Effects of Splenectomy and Beta-Adrenoceptor Blockade on Cardiac Output Response to Acute Hypoxemia

Liang, Chang‐seng; Huckabee, William E.

doi:10.1172/jci107512

Cited by 8 publications

(12 citation statements)

References 18 publications

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“…Similarly, it decreases during severe hypoxia, probably a result of adrenergic stimulation (40). The increases in cardiac output and myocardial contractility during hypoxia probably are related to autoregulation ofthe peripheral vascular beds (41) and stimulation of the sympathetic nervous system (1,28,42,43). Results of the present study suggest that the systemic hemodynamic effects of hypoxia probably are not causally related to the accumulation of glycolytic metabolites or of other metabolites which are also affected by fluoroacetate.…”

Section: Resultsmentioning

confidence: 61%

“…Similarly, it is known that a shift from fatty acid oxidation to increased glycolysis occurs during hypoxia (22)(23)(24), probably partly because of the highly accelerated activity of phosphofructokinase (23) relative to that of thiokinase. However, neither total body nor myocardial oxygen consumption changes significantly in intact animals during mild to moderately severe hypoxia (25)(26)(27)(28), partly because the increased flow compensates for the reduction in arterial oxygen content (26). Likewise, oxygen consumption did not change after fluoroacetate administration in the present experiments.…”

Section: Resultsmentioning

confidence: 99%

“…Adult male dogs weighing [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31] kg after overnight fast were anesthetized with intravenous chloralose (60 mg/kg) after induction with vaporized halothane (Fluothane, Ayerst Laboratories, New York). The trachea was cannulated with a T-tube connected to a Benedict-Roth spirometer filled with 100% oxygen to record the rate of oxygen consumption.…”

Section: Methodsmentioning

confidence: 99%

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Metabolic control of circulation. Effects of iodoacetate and fluoroacetate.

Liang¹

1977

J. Clin. Invest.

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A B S T R A C T The circulatory effects of selective metabolic inhibition of glycolysis and of the tricarboxylic acid cycle by iodoacetate and fluoroacetate were studied in intact chloralose-anesthetized dogs. Pulmonary arterial blood pressure and vascular resistance increased after administration of both inhibitors, but neither systemic hemodynamics nor myocardial contractility changed significantly. Coronary blood flow did not change after iodoacetate administration but increased four-to fivefold after fluoroacetate. Administration of normal saline had no effect on any of the parameters. The changes in pulmonary arterial blood pressure and coronary blood flow after fluoroacetate were not mediated via the autonomic nerves or adrenergic neurohumors because they still occurred after autonomic nervous system inhibition. Neither myocardial oxygen consumption nor left ventricular work changed. A selective increase in myocardial blood flow also occurred in conscious dogs after fluoroacetate administration; hepatic artery flow was reduced, but other organ flows did not change significantly. These results indicate that pulmonary pressor and coronary dilator effects may be produced in intact dogs by selective metabolic blockade, in the absence of reduced oxygen supply or impairment in the electron transport system. These results also suggest that the increases in pulmonary arterial blood pressure, coronary blood flow, and cardiac output that occur during hypoxia probably are related to separate metabolic events in the tissue.

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Section: Resultsmentioning

confidence: 61%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Metabolic control of circulation. Effects of iodoacetate and fluoroacetate.

Liang¹

1977

J. Clin. Invest.

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“…We did not investigate the possible role played by the spleen in augmenting the CO increase during hypoxia. Splenic contraction contributes to increased CO by increasing effective blood volume and cardiac filling pressures (Liang and Huckabee, 1973), but how this might have been altered by autonomic blockade was not evaluated. Histological evidence suggests that sympathetic terminals in the spleen may be more resistant to 60HDA than those in other tissues (Kostrzewa and Jacobowitz, 1974).…”

Section: Discussionmentioning

confidence: 99%

Autonomic cardiovascular control during hypoxia in the dog.

Hammill¹,

Wagner²,

Latham³

et al. 1979

Circulation Research

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SUMMARYThe mechanisms controlling cardiovascular responses to hypoxia are poorly understood. We studied effects of parasympathetdc blockade by atropine (Px) and sympathectomy by adrenalectomy plus 6-hydroxydopamine (Sx) in five unanesthetdzed dogs acutely exposed to hypoxic conditions (Paoi -35 mm Hg). In intact dogs during hypoxia, heart rate increased by 55 ± 10 (SEM) beats/min. After either Px or Sx, heart rate increased by only 34 ± 4 beats/min during hypoxia. Combined Sx and Px abolished the heart rate response to hypoxia. In intact dogs, hypoxia decreased stroke volume by 6 ± 1 ml. After Sx, hypoxia still decreased stroke volume (5 ± 1 ml), but stroke volume increased during Px (5 ± 2 ml). The stroke volume response was eliminated by Sx plus Px. Cardiac output increased during hypoxia alone (1.2 ± 0.2 liters/min) and in the presence of Px (2.0 ± 0.5 liters/min) and Sx (0.8 ± 0.3 liter/min); this response was abolished by Sx plus Px. Systemic arterial pressure increased during hypoxia alone (16 ± 4 mm Hg) and in the presence of Px (21 ± 7 mm Hg), but failed to change during either Sx or Sx plus Px. Total systemic vascular resistance fell during hypoxia alone (5 ± 2 mm Hg/ liter per min) and in the presence of Px (3 ± 1 mm Hg/liter per min and Sx (5 ± 2 mm Hg/liter per min), but failed to fall during Sx plus Px. We conclude that the autonomic nervous system plays a major role in mediating these cardiovascular systemic responses to hypoxia. The pattern of responses suggests that sympathetic activity increases heart rate, stroke volume, cardiac output, and blood pressure during hypoxia. whereas decreased parasympathetic activity increases heart rate and cardiac output and decreases stroke volume. If both components of the autonomic system are blocked, the systemic hypoxic response is eliminated. Ore Res 44: 569-676, 1979

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“…Recently one of us has demonstrated that this splenic substance plays an important role in regulating the cardiac output response to generalized hypoxia (12,13). The purpose of the present study was to inves tigate the possible role of myocardial adenylate cyclase-adenosine 3',5'-monophosphate (cyclic AMP) system in the cardiac output response to generalized hypoxemia.…”

mentioning

confidence: 94%

Effects of Arterial Hypoxemia and Splenic Nerve Stimulation on Myocardial Adenosine 3,5’-Monophosphate in Dogs

Liang¹,

Volicer²

1975

Pharmacology

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Epinephrine infusion, 5-percent oxygen breathing, and splenic nerve stimulation were employed to increase cardiac output by 50–100 % in anesthetized dogs. Epinephrine infusion, as expected, increased plasma and myocardial cyclic AMP concentrations. Arterial hypoxemia increased cyclic AMP concentration in plasma but not in the heart. Practolol pretreatment abolished the increase in plasma cyclic AMP concentration and reduced the rise in cardiac output during hypoxemia. Splenic nerve stimulation was not associated with increases in either plasma or myocardial cyclic AMP. Adenylate cyclase activity was increased by addition of plasma into the incubation medium. However, splenic venous plasma obtained during splenic nerve stimulation did not increase adenylate cyclase activity more than control plasma obtained before stimulation. We conclude that the positive inotropic action of arterial hypoxemia and splenic nerve stimulation does not depend on the adenylate cyclase-cyclic AMP system.

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Effects of Splenectomy and Beta-Adrenoceptor Blockade on Cardiac Output Response to Acute Hypoxemia

Cited by 8 publications

References 18 publications

Metabolic control of circulation. Effects of iodoacetate and fluoroacetate.

Metabolic control of circulation. Effects of iodoacetate and fluoroacetate.

Autonomic cardiovascular control during hypoxia in the dog.

Effects of Arterial Hypoxemia and Splenic Nerve Stimulation on Myocardial Adenosine 3,5’-Monophosphate in Dogs

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Effects of Splenectomy and Beta-Adrenoceptor Blockade on Cardiac Output Response to Acute Hypoxemia

Cited by 8 publications

References 18 publications

Metabolic control of circulation. Effects of iodoacetate and fluoroacetate.

Metabolic control of circulation. Effects of iodoacetate and fluoroacetate.

Autonomic cardiovascular control during hypoxia in the dog.

Effects of Arterial Hypoxemia and Splenic Nerve Stimulation on Myocardial Adenosine 3,5&rsquo;-Monophosphate in Dogs

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Effects of Arterial Hypoxemia and Splenic Nerve Stimulation on Myocardial Adenosine 3,5’-Monophosphate in Dogs