PULMONARY VASCULAR RESPONSE TO CYCLOOXYGENASE PATHWAY INHIBITION MEASURED IN CONSCIOUS DOGS IS MODIFIED DURING PENTOBARBITAL ANESTHESIA

1988 ◽  
Vol 69 (3A) ◽  
pp. A127-A127
Author(s):  
D. P. Nyhan ◽  
B. B. Chen ◽  
D. M. Fehr ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Conscious Dogs ◽  
Vascular Response ◽  
Pentobarbital Anesthesia ◽  
Pathway Inhibition

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)

scholarly journals PULMONARY VASCULAR RESPONSE TO INCREASING CARDIAC INDEX FOLLOWING SYSTEMIC HYPOTENSION IS MODIFIED BY PENTOBARBITAL ANESTHESIA

1987 ◽  
Vol 21 (4) ◽  
pp. 205A-205A
Author(s):  
Daniel P Nyhan ◽  
Bessie B Chen ◽  
Harold M Coll ◽  
Patrick W Clougherty ◽  
Paul A Murray
Keyword(s):  
Cardiac Index ◽  
Vascular Response ◽  
Systemic Hypotension ◽  
Pentobarbital Anesthesia

Episodic secretion of parathyroid hormone in the dog

1981 ◽  
Vol 241 (3) ◽  
pp. E171-E177
Author(s):  
J. Fox ◽  
K. P. Offord ◽  
H. Heath
Keyword(s):  
Spectral Analysis ◽  
Parathyroid Hormone ◽  
Conscious Dogs ◽  
Blood Samples ◽  
Pentobarbital Anesthesia ◽  
Ipth Concentration

This study was designed to determine whether parathyroid hormone (PTH) is secreted episodically, to characterize any such rhythms, and to see whether the rhythms can be altered by stimulating PTH secretion using constant hypocalcemia. We collected blood samples at 1-min intervals for 1 h from the precava or postcava of conscious dogs during normocalcemia or induced, constant hypocalcemia. In two anesthetized normocalcemic dogs we catheterized a caudal thyroid vein and collected all the effluent blood in 1-min fractions. Immunoreactive PTH (IPTH) concentrations were determined in quadruplicate, and the results were subjected to spectral analysis. In both the precava and postcava of normocalcemic dogs, there were regular oscillations in IPTH levels with a period of 12 min (range, 10–15 min) and a +/- 14% variation about the overall mean. Although significant two- to fourfold changes in IPTH levels still occurred during constant hypocalcemia, there was no significant rhythmicity. Significant cycles in IPTH concentration (mean 8.4-min period) were observed in thyroid venous effluent plasma during normocalcemia, confirming that the phenomenon represented episodic secretion that was not affected by pentobarbital anesthesia.

Role of EDRF/NO in parasympathetic coronary vasodilation following carotid chemoreflex activation in conscious dogs

1994 ◽  
Vol 267 (2) ◽  
pp. H605-H613 ◽  
Author(s):  
W. Shen ◽  
M. Ochoa ◽  
X. Xu ◽  
J. Wang ◽  
T. H. Hintze
Keyword(s):  
Vagus Nerve ◽  
Conscious Dogs ◽  
Coronary Resistance ◽  
Vascular Response ◽  
Coronary Vasodilation ◽  
Relaxing Factor ◽  
Anesthetized Dogs ◽  
Endothelium Derived Relaxing Factor ◽  
Stimulation Of

The role of endothelium-derived relaxing factor (EDRF) in parasympathetic coronary vasodilation following carotid chemoreflex activation induced by nicotine in conscious dogs and stimulation of the vagus nerve in anesthetized dogs was studied. Injection of nicotine (11 +/- 4 micrograms) into the carotid artery increased coronary blood flow (CBF) by 126 +/- 16% from 28 +/- 3 ml/min and reduced late diastolic coronary resistance (LDCR) by 43 +/- 4% from 3.58 +/- 0.52 mmHg.ml-1.min, accompanied by a significant increase in mean arterial pressure and a decrease in heart rate (all P < 0.01). Pacing and propranolol did not change the coronary vascular response to chemoreflex activation. There were still increases in CBF by 113 +/- 17% from 29 +/- 3 ml/min and decreases in LDCR by 41 +/- 5% from 3.13 +/- 0.52 mmHg.ml-1.min (all P < 0.01). After infusion of N omega-nitro-L-arginine (L-NNA) (30 mg/kg), the increase in CBF following chemoreflex activation was only 23 +/- 3% from 37 +/- 3 ml/min, and the fall in LDCR was 19 +/- 3% from 3.09 +/- 0.51 mmHg.ml-1.min. Stimulation of the vagus nerve showed a relationship between stimulation frequency and coronary vasodilation that was significantly inhibited by L-NNA. Thus EDRF plays an important role in mediating parasympathetic coronary vasodilation during chemoreflex activation and perhaps during many reflexes that cause vagal cholinergic vasodilation in the heart.

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.

scholarly journals Effects of Experimentally Produced Heart Failure on the Peripheral Vascular Response to Severe Exercise in Conscious Dogs

1972 ◽  
Vol 31 (2) ◽  
pp. 186-194 ◽  
Author(s):  
Charles B. Higgins ◽  
Stephen F. Vatner ◽  
Dean Franklin ◽  
Eugene Braunwald
Keyword(s):  
Heart Failure ◽  
Conscious Dogs ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Severe Exercise

AVP-induced pulmonary vasodilation during specific V1 receptor block in conscious dogs

1987 ◽  
Vol 253 (3) ◽  
pp. H493-H499
Author(s):  
D. P. Nyhan ◽  
P. W. Clougherty ◽  
P. A. Murray
Keyword(s):  
Vena Cava ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Conscious Dogs ◽  
Beta Adrenergic ◽  
Pulmonary Vasodilation ◽  
Vasodilator Response ◽  
Pulmonary Vasodilator ◽  
Receptor Block ◽  
Pathway Inhibition

Our objectives were 1) to determine whether exogenously administered arginine vasopressin (AVP) can exert a vasoactive influence on the pulmonary circulation of conscious dogs during specific vasopressinergic-1 (V1) receptor block, and 2) to assess the extent to which the pulmonary vascular response to AVP during V1 receptor block is mediated by either sympathetic beta-adrenergic or cholinergic receptor activation or by cyclooxygenase pathway activation. 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 to reduce Q. In dogs pretreated with a specific V1 receptor antagonist [d(CH2)5 AVP, 10 micrograms/kg iv], AVP infusion (7.6 ng.kg-1 X min-1 iv) increased (P less than 0.01) Q from 139 +/- 6 to 175 +/- 8 ml.min-1 X kg-1, and decreased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure: PAP-PCWP) over the entire range of Q studied (140 to 80 ml.min-1 X kg-1). This pulmonary vasodilator response to AVP during V1 block was also observed following sympathetic beta-adrenergic block alone, following combined sympathetic beta-adrenergic and cholinergic block, and following cyclooxygenase pathway inhibition. Thus exogenous administration of AVP during specific V1 receptor block results in active, nonflow-dependent pulmonary vasodilation. This pulmonary vasodilator response is not mediated by reflex activation of sympathetic beta-adrenergic or cholinergic receptors or by metabolites of the cyclooxygenase pathway over a broad range of Q.

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