Comparison of renal responses to 5% saline infusions into vena portae and vena cava in conscious dogs

1978 ◽  
Vol 374 (1) ◽  
pp. 23-29 ◽  
Author(s):  
F. W. Kapteina ◽  
W. Motz ◽  
D. Schwartz-Porsche ◽  
O. H. Gauer
Keyword(s):  
Vena Cava ◽  
Conscious Dogs ◽  
Renal Responses ◽  
Vena Portae

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.

Arterial baroreceptors control plasma vasopressin responses to graded hypotension in conscious dogs

2000 ◽  
Vol 278 (2) ◽  
pp. R469-R475 ◽  
Author(s):  
Terry N. Thrasher ◽  
Hong-Gen Chen ◽  
Lanny C. Keil
Keyword(s):  
Inferior Vena ◽  
Control Period ◽  
Vena Cava ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Inferior Vena Caval ◽  
Arterial Baroreceptors ◽  
Treatment Conditions ◽  
The Individual

We studied the role of cardiac and arterial baroreceptors in the reflex control of arginine vasopressin (AVP) and renin secretion during graded hypotension in conscious dogs. The dogs were prepared with Silastic cuffs on the thoracic inferior vena cava and catheters in the pericardial space. Each experiment consisted of a control period followed by four periods of inferior vena caval constriction, during which mean arterial pressure (MAP) was reduced in increments of ∼10 mmHg. The hormonal responses were measured in five dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD+CD. The individual slopes relating MAP to plasma AVP and plasma renin activity (PRA) were used to compare the treatment effects using a 2 × 2 factorial analysis. There was a significant ( P < 0.01) effect of SAD on the slope relating plasma AVP to MAP but no effect of CD and no SAD × CD interaction. In contrast, the slope relating PRA and MAP was increased ( P < 0.05) by SAD but was not affected by CD. These results support the hypothesis that stimulation of AVP secretion in response to graded hypotension is primarily driven by unloading arterial baroreceptors in the dog.

Pentobarbital anesthesia alters pulmonary vascular response to neural antagonists

1989 ◽  
Vol 256 (5) ◽  
pp. H1384-H1392 ◽  
Author(s):  
D. P. Nyhan ◽  
H. M. Goll ◽  
B. B. Chen ◽  
D. M. Fehr ◽  
P. W. Clougherty ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Vena Cava ◽  
Cholinergic Receptor ◽  
Conscious Dogs ◽  
Base Line ◽  
Pentobarbital Anesthesia ◽  
Pulmonary Vasodilation ◽  
Receptor Block ◽  
Pentobarbital Sodium Anesthesia ◽  
Line P

We investigated the effects of pentobarbital sodium anesthesia on vasoregulation of the pulmonary circulation. Our specific objectives were to 1) assess the net effect of pentobarbital on the base-line pulmonary vascular pressure-to-cardiac index (P/Q) relationship compared with that measured in conscious dogs, and 2) determine whether autonomic nervous system (ANS) regulation of the intact P/Q relationship is altered during pentobarbital. P/Q plots were constructed by graded constriction of the thoracic inferior vena cava, which produced stepwise decreases in Q. Pentobarbital (30 mg/kg iv) had no net effect on the base-line P/Q relationship. In contrast, changes in the conscious intact P/Q relationship in response to ANS antagonists were markedly altered during pentobarbital. Sympathetic alpha-adrenergic receptor block with prazosin caused active pulmonary vasodilation (P less than 0.01) in conscious dogs but caused vasoconstriction (P less than 0.01) during pentobarbital. Sympathetic beta-adrenergic receptor block with propranolol caused active pulmonary vasoconstriction (P less than 0.01) in both groups, but the magnitude of the vasoconstriction was attenuated (P less than 0.05) during pentobarbital at most levels of Q. Finally, cholinergic receptor block with atropine resulted in active pulmonary vasodilation (P less than 0.01) in conscious dogs, whereas vasoconstriction (P less than 0.01) was observed during pentobarbital. Thus, although pentobarbital had no net effect on the base-line P/Q relationship measured in conscious dogs, ANS regulation of the intact pulmonary vascular P/Q relationship was altered during pentobarbital anesthesia.

Sodium channel enhancer restores baroreflex sensitivity in conscious dogs with heart failure

2005 ◽  
Vol 288 (4) ◽  
pp. H1508-H1514 ◽  
Author(s):  
Weiqun Shen ◽  
Robert M. Gill ◽  
Jian-Ping Zhang ◽  
Bonita D. Jones ◽  
Angela K. Corbly ◽  
...  
Keyword(s):  
Heart Failure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Vena Cava ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Inotropic Effect ◽  
Pulse Interval ◽  
Adrenergic Blockade ◽  
Before And After

We compared the cardiac inotropic, lusitropic, and chronotropic responses to the Na+ channel enhancer LY-368052 in conscious dogs before and after development of congestive heart failure (CHF). We also examined the effect of LY-368052 on baroreflex sensitivity and the efferent neural mechanisms of the bradycardic response in heart failure. Dogs were chronically instrumented, and heart failure was induced by right ventricular pacing at 240 beats/min for 3–4 wk. LY-368052 dose-dependently increased left ventricular contractile performance before and after the development of CHF to a similar extent. The inotropic effect of LY-368052 in heart failure was not altered by either ganglionic or β-adrenergic receptor blockade. LY-368052 improved cardiac relaxation and induced bradycardia in dogs with heart failure but not in normal dogs. The negative chronotropic effect of LY-368052 was eliminated by ganglionic blockade but not β-adrenergic blockade, suggesting that the bradycardia was mediated by the autonomic nervous system via enhanced parasympathetic tone. Baroreflex sensitivity was assessed as the pulse interval-mean arterial pressure slope in response to temporary pharmacological (nitroglycerin or phenylephrine) and mechanical (brief occlusion of inferior vena cava) alterations of arterial pressure in conscious dogs before and after development of heart failure. Baroreflex sensitivity was significantly depressed in heart failure and restored completely by acute treatment with LY-368052. Thus the Na+ channel enhancer LY-368052 maintains its β-receptor-independent inotropic effect in chronic CHF and specifically improves ventricular relaxation and depressed baroreflex function.

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.

Pulmonary vasoactive effects of exogenous and endogenous AVP in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. H1009-H1016
Author(s):  
D. P. Nyhan ◽  
H. S. Geller ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Pressure ◽  
Entire Range ◽  
Enzyme Inhibitor ◽  
Vena Cava ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Similar Response ◽  
Autonomic Nervous

Our objectives were to investigate the extent to which both exogenously administered and endogenously released arginine vasopressin (AVP) exert a direct, vasoactive influence on the pulmonary circulation of conscious dogs. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by stepwise constriction of the thoracic inferior vena cava (IVC) to reduce Q. In intact dogs, AVP infusion (7.6 ng X kg-1 X min-1 iv) increased (P less than 0.01) plasma AVP from 2.3 +/- 0.4 to 280 +/- 23 pg/ml, and increased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure minus pulmonary capillary wedge pressure, PAP-PCWP) over the entire range of Q studied. Following administration of autonomic nervous system antagonists and a converting-enzyme inhibitor, exogenous AVP again increased (P less than 0.01) PAP-PCWP over the entire range of Q. Generation of P/Q plots via IVC constriction resulted in systemic hypotension (58 +/- 4 mmHg) and a concomitant increase (P less than 0.01) in endogenous AVP release from 2.1 +/- 0.2 to 109 +/- 22 pg/ml. Following administration of the specific AVP receptor antagonist [d(CH2)5]AVP (10 micrograms/kg iv), systemic arterial pressure, but not PAP - PCWP, was decreased to significantly lower levels as Q was reduced during IVC constriction. A similar response was observed in dogs pretreated with the neurohumoral blockers. Thus exogenous administration of AVP results in active, non-flow-dependent pulmonary vasoconstriction. This effect is not dependent on reflex activation of the autonomic nervous system or on the increased production of angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Halothane anesthesia abolishes pulmonary vascular responses to neural antagonists

1992 ◽  
Vol 262 (1) ◽  
pp. H117-H122 ◽  
Author(s):  
B. B. Chen ◽  
D. P. Nyhan ◽  
D. M. Fehr ◽  
P. A. Murray
Keyword(s):  
Entire Range ◽  
Vena Cava ◽  
Cholinergic Receptor ◽  
Conscious State ◽  
Conscious Dogs ◽  
Halothane Anesthesia ◽  
Pulmonary Vasodilation ◽  
Inhalational Anesthetic ◽  
Pulmonary Arterial ◽  
End Tidal

We investigated the effects of the inhalational anesthetic halothane on autonomic nervous system (ANS) regulation of the baseline pulmonary vascular pressure-flow (P/Q) relationship compared with that measured in the conscious state. Multipoint pulmonary vascular P/Q plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q. P/Q plots were generated in the same dogs in the conscious state and during halothane anesthesia (approximately 1.2% end tidal) in the intact (no drug) condition and after administration of selective ANS antagonists. In conscious dogs, sympathetic alpha 1-adrenoreceptor block with prazosin decreased (P less than 0.01) the pulmonary vascular pressure gradient [pulmonary arterial pressure-pulmonary arterial wedge pressure (PAP-PAWP)] over the entire range of Q studied; i.e., inhibition of endogenous alpha 1-adrenoreceptor activity caused pulmonary vasodilation. In contrast, alpha 1-adrenoreceptor block had no effect on PAP-PAWP at any value of Q during halothane anesthesia. In conscious dogs, sympathetic beta-adrenoreceptor block with propranolol increased (P less than 0.01) PAP-PAWP over the entire range of Q studied; i.e., inhibition of endogenous beta-adrenoreceptor activity resulted in pulmonary vasoconstriction. However, beta-adrenoreceptor block had no effect on PAP-PAWP at any value of Q during halothane anesthesia. Finally, cholinergic receptor block with atropine decreased (P less than 0.05) PAP-PAWP at values of Q greater than 100 ml.min-1.kg-1 in conscious dogs but had no effect on PAP-PAWP at any value of Q during halothane anesthesia. These results indicate that endogenous ANS regulation of the baseline pulmonary vascular P/Q relationship observed in conscious dogs is abolished during halothane anesthesia.

Bradykinin actively modulates pulmonary vascular pressure-cardiac index relationships

1987 ◽  
Vol 63 (1) ◽  
pp. 145-151 ◽  
Author(s):  
D. P. Nyhan ◽  
P. W. Clougherty ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Cardiac Index ◽  
Arterial Pressure ◽  
Pulmonary Capillary Wedge Pressure ◽  
Pulmonary Arterial Pressure ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Beta Adrenergic ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Our objectives were to investigate the pulmonary vascular effects of exogenously administered bradykinin at normal and reduced levels of cardiac index in intact conscious dogs and to assess the extent to which the pulmonary vascular response to bradykinin is the result of either cyclooxygenase pathway activation or reflex activation of sympathetic beta-adrenergic and -cholinergic receptors. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by step-wise constriction of the thoracic inferior vena cava to reduce Q. In intact dogs, bradykinin (2 micrograms X kg-1 X min-1 iv) caused systemic vasodilation, i.e., systemic arterial pressure was slightly decreased (P less than 0.05), Q was markedly increased (P less than 0.01), and mixed venous PO2 and oxygen saturation (SO2) were increased (P less than 0.01). Bradykinin decreased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) over the entire range of Q studied (140–60 ml X min-1 X kg-1) in intact dogs. During cyclooxygenase pathway inhibition with indomethacin, bradykinin again decreased (P less than 0.05) pulmonary arterial pressure-pulmonary capillary wedge pressure at every level of Q, although the magnitude of the vasodilator response was diminished at lower levels of Q (60 ml X min-1 X kg-1). Following combined administration of sympathetic beta-adrenergic and -cholinergic receptor antagonists, bradykinin still decreased (P less than 0.01) pulmonary arterial pressure-pulmonary capillary wedge pressure over the range of Q from 160 to 60 ml X min-1 X kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Multipoint pulmonary vascular pressure-cardiac output plots in conscious dogs

1985 ◽  
Vol 249 (2) ◽  
pp. H351-H357 ◽  
Author(s):  
R. F. Lodato ◽  
J. R. Michael ◽  
P. A. Murray
Keyword(s):  
Cardiac Output ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Vasomotor Tone ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Induced Changes ◽  
Arterial Po2

To characterize quantitatively the relationships among pulmonary vascular pressures (P) and cardiac output (Q) in conscious dogs, multipoint plots of pulmonary arterial (PAP), pulmonary capillary wedge (PCWP), PAP - PCWP, and left atrial (LAP) pressure versus Q were generated by graded constriction of the thoracic inferior vena cava (IVC) to vary Q. Slopes and extrapolated pressure intercepts from linear regression fits to the P/Q plots were determined for three inspired oxygen tensions: normoxia, hyperoxia, and hypoxia. During normoxia (arterial Po2 87 +/- 1 Torr), the extrapolated pressure intercepts for PAP, PCWP, and PAP - PCWP were virtually 0 mmHg, and for LAP, substantially negative (-5.5 +/- 1.1 mmHg; P less than 0.01). Hyperoxia (Po2 365 +/- 28 Torr) had no effect on any of the P/Q plots. In contrast, hypoxia (Po2 51 +/- 1 Torr) significantly increased the intercepts (P less than 0.01) as well as the slopes (P less than 0.05) of PAP and PAP - PCWP versus Q, but produced only minor changes in PCWP and LAP versus Q. These hypoxia-induced changes in intercepts, perhaps related to changes in critical closing pressures, demonstrate the limitations of pulmonary vascular resistance calculations (quotient of pressure gradient and Q) in quantifying changes in pulmonary vasomotor tone. In this way, the IVC constriction technique provides a more complete description of P/Q relationships than that permitted by simple calculations of pulmonary vascular resistance. We conclude that this technique can be utilized to investigate the effects of other physiological and pharmacological interventions on pulmonary vasomotor tone in conscious dogs.

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