neurons were rare and confirmed a diffuse AVP afferent innervation of the sympathoexcitatory area. Microinjection of AVP into the nRVL in anesthetized rats produced a large dose-related increase in AP different from control at a dose of 1 pmol or higher. AVP injected intravenously elevated AP only at significantly higher doses. Microinjections of AVP into the nucleus tractus solitarii (NTS) had a smaller effect whereas into the caudal ventrolateral medulla exerted no effect on AP. Bilateral microinjections of an AVP antagonist, d(CH2)5[Tyr(Me)2]AVP into the nRVL produced no change in AP but blocked the increase produced by subsequent injections of AVP. An acute hemorrhage produced by withdrawal of 2 ml of blood from the femoral vein did not alter AP. However, bilateral microinjections of the AVP antagonist into the nRVL 5 min after hemorrhage decreased AP. In contrast, the AVP-antagonist injected intravenously after hemorrhage had no effect on AP. Our data suggest that under conditions demanding increased sympathetic drive to maintain AP, such as hemorrhage, a functional AVP receptor mechanism via terminals in the nRVL may be activated to restore normal levels of AP.

Topics: Animals; Arginine Vasopressin; Axonal Transport; Axons; Blood Pressure; Brain; Fluorescent Antibody Technique; Hemorrhage; Male; Medulla Oblongata; Microinjections; Neurons; Rats; Rats, Sprague-Dawley; Rats, Wistar; Synapses

During initial stages of hemorrhage in the rat, cardiovascular compensation leads to a tachycardia (mean +/- SE, 5.2 +/- 0.7%; n = 23) that helps prevent a large fall in blood pressure. This compensatory phase is followed by a decompensatory phase in which mean arterial pressure and heart rate fall. A rise in arginine vasopressin (AVP) levels has been postulated as the cause of this hemorrhage-induced bradycardia (HIB). The object of the present study was to determine whether interference with AVP release by alcohol anesthesia or neurohypophysectomy or by blockade of AVP receptors in the plasma or cerebral spinal fluid could attenuate HIB. Male Wistar rats were anesthetized with pentobarbital, surgically prepared, and bled to maintain a blood pressure of 40-50 mm Hg. After hemorrhage, heart rate decreased 15 +/- 2% (n = 6) with alcohol anesthesia compared with 32 +/- 3% (n = 7) with pentobarbital. After neurohypophysectomy, however, HIB remained unchanged (-15 +/- 2%; n = 5) compared with sham-operated controls (-19 +/- 3%; n = 6). Peripheral administration of two nonselective V1/V2 antagonists and one V2 antagonist had no effect on HIB, whereas a V1 antagonist significantly attenuated the heart rate decrease (-15 +/- 4%; n = 6) compared with controls (-32 +/- 3%; n = 7). None of the AVP antagonists tested at one tenth the peripheral dose had any effect on HIB when administered into the lateral ventricle of the brain, although a mixed serotonin, dopamine, and catecholamine antagonist, spiperone, potentiated the response. It was concluded that although peripheral release of AVP may be partially involved in the heart rate response to hemorrhage, central AVP release and central AVP receptors were not involved in HIB.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Drinking; Electrocardiography; Ethanol; Heart Rate; Hemorrhage; Male; Pentobarbital; Pituitary Gland, Posterior; Rats; Rats, Wistar; Receptors, Angiotensin; Receptors, Vasopressin; Spiperone; Vasopressins

We investigated possible interactions between arginine vasopressin (AVP) and endogenous opioid peptides during rapid hypotensive hemorrhage and subsequent opioid receptor blockade in conscious rabbits. Plasma AVP concentration did not change after normotensive hemorrhage but increased after hypotensive hemorrhage. Blockade of V1-AVP receptors (AVPX) did not affect prehemorrhage arterial pressure, heart rate, or hindquarter blood flow and vascular resistance. AVPX did not alter the hemodynamic response to hemorrhage or the blood loss required to reduce mean arterial pressure to less than 40 mmHg. However, hindquarter blood flow was higher and mean arterial pressure and hindquarter resistance lower after hypotensive hemorrhage in AVPX-treated animals. These differences were maintained after naloxone or saline injection. Naloxone increased mean arterial pressure and hindquarter resistance and decreased heart rate with or without AVPX. At 2 min postinjection, plasma AVP values were greater after saline than after naloxone. When naloxone's pressor response was reduced by alpha-adrenergic blockade, plasma AVP values were higher after naloxone than after saline. Thus AVP was not vital to maintenance of blood pressure during rapid normotensive hemorrhage or to the abrupt decrease in arterial blood pressure and resistance after rapid hypotensive hemorrhage. AVP release was important to spontaneous recovery from acute hypotensive hemorrhage but only of minor importance to naloxone's pressor response. Finally, AVP release appeared to be inhibited by endogenous opioids during acute hemorrhagic hypotension.

Topics: Animals; Arginine Vasopressin; Drug Interactions; Endorphins; Hemodynamics; Hemorrhage; Hypotension; Naloxone; Narcotic Antagonists; Rabbits; Rest

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

Topics: Animals; Animals, Newborn; Arginine Vasopressin; Biomechanical Phenomena; Blood Pressure; Cardiac Output; Cerebrovascular Circulation; Hemorrhage; Hypotension; Indomethacin; Lypressin; Oxygen Consumption; Prostaglandins; Swine; Vascular Resistance; Vasopressins

The present study examined the effects of central and peripheral administration of a vascular (V1) vasopressin (AVP) receptor antagonist on blood pressure, heart rate, and AVP levels in conscious rats. Rats subjected to rapid arterial haemorrhage were administered the AVP V1 antagonist [d(CH2)5Tyr(Me)AVP] either 5 min pre- or 20 min posthaemorrhage. Mean arterial blood pressure (MAP) was monitored for 45 min, after which the animals were killed and selected brain regions and plasma taken for AVP measurement. Intravenous (i.v.) administration of d(CH2)5Tyr(Me)AVP at 10 micrograms kg-1, but not 100 ng kg-1, significantly reduced MAP between 20 and 45 min posthaemorrhage compared with saline-treated controls. In contrast, administration of d(CH2)5Tyr(Me)AVP at 100 ng kg-1 intracerebroventricularly caused an attenuated MAP recovery to haemorrhage comparable with the effect of the antagonist at 10 micrograms kg-1 i.v. Haemorrhage caused a marked increase in circulating AVP levels, which was further enhanced in rats treated with the V1 antagonist at 10 micrograms kg-1 i.v., but no change in AVP levels of selected brain regions. The results indicate a role for AVP in MAP recovery following haemorrhage which may be centrally mediated.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Brain; Chromatography, High Pressure Liquid; Female; Heart Rate; Hemodynamics; Hemorrhage; Hypothalamus; Injections, Intravenous; Injections, Intraventricular; Radioimmunoassay; Rats; Vasopressins

We examined the hypothesis that V2-like receptors might contribute to the hemodynamic response seen after blockade of the vasoconstrictor (V1) effect of arginine vasopressin (AVP) in nonhypotensive hemorrhage. Seven chronically instrumented dogs were bled 15 ml/kg within 15 min on two different days, at least 3 days apart, and then injected either with the V1 antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-methyl)tyrosine]AVP [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg] or with the combined V1+V2 antagonist [1(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-ethyl)-D-tyrosine)4-valine]AVP [d(CH2)5-D-Tyr-(Et)VAVP (10 micrograms/kg)]. Mean arterial pressure, heart rate, and cardiac output (electromagnetic flowmeter) were measured before as well as after hemorrhage and for 10 min after antagonist administration. Both antagonists given after hemorrhage significantly decreased mean arterial pressure as well as total peripheral resistance and increased cardiac output. The V1 antagonist also increased heart rate significantly. No significant hemodynamic changes were measured in another group of six dogs in the absence of antagonist treatment. Although hemodynamic changes tended to be greater with the V1 antagonist than with the combined V1+V2 antagonist, a significant difference between the two analogues was established only for heart rate. These results indicate that in hemorrhage interaction with V2-like receptors plays only a modest role in the hemodynamic changes after V1 blockade in conscious dogs, contrary to what was found in dehydration.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Cardiac Output; Dogs; Heart Rate; Hemodynamics; Hemorrhage; Male; Receptors, Angiotensin; Receptors, Vasopressin; Reference Values; Vascular Resistance

The effect of arginine vasopressin (AVP) pressor blockade on the response to graded hemorrhage was investigated on conscious, unstressed, freely moving rats. The parameters studied were mean arterial pressure (MAP), heart rate (HR), blood velocity in the ascending aorta (ABV), and plasma concentrations of AVP (pAVP), renin (PRC), corticosterone (pCS), and catecholamines. After the first hemorrhage (0.75% of body wt over 5 min), MAP remained unchanged while ABV declined and HR increased. The two subsequent hemorrhages brought about significant reduction in MAP, HR, and ABV. pAVP, pCS, and PRC increased gradually during the experiment, while plasma catecholamine levels remained unchanged except for epinephrine, which increased after the third hemorrhage. After pretreatment with the AVP-pressor antagonist, [d(CH2)5Tyr(Me)]AVP, the hemorrhage-induced cardiovascular changes were practically identical to those seen in control animals. Results with AVP blockade performed after the third hemorrhage were also negative. A pressor role of AVP after hypotensive hemorrhage could only be revealed in the presence of converting-enzyme inhibition and alpha-adrenergic blockade. In addition, [d(CH2)5Tyr(Me)]AVP did not modify the effect of hemorrhage on pCS and catecholamines and caused only a slight enhancement of the increase in PRC. It is concluded that conscious, nonstressed rats, if all compensatory mechanisms are allowed full expression, exhibit a normal cardiovascular compensatory response to hemorrhage in the absence of functional AVP pressor receptors.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Captopril; Cardiac Output; Cardiovascular System; Catecholamines; Corticosterone; Female; Heart Rate; Hemorrhage; Phentolamine; Rats; Renin

The cardiovascular effects of an acute haemorrhage (2% of the body weight) were studied over a 60 min period in three groups of rats: (a) Brattleboro rats with hereditary hypothalamic diabetes insipidus (b.d.i.) lacking circulating vasopressin, (b) control rats of the parent Long Evans (l.e.) strain, and (c) l.e. rats treated with an antagonist of the vascular action of vasopressin. Prior to the haemorrhage there were no significant differences between the three groups of rats with respect to mean arterial blood pressure, cardiac output, stroke volume or total peripheral resistance. Following the haemorrhage cardiac output and stroke volume were severely reduced in all three groups of rats. Total peripheral resistance was relatively unaffected in antagonist-treated l.e. rats and b.d.i. rats, but rose substantially in response to the loss of blood in the control l.e. group. Both total peripheral resistance and mean arterial blood pressure were markedly greater in the untreated l.e. control rats than in the other two groups of animals during the first 20 min after haemorrhage. The mean heart rate measured in Brattleboro rats was elevated compared with that of control l.e. rats throughout the experiment and, in addition, significantly greater than that of antagonist-treated l.e. rats during the first 40 min after the haemorrhage. Survival rate for the b.d.i. rats following the 2% haemorrhage was lower than that for l.e. control rats and antagonist-treated l.e. rats. The results indicate that the recovery of the blood pressure following an acute arterial haemorrhage is significantly influenced by vasopressin, particularly during the first 20 min, and that the predominant effect of the hormone is to increase the total peripheral resistance. The higher mortality associated with volume depletion in the b.d.i. rats is unlikely to be directly related to the absence of the vascular action of vasopressin, since administration of the vasopressin antagonist to normal l.e. rats does not reduce their survival rate.

Topics: Anesthesia, General; Animals; Arginine Vasopressin; Blood Pressure; Diabetes Insipidus; Hemodynamics; Hemorrhage; Male; Rats; Rats, Brattleboro; Time Factors

To determine if the posterior pituitary hormone vasopressin is important for maintaining fetal cardiovascular homeostasis during hypovolemic stress, in seven chronically catheterized fetal lambs we induced hemorrhage of 20% of estimated blood volume in the presence and in the absence of a potent antagonist to the pressor effects of vasopressin. The study was a paired crossover design with at least 48 hours separating experiments in the same animal. Injection of the vasopressin antagonist did not alter basal fetal heart rate or arterial blood pressure, but hemorrhage of 2% of estimated fetal blood volume per minute for 10 minutes produced a greater fall in blood pressure (13 +/- 2 versus 10 +/- 2 torr, p less than 0.05) when the blocker was present than when it was absent. Arterial blood pressure remained below control levels longer following hemorrhage when the fetuses were pretreated with the antagonist (49.7 +/- 6 versus 26.6 +/- 6 minutes, p less than 0.01), and the integrated fall in arterial blood pressure with hemorrhage was greatest (283 +/- 53 versus 169 +/- 57 mm Hg . min p less than 0.01) when the blocker was used. The fall in heart rate following hemorrhage was similar with and without blocker pretreatment. These results indicate that vasopressin plays a physiologic role in blood pressure regulation in fetal lambs during periods of hypovolemia.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Cardiovascular System; Catheters, Indwelling; Female; Fetal Diseases; Fetus; Heart Rate; Hematocrit; Hemorrhage; Homeostasis; Hydrogen-Ion Concentration; Pregnancy; Sheep; Time Factors; Vasopressins

The effects of hemorrhagic hypotension on mean arterial pressure (MAP), cardiac output (CO), and its distribution were investigated in halothane-anesthetized rats using the radioactive microsphere technique. Hemorrhage (12 ml/kg) decreased MAP and CO, increased total peripheral resistance (TPR), and decreased blood flow (BF) to the heart, stomach, intestine, kidneys, skin, cecum, and colon. The effects of antagonists of vasopressin and the renin-angiotensin system on peripheral circulation following hypotensive hemorrhage were also examined using d(CH2)5Tyr(Me)AVP and saralasin, respectively. Injection of the vasopressin antagonist caused a reduction of MAP by reducing TPR and caused an increase of percent distribution of CO to the stomach, skin, cecum, and colon. Intravenous infusion of saralasin caused significant reductions of MAP by reducing TPR. Saralasin caused an increase of percent distribution of CO to the kidneys. The results show that both vasopressin and the renin-angiotensin systems participate in the control of MAP and peripheral vascular resistance following hypotensive hemorrhage in anesthetized rats.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Cardiac Output; Hemorrhage; Organ Specificity; Rats; Rats, Inbred Strains; Regional Blood Flow; Saralasin; Vascular Resistance