Cardiovascular Effects of Vasopressin Infused into the Vertebral Circulation of Conscious Dogs

1981 ◽  
Vol 61 (3) ◽  
pp. 345-347 ◽  
Author(s):  
J. F. Liard ◽  
O. Dériaz ◽  
M. Tschopp ◽  
J. Schoun
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Inferior Vena ◽  
Vena Cava ◽  
Electromagnetic Flowmeter ◽  
Cardiovascular Effects ◽  
Conscious Dogs ◽  
Left Vertebral Artery ◽  
Plasma Vasopressin ◽  
The Central Nervous System

1. Seven conscious dogs received arginine-vasopressin infusions (100 and 1000 fmol min−1 kg−1) through catheters implanted in the left vertebral artery or the inferior vena cava while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. Despite similar increases in plasma vasopressin concentrations, intravertebral administration induced a lesser increase in mean arterial pressure and a greater decrease in heart rate than the same infusion given intravenously. 3. These results suggest that vasopressin has an effect on structures of the central nervous system involved in cardiovascular control, possibly by affecting the baroreceptor reflex.

ARTERIAL AND VENOUS BLOOD PRESSURE RESPONSES DURING A REDUCTION IN BLOOD VOLUME AND HYPOXIA AND HYPERCAPNIA IN INFANTS DURING THE FIRST TWO DAYS OF LIFE

PEDIATRICS ◽  
1966 ◽  
Vol 37 (5) ◽  
pp. 733-742
Author(s):  
Maureen Young ◽  
Dennis Cottom
Keyword(s):  
Heart Rate ◽  
Inferior Vena Cava ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Inferior Vena ◽  
Recovery Period ◽  
Vena Cava ◽  
Ductus Venosus ◽  
Volume Distribution ◽  
The Mean

In 46 normal full-term infants (0.5-36.5 hours of age) the mean systolic pressure in the lower aorta, catheterized through the umbilical artery, was 70 S.D. ± 8 mm Hg and the mean diastolic pressure 44 S.D. ± 7 mm Hg. The mean venous pressure in the thoracic inferior vena cava, catheterized through the umbilical vein and ductus venosus was 1.4 S.D. ± 2 cm H2O. Higher pressures were recorded in the portal sinus. The mean arterial O2 tension in the lower aorta was 84 S.D. ± 13 mm Hg and the mean CO2 tension 37 S.D. ± 7 mm Hg. The mean rectal temperature was 36.2 S.D. ± 0.7°C. Arterial pressure tracings recorded during, and in the recovery period following, a 10% reduction in blood volume suggest that vasomoter baroreceptor responses to a reduction in pulse pressure are not very active during the first 2 days of life. Cardiac responses are more active. In contrast to the adult, passive tipping of the newborn infant into the head-up position caused little change in the inferior vena cava pressure or in the arterial pressure. An increase in intratracheal pressure of 7-10 cm H2O caused immediate bradycardia. Frequently the heart rate was halved but little fall in mean pressure occurred over 10 seconds. Breathing hypoxic mixtures caused hypotension and tachycardia. Hypotension was observed with no change in heart rate when the arterial CO2 was raised simultaneously. Differences in blood volume distribution, and the relative size of the circulatory beds under reflex and chemical control, possibly share with the apparent unresponsiveness of the peripheral vessels in causing the differences in responses observed between the infant and the adult.

Central nervous system cardiovascular effects of bombesin in conscious rats

1985 ◽  
Vol 248 (4) ◽  
pp. H425-H431 ◽  
Author(s):  
L. A. Fisher ◽  
C. R. Cave ◽  
M. R. Brown
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Circulation ◽  
Alpha Adrenergic Receptors ◽  
The Central Nervous System ◽  
Atropine Methyl Nitrate

The effects of intracerebroventricular administration of bombesin on mean arterial pressure and heart rate were studied in conscious, freely moving rats. Injection of bombesin produced dose-dependent elevations of mean arterial pressure and reductions of heart rate. These effects were not caused by leakage of bombesin into the peripheral circulation. Adrenalectomy abolished the pressor action of bombesin but did not alter bombesin-induced bradycardia. Systemic phentolamine pretreatment prevented bombesin-induced changes of mean arterial pressure, whereas rats treated intravenously with captopril or a vasopressin antagonist still exhibited pressor responses to bombesin administration. Bombesin-induced bradycardia was partially antagonized by intravenous atropine methyl nitrate administration, whereas systemic injections of propranolol did not modify this response. It is concluded that bombesin acts within the central nervous system to elevate mean arterial pressure through an adrenal-dependent mechanism involving alpha-adrenergic receptors and to reduce heart rate through an adrenal-independent mechanism involving, at least in part, cardiac parasympathetic nervous activation.

V1 vs. combined V1+V2 vasopressin blockade after hemorrhage in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1325-H1329
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Conscious Dogs ◽  
Hemodynamic Changes ◽  
Significant Difference ◽  
V2 Antagonist

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.

Altered heart rate-arterial pressure relation during head-out water immersion in conscious dog

1988 ◽  
Vol 254 (4) ◽  
pp. R595-R601 ◽  
Author(s):  
H. Yoshino ◽  
D. C. Curran-Everett ◽  
S. K. Hong ◽  
J. A. Krasney
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Inferior Vena ◽  
Water Immersion ◽  
Vena Cava ◽  
Systolic Arterial Pressure ◽  
Baroreflex Control ◽  
Rate Range ◽  
Average Gain ◽  
Cholinergic Regulation

The influence of head-out water immersion (WI) (37 degrees C) on baroreflex control of heart rate was studied in five trained, instrumented, conscious dogs. Arterial pressure was raised and lowered using occluder cuffs implanted around the aorta and inferior vena cava. Function curves relating transmural systolic arterial pressure (TSAP = systolic arterial pressure-pleural pressure) to heart rate (HR) were constructed to compare responses in air and during WI. The resting TSAP in air [142 +/- 8 mmHg (mean +/- SE) at 78 +/- 6 beats/min] increased significantly during WI (161 +/- 9 mmHg at 109 +/- 9 beats/min). During WI, the saturation TSAP at the bradycardia plateau of the relation increased significantly, by 19 mmHg, whereas the average gain (slope) of the relation decreased significantly, from -1.426 to -0.752 beats.min-1.mmHg-1. Therefore, WI elicits both a resetting and a decrease of the average gain of the TSAP-HR relation. The heart rate range increased during WI as well. After cholinergic blockade with atropine, WI did not elicit a resetting of the relation and the change in average gain was abolished. However, after beta 1-blockade with metoprolol, the resting TSAP increased significantly during WI and resetting persisted, but the decrease of average gain was abolished. Therefore, the alteration of the TSAP-HR relation in WI is achieved via a modulation of both adrenergic and cholinergic regulation of HR.

Effect of hypoxic hypoxia on systemic vasculature

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Drainage ◽  
Hypoxic Hypoxia ◽  
Venous Compliance ◽  
Flow Curves ◽  
Pressure Flow

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.

Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H815-H822 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Cervical Vagotomy ◽  
Curve Upward ◽  
Sinus Pressure

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

Combined neurohumoral block modulates pulmonary vascular P/Q relationship in conscious dogs

1988 ◽  
Vol 255 (5) ◽  
pp. H1084-H1090
Author(s):  
H. S. Geller ◽  
D. P. Nyhan ◽  
H. M. Goll ◽  
P. W. Clougherty ◽  
B. B. Chen ◽  
...  
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Vascular Response ◽  
Cyclooxygenase Inhibition ◽  
Pulmonary Vasodilation ◽  
Vascular Regulation ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Vasodilator ◽  
Pathway Inhibition

Our objective was to investigate the integrated pulmonary vascular response of conscious dogs to combined inhibition of the autonomic nervous system, arginine vasopressin (V1) receptors (vasopressinergic V1), and converting enzyme to identify the overall influence of these three major neurohumoral mechanisms in vascular regulation of the pulmonary circulation. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were generated by graded constriction of the thoracic inferior vena cava, which produced stepwise decreases in Q. When compared with the P/Q relationship measured in intact conscious dogs, combined neurohumoral block resulted in active, nonflow-dependent pulmonary vasodilation. A second objective was to assess the extent to which cyclooxygenase pathway inhibition modified both the intact P/Q relationship and the pulmonary vasodilator response to combined neurohumoral block. Cyclooxygenase inhibition alone (either indomethacin or sodium meclofenamate) resulted in active, nonflow-dependent pulmonary vasoconstriction. Moreover, the pulmonary vasodilation in response to combined neurohumoral block was entirely abolished following cyclooxygenase inhibition. Thus the integrated pulmonary vascular response of conscious dogs to combined neurohumoral block is active vasodilation. This response appears to be mediated by metabolites of the cyclooxygenase pathway.

Prostaglandin D2 inhibits hypoxic pulmonary vasoconstriction in neonatal lambs

1983 ◽  
Vol 54 (6) ◽  
pp. 1585-1589 ◽  
Author(s):  
J. B. Philips ◽  
R. K. Lyrene ◽  
M. McDevitt ◽  
W. Perlis ◽  
C. Satterwhite ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Inferior Vena ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Vena Cava ◽  
Systemic Arterial Pressure ◽  
Prostaglandin D2 ◽  
Pulmonary Vasoconstriction ◽  
Neonatal Lambs

Intrapulmonary injections of prostaglandin D2 (PGD2) reduce pulmonary arterial pressure and resistance in fetal and hypoxic neonatal lambs without affecting systemic arterial pressure. This apparently specific pulmonary effect of PGD2 could be explained by inactivation of the agent during passage through the pulmonary capillary bed. We therefore studied the effects of both pulmonary and systemic infusions of PGD2 on the acute vascular response to a 1-min episode of hypoxia in newborn lambs. Since PGD2 has been reported to be a pulmonary vasoconstrictor in normoxic lambs, we also evaluated its effects during normoxemia. Pulmonary vascular pressures were not affected by either 1- or 10-micrograms . kg-1 . min-1 infusions into the left atrium or inferior vena cava during normoxia. Infusion of 1 microgram . kg-1 . min-1 PGD2 into the inferior vena cava decreased pulmonary vascular resistance and increased systemic arterial pressure. These two parameters were unchanged with the other three infusion regimens. Mean pulmonary vascular resistance rose 83% with hypoxia and no PGD2. PGD2 prevented any change in pulmonary vascular resistance with hypoxia, while systemic arterial pressure increased (1-microgram . kg-1 . min-1 doses) or was unchanged. Thus PGD2 specifically prevents hypoxic pulmonary vasoconstriction while maintaining systemic pressures, regardless of infusion site. PGD2 may be indicated in treatment of persistent pulmonary hypertension of the newborn and other pulmonary hypertensive disorders.

Prostacyclin reduces "preload" in conscious dogs via a vagal reflex mechanism

1987 ◽  
Vol 253 (6) ◽  
pp. H1477-H1483
Author(s):  
D. M. Nganele ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Reflex Mechanism ◽  
Capacitance Vessels ◽  
Preload Reduction ◽  
Cardiopulmonary Receptors ◽  
Electrical Pacing

The purpose of this study was to determine the effects of prostacyclin on left ventricular (LV) preload in conscious dogs. LV end-diastolic diameter (LV EDD) was used as an index of preload. Because prostacyclin reduces arterial pressure, data were sampled when mean arterial pressure, heart rate, and first derivative of LV pressure (dP/dt) had returned to control levels. There was no dose-response relationship in the preload reduction to prostacyclin, the threshold dose being 0.1 microgram/kg. Intravenous prostacyclin (2.0 micrograms/kg) reduced LV EDD 2.9 +/- 0.5% from 36 +/- 2.2 mm, (P less than 0.01). With heart rate held constant (146 +/- 2.5 beats/min) by electrical pacing, prostacyclin still reduced LV EDD by 4.0 +/- 1.0% from 32 +/- 2.5 mm (P less than 0.05). Intravenous administration of arachidonic acid (500 micrograms/kg) gave similar results. The magnitude of the preload response to prostacyclin was similar to that of nitroglycerin (25 micrograms/kg). Prazosin (1 mg/kg) or bilateral cervical vagal section completely abolished the preload response to prostacyclin but not to nitroglycerin. We, therefore, propose a mechanism where prostacyclin activates cardiopulmonary receptors with vagal afferents that results in a withdrawal of peripheral sympathetic tone to capacitance vessels to reduce preload, in contrast to nitroglycerin, whose mechanism of action is most probably a direct effect on capacitance vessels.

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