HALOTHANE ANESTHESIA CAUSES ACTIVE PULMONARY VASOCONSTRICTION COMPARED TO THAT MEASURED IN CONSCIOUS DOGS

1988 ◽  
Vol 69 (3A) ◽  
pp. A799-A799
Author(s):  
B. B. Chen ◽  
D. P. Nyhan ◽  
H. M. Goll ◽  
D. M. Fehr ◽  
P. A. Murray
Keyword(s):  
Conscious Dogs ◽  
Halothane Anesthesia ◽  
Pulmonary Vasoconstriction

Anesthesia alters pulmonary vasoregulation by angiotensin II and captopril

1992 ◽  
Vol 72 (2) ◽  
pp. 636-642 ◽  
Author(s):  
D. P. Nyhan ◽  
B. B. Chen ◽  
D. M. Fehr ◽  
P. Rock ◽  
P. A. Murray
Keyword(s):  
Angiotensin Ii ◽  
Conscious Dogs ◽  
Angiotensin Converting Enzyme Inhibition ◽  
General Anesthetic ◽  
Halothane Anesthesia ◽  
Pentobarbital Sodium ◽  
Measured Range ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial

We investigated the effects of an intravenous (pentobarbital sodium) and inhalational (halothane) general anesthetic on the pulmonary vascular responses to angiotensin II and angiotensin-converting enzyme inhibition (CEI). Multipoint pulmonary vascular pressure-flow (P/Q) plots were generated in conscious pentobarbital- (30 mg/kg iv) and halothane-anesthetized (approximately 1.2% end-tidal) dogs in the intact (no drug) condition, during angiotensin II administration (60 ng.kg-1.min-1 iv), and during CEI (captopril 1 mg/kg plus 1 mg.kg-1.h-1 iv). In conscious dogs, angiotensin II increased (P less than 0.001) the pulmonary vascular pressure gradient [pulmonary arterial pressure--pulmonary arterial wedge pressure (PAP-PAWP)] over the empirically measured range of Q; i.e., angiotensin II caused pulmonary vasoconstriction. Pulmonary vasoconstriction (P less than 0.01) in response to angiotensin II was also observed during pentobarbital sodium anesthesia. In contrast, angiotensin II had no effect on the P/Q relationship during halothane anesthesia. In conscious dogs, CEI decreased (P less than 0.001) PAP-PAWP over the empirically measured range of Q; i.e., CEI caused pulmonary vasodilation. However, CEI caused pulmonary vasoconstriction (P less than 0.02) during pentobarbital sodium and had no effect on the P/Q relationship during halothane. Thus, compared with the conscious state, the pulmonary vasoconstrictor response to angiotensin II is unchanged or abolished, and the pulmonary vasodilator response to CEI is reversed to vasoconstriction or abolished during pentobarbital sodium and halothane anesthesia, respectively.

Halothane anesthesia causes active flow-independent pulmonary vasoconstriction

1990 ◽  
Vol 259 (1) ◽  
pp. H74-H83
Author(s):  
B. B. Chen ◽  
D. P. Nyhan ◽  
D. M. Fehr ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Vena Cava ◽  
Conscious State ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Halothane Anesthesia ◽  
Controlled Ventilation ◽  
Pulmonary Vasoconstriction ◽  
Neurohumoral Activation ◽  
Active Flow

We utilized multipoint pulmonary vascular pressure-flow (P/Q) plots to investigate the effects of halothane anesthesia on the pulmonary circulation. Our first objective was to assess the extent to which the P/Q relationship measured in conscious dogs is altered during halothane anesthesia. P/Q plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q. Compared with conscious dogs, halothane (approximately 1.2% end-tidal) resulted in active, flow-independent pulmonary vasoconstriction (P less than 0.01) at all levels of Q. Halothane also decreased (P less than 0.01) systemic arterial pressure and Q. Thus our second objective was to determine whether the halothane-induced pulmonary vasoconstriction was mediated by reflex neurohumoral activation or by metabolites of the cyclooxygenase pathway. However, the magnitude of halothane-induced pulmonary vasoconstriction was not significantly reduced by sympathetic alpha-adrenoreceptor block, angiotensin converting-enzyme inhibition, combined arginine vasopressin V1 + V2 receptor block, or by cyclooxygenase inhibition. Finally, halothane-induced pulmonary vasoconstriction (P less than 0.01) was also observed when compared with pentobarbital-anesthetized dogs during controlled ventilation. Thus, compared with the conscious state, halothane anesthesia causes active flow-independent pulmonary vasoconstriction that is not mediated by reflex neurohumoral activation, by metabolites of the cyclooxygenase pathway, nor is it due to the effects of general anesthesia and controlled ventilation.

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.

Pentobarbital anesthesia modifies pulmonary vasoregulation after hypoperfusion

1988 ◽  
Vol 255 (3) ◽  
pp. H569-H576
Author(s):  
B. B. Chen ◽  
D. P. Nyhan ◽  
H. M. Goll ◽  
P. W. Clougherty ◽  
D. M. Fehr ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Adrenergic Receptor ◽  
Conscious State ◽  
Conscious Dogs ◽  
Mixed Venous Blood ◽  
Vascular Response ◽  
Beta Adrenergic ◽  
Pentobarbital Anesthesia ◽  
Pulmonary Vasoconstriction ◽  
Receptor Block

Our objectives were 1) to investigate the extent to which the pulmonary vascular response to increasing cardiac index after a period of hypotension and hypoperfusion (defined as reperfusion) measured in conscious dogs is altered during pentobarbital sodium anesthesia, and 2) to determine whether pentobarbital anesthesia modifies autonomic nervous system (ANS) regulation of the pulmonary circulation during reperfusion. Base-line and reperfusion pulmonary vascular pressure-cardiac index (P/Q) plots were generated by stepwise inflation and deflation, respectively, of an inferior vena caval occluder to vary Q in conscious and pentobarbital-anesthetized (30 mg/kg iv) dogs. During pentobarbital anesthesia, controlled ventilation (without positive end-expiratory pressure) allowed matching of systemic arterial and mixed venous blood gases to conscious values. Marked pulmonary vasoconstriction (P less than 0.01) was observed during reperfusion in pentobarbital-anesthetized but not in conscious dogs. Both sympathetic alpha-adrenergic receptor block and total ANS ganglionic block attenuated, but did not abolish, the pulmonary vasoconstriction during reperfusion in pentobarbital-anesthetized dogs. Neither sympathetic beta-adrenergic receptor block nor cholinergic receptor block enhanced the magnitude of the pulmonary vasoconstrictor response to reperfusion during pentobarbital anesthesia. Thus, in contrast to the conscious state, the pulmonary vascular response to reperfusion is characterized by active, non-flow-dependent pulmonary vasoconstriction during pentobarbital anesthesia. This response is primarily, but not exclusively, mediated by sympathetic alpha-adrenergic vasoconstriction and is not offset by either sympathetic beta-adrenergic or cholinergic vasodilation. These results indicate, that, compared with the conscious state, pentobarbital anesthesia modifies pulmonary vasoregulation, during reperfusion following hypotension and hypoperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute and chronic pulmonary vasoconstriction after left lung autotransplantation in conscious dogs

1992 ◽  
Vol 73 (2) ◽  
pp. 603-609 ◽  
Author(s):  
P. A. Murray ◽  
R. S. Stuart ◽  
C. D. Fraser ◽  
D. M. Fehr ◽  
B. B. Chen ◽  
...  
Keyword(s):  
Left Lung ◽  
Blood Gases ◽  
Conscious Dogs ◽  
Specific Effects ◽  
Vascular Regulation ◽  
Post Surgery ◽  
Pulmonary Vasoconstriction ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Active Flow

We investigated the acute and chronic effects of left lung autotransplantation (LLA) on the left pulmonary vascular pressure-flow (LP/Q) relationship in conscious dogs. Continuous LP/Q plots were generated in chronically instrumented conscious dogs 2 days, 2 wk, 1 mo, and 2 mo after LLA. Identically instrumented normal conscious dogs were studied at equal time points post-surgery. LLA had little or no effect on baseline systemic hemodynamics or blood gases. In contrast, compared with normal conscious dogs, striking active flow-independent pulmonary vasoconstriction was observed 2 days post-LLA. The slope of the LP/Q relationship was increased from a normal value of 0.275 +/- 0.021 to 0.699 +/- 0.137 mmHg.ml-1.min-1.kg-1 2 days post-LLA. Pulmonary vasoconstriction of similar magnitude was also observed on a chronic basis at 2 wk, 1 mo, and even 2 mo post-LLA. Pulmonary vasoconstriction post-LLA was not due to fixed resistance at the left pulmonary arterial or venous anastomotic sites. Finally, systemic arterial blood gases were unchanged when total pulmonary blood flow was directed to exclusively perfuse the transplanted left lung. Thus, LLA results in both acute and chronic pulmonary vasoconstriction in conscious dogs. LLA should serve as a useful stable experimental model to assess the specific effects of surgical transplantation on pulmonary vascular regulation.

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.

scholarly journals Halothane anesthesia does not suppress sympathetic activation produced by neuroglucopenia

1987 ◽  
Vol 252 (5) ◽  
pp. E667-E672 ◽  
Author(s):  
P. J. Havel ◽  
D. E. Flatness ◽  
J. B. Halter ◽  
J. D. Best ◽  
R. C. Veith ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Endocrine Pancreas ◽  
Conscious Dogs ◽  
Sympathetic Activation ◽  
Plasma Epinephrine ◽  
Halothane Anesthesia ◽  
Pentobarbital Sodium ◽  
Sympathetic Response ◽  
Sympathetic Control ◽  
Anesthetized Dogs

To determine the suitability of halothane anesthesia for studies of sympathetic control of the endocrine pancreas in dogs, we assessed the effect of halothane anesthesia (0.8% inspired concentration) on the sympathetic response to central neuroglucopenia. In dogs anesthetized with halothane, intravenous administration of the neuroglucopenic agent, 2-deoxy-D-glucose (2-DG; 100 mg/kg), produced increases of both systemic plasma epinephrine (EPI; delta = 269 +/- 86 pg/ml, P less than 0.025) and norepinephrine (NE; delta = 157 +/- 55 pg/ml, P less than 0.025) equivalent to those previously observed in conscious dogs. Measurement of plasma NE kinetics revealed that the plasma NE response to 2-DG during halothane was due to an increase in the rate of NE appearance that was identical to that of conscious dogs, rather than to an impairment of NE clearance. In contrast, 2-DG at this dose did not increase plasma EPI or NE levels in dogs anesthetized with pentobarbital sodium (30 mg/kg). Plasma glucose increased modestly after 2-DG (100 mg/kg) in both conscious and halothane-anesthetized dogs but not in the pentobarbital-anesthetized dogs. Although 2-DG at a threefold higher dose (300 mg/kg) caused plasma EPI, NE, and glucose (delta = 12 +/- 3 mg/dl, P less than 0.001) to increase in pentobarbital-anesthetized dogs, the responses to this higher dose of 2-DG were all significantly larger in halothane-anesthetized dogs (delta of plasma glucose = 30 +/- 8 mg/dl, P less than 0.005; P less than 0.0025 vs. pentobarbital).(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic nervous system pulmonary vasoregulation after hypoperfusion in conscious dogs

1988 ◽  
Vol 254 (5) ◽  
pp. H976-H983
Author(s):  
P. W. Clougherty ◽  
D. P. Nyhan ◽  
B. B. Chen ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Cardiac Index ◽  
Cholinergic Receptor ◽  
Conscious Dogs ◽  
Base Line ◽  
Beta Adrenergic ◽  
Autonomic Nervous ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasoconstriction

We investigated the role of the autonomic nervous system (ANS) in the pulmonary vascular response to increasing cardiac index after a period of hypoperfusion (defined as reperfusion) in conscious dogs. Base-line and reperfusion pulmonary vascular pressure-cardiac index (P/Q) plots were generated by stepwise constriction and release, respectively, of an inferior vena caval occluder to vary Q. Surprisingly, after 10-15 min of hypoperfusion (Q decreased from 139 +/- 9 to 46 +/- 3 ml.min-1.kg-1), the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) was unchanged over a broad range of Q during reperfusion compared with base line when the ANS was intact. In contrast, pulmonary vasoconstriction was observed during reperfusion after combined sympathetic beta-adrenergic and cholinergic receptor block, after beta-block alone, but not after cholinergic block alone. The pulmonary vasoconstriction during reperfusion was entirely abolished by combined sympathetic alpha- and beta-block. Although sympathetic alpha-block alone caused pulmonary vasodilation compared with the intact, base-line P/Q relationship, no further vasodilation was observed during reperfusion. Thus the ANS actively regulates the pulmonary circulation during reperfusion in conscious dogs. With the ANS intact, sympathetic beta-adrenergic vasodilation offsets alpha-adrenergic vasoconstriction and prevents pulmonary vasoconstriction during reperfusion.

Neurohumoral regulation of the pulmonary circulation during circulatory hypotension in conscious dogs

1993 ◽  
Vol 75 (4) ◽  
pp. 1675-1682 ◽  
Author(s):  
W. P. Peterson ◽  
G. A. Trempy ◽  
K. Nishiwaki ◽  
D. P. Nyhan ◽  
P. A. Murray
Keyword(s):  
Angiotensin Ii ◽  
Muscarinic Receptor ◽  
Arginine Vasopressin ◽  
Pulmonary Circulation ◽  
Vena Cava ◽  
Receptor Activation ◽  
Conscious Dogs ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Vasodilator ◽  
Receptor Block

We investigated the effects of circulatory hypotension (HYPO) on the left pulmonary vascular pressure-flow relationship in chronically instrumented conscious dogs and the role of five neurohumoral mechanisms in either mediating or modulating the response to this stimulus. HYPO was induced by acute (approximately 15-min) inflation of a hydraulic occluder implanted around the thoracic inferior vena cava, which decreased systemic arterial pressure to approximately 55 mmHg. HYPO resulted in active pulmonary vasoconstriction (53–66%; P < 0.01) in intact conscious dogs. Sympathetic alpha 1-adrenoreceptor block reduced (P < 0.01) the magnitude of HYPO-induced pulmonary vasoconstriction by 91–99%. Neither sympathetic beta-adrenoreceptor block nor cholinergic muscarinic receptor block had any significant effect on the magnitude of HYPO-induced pulmonary vasoconstriction. Surprisingly, angiotensin II receptor block increased (P < 0.05) HYPO-induced pulmonary vasoconstriction by 69–91%. In contrast, arginine vasopressin V1-receptor block reduced (P < 0.05) HYPO-induced pulmonary vasoconstriction by 34–41%. These results indicate that the pulmonary circulation of intact conscious dogs is actively regulated by three distinct neurohumoral mechanisms during HYPO. Sympathetic alpha 1-adrenoreceptor activation is the primary mediator of HYPO-induced pulmonary vasoconstriction. Angiotensin II and arginine vasopressin exert opposing pulmonary vasodilator and vasoconstrictor effects during HYPO, whereas sympathetic beta-adrenoreceptor and cholinergic muscarinic receptor activation do not appear to modulate the pulmonary vascular response to HYPO.

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