Effects of myocardial hypoxia on left ventricular performance

Ng, M. L.; Levy, M. N.; Degeest, H; Zieske, Harrison

doi:10.1152/ajplegacy.1966.211.1.43

Cited by 28 publications

(5 citation statements)

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“…In our previous experiment we did not demonstrate any further increase in CI with either dopamine or epinephrine infusions during hypoxia with arterial oxygen saturation between 45% and 50% [ 9 ]. The difference in the effects of hypoxia on the responses to inotropes of cardiac output in this and the previous study might well be related to the difference in the severity of the hypoxia [ 22 ].…”

Section: Discussionmentioning

confidence: 86%

The effects of dopamine and epinephrine on hemodynamics and oxygen metabolism in hypoxic anesthetized piglets

Cheung

Barrington

2001

Crit Care

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CI = cardiac index; EO 2 = oxygen extraction; HAFI = hepatic arterial flow index; hepatic DO 2 = hepatic oxygen delivery; hepatic DO 2 ratio = ratio of hepatic arterial oxygen delivery to total hepatic oxygen delivery; MVRI = mesenteric vascular resistance index; PAP = mean pulmonary arterial pressure; PVFI = portal venous flow index; PVRI = pulmonary vascular resistance index; S a O 2 = arterial saturation; SAP = mean systemic arterial pressure; S p O 2 = portal venous saturation; S v O 2 = mixed venous saturation; SVRI = systemic vascular resistance index; VO 2 = oxygen consumption; THFI = total hepatic flow index.Available online http://ccforum.com/content/5/3/158 AbstractBackground: The most appropriate inotropic agent for use in the newborn is uncertain. Dopamine and epinephrine are commonly used, but have unknown effects during hypoxia and pulmonary hypertension; the effects on the splanchnic circulation, in particular, are unclear. Methods: The effects on the systemic, pulmonary, hepatic, and mesenteric circulations of infusions of dopamine and epinephrine (adrenaline) were compared in 17 newborn piglets. Three groups [control (n = 5), dopamine (n = 6) and epinephrine (n = 6)] of fentanyl anesthetized newborn piglets were instrumented to measure cardiac index (CI), hepatic arterial and portal venous blood flow, mean systemic arterial pressure (SAP), mean pulmonary arterial pressure (PAP), and arterial, portal and mixed venous oxygen saturations. Systemic, pulmonary, and mesenteric vascular resistance indices [systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), mesenteric vascular resistance index (MVRI)], and systemic and splanchnic oxygen extraction and consumption were calculated. Alveolar hypoxia was induced, with arterial oxygen saturation being maintained at 55-65%. After 1 h of stabilization during hypoxia, each animal received either dopamine or epinephrine; randomly administered doses of 2, 10, and 32 µg kg -1 min -1 and 0.2, 1.0, and 3.2 µg kg -1 min -1 respectively were infused for 1 h at each dose. Results were compared with the 1 h hypoxia values by two-way analysis of variance. Results: Epinephrine increased CI at all doses, with no significant effects on SAP and SVRI. Although epinephrine increased PAP at 3.2 µg kg -1 min -1 , it had no effect on PVRI. Dopamine had no effect on CI, SAP, and SVRI, but increased PAP at all doses and PVRI at 32 µg kg -1 min -1 . The SAP/PAP ratio was decreased with 32 µg kg -1 min -1 dopamine, whereas epinephrine did not affect the ratio. In the mesenteric circulation, dopamine at 32 µg kg -1 min -1 increased portal venous flow and total hepatic blood flow and oxygen delivery, and decreased MVRI; epinephrine had no effect on these variables. Epinephrine increased hepatic arterial flow at 0.2 µg kg -1 min -1 ; dopamine had no effect on hepatic arterial flow at any dose. Despite these hemodynamic changes, there were no differences in systemic or splanchnic oxygen extraction or consumption at any dose of dopamine or epinephrine. ...

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Section: Discussionmentioning

confidence: 86%

The effects of dopamine and epinephrine on hemodynamics and oxygen metabolism in hypoxic anesthetized piglets

Cheung

Barrington

2001

Crit Care

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“…It is clear that an increase in left ventricular peak pressure, when enddiastolic pressure and outflow resistance are constant, indicates an increase in the force of contraction from the same initial fibre length. DeGeest, Levy & Zieske (1965) used left ventricular peak pressure in an isovolumetric ventricle to indicate inotropic changes during stimulation of carotid chemoreceptors and Ng, Levy, DeGeest & Zieske (1966) used it in a similar denervated preparation to indicate inotropic changes associated with the effects of hypoxia on the myocardium.…”

Section: Discussionmentioning

confidence: 99%

Inotropic changes in the left ventricle: the effect of changes in heart rate, aortic pressure and end‐diastolic pressure

Furnival¹,

Linden²,

Snow³

1970

The Journal of Physiology

155

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SUMMARY1. Under conditions where heart rate, mean aortic pressure and enddiastolic pressure in the left ventricle are held constant, the intravenous infusion of isoprenaline is accompanied by large changes in dP/dt max in the left ventricle.2. Under similar conditions, during stepwise increments in the rate of infusion of isoprenaline the changes in dP/dt max (measured at a constant paced heart rate) were proportional to changes in the free (intrinsic) heart rate. It is concluded that dP/dt max is a quantitative index of inotropic changes in the left ventricle.3. In comparison to dP/dt max, three other variables which have been used to indicate inotropic changes in the heart (peak pressure in the left ventricle, duration of systole and stroke work at constant end-diastolic pressure), were shown to be unreliable indices of inotropic changes.4. Using dP/dt max to indicate inotropic changes, alteration in the heart rate while mean aortic pressure and end-diastolic pressure in the left ventricle were held constant, and in mean aortic pressure while heart rate and end-diastolic pressure in the left ventricle were held constant, were each shown to be accompanied by small inotropic changes in the heart.5. Under similar conditions, changes in end-diastolic pressure in the left ventricle alone were not accompanied by inotropic changes as indicated by dP/dt max.

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“…on the heart rate and cardiac output increases observed in dogs anaesthetized with pentobarbitone, after 20 min at Pa Oa 30 mm Hg. Myocardial hypoxia, whether caused by a decrease in coronary blood flow or a reduction in arterial oxygen content, eventually results in depression of myocardial contractility (Tennant and Wiggers, 1935;Bing, 1965;Case, 1966;Ng, Levy and Degeest, 1966). Similar depression occurs in isolated cardiac muscle preparations during hypoxia (Tyberg et al, 1970;Henderson 1974;Nayler, 1974).…”

Section: Discussionmentioning

confidence: 93%

“…However, there have been occasional reports of transient increases in contractility when heart preparations isolated from humoral influences were first subjected to hypoxia. Ng, Levy and Degeest (1966) snowed that when heart rate was maintained constant by atrial pacing, perfusion of the coronary circulation of dogs with blood at Po 2 40 mm Hg increased contractility, but that reduction of the Po 2 of the perfusing blood to 25 mm Hg resulted in cardiac depression. Cross and colleagues (1963) found that there was a transient increase in the spontaneous heart rate and contractility of the isolated, perfused dog heart when the coronary artery Po 2 was reduced to 25 mm Hg, but that depression ensued after 1 or 2 min.…”

Section: Discussionmentioning

confidence: 99%

Haemodynamic Interactions of High-Dose Propranolol Pretreatment and Anaesthesia in the Dog Ii: The Effects of Acute Arterial Hypoxaemia at Increasing Depths of Halothane Anaesthesia

Roberts

Foëx

Clarke

et al. 1976

British Journal of Anaesthesia

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Beta-adrenergic blockade may impair the normal cardiovascular response to hypoxia occurring during general anaesthesia. The haemodynamic effects of acute hypoxia, induced by a 90-s period of ventilation with nitrogen, were studied during increasing depths of halothane anaesthesia up to a maximum of 2.5% inspired halothane in dogs chronically implanted with intracardiac catheters, a left-ventricular pressure transducer and an aortic blood flow transducer. An untreated group of dogs and a group which had been treated for 3 weeks with propranolol 20 mg/kg/day were compared. The beta-blocked group had lesser cardiac output values, left-ventricular contractility indices, external left-ventricular work and peak left-ventricular power at all depths of anaesthesia except 2.5% halothane, but both groups responded to hypoxia similarly at each depth of anaesthesia. Cardiac performance was enhanced in both groups during acute hypoxia. No adverse haemodynamic effect of the combination of propranolol, halothane and hypoxia was demonstrated.

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Effects of myocardial hypoxia on left ventricular performance

Cited by 28 publications

References 0 publications

The effects of dopamine and epinephrine on hemodynamics and oxygen metabolism in hypoxic anesthetized piglets

The effects of dopamine and epinephrine on hemodynamics and oxygen metabolism in hypoxic anesthetized piglets

Inotropic changes in the left ventricle: the effect of changes in heart rate, aortic pressure and end‐diastolic pressure

Haemodynamic Interactions of High-Dose Propranolol Pretreatment and Anaesthesia in the Dog Ii: The Effects of Acute Arterial Hypoxaemia at Increasing Depths of Halothane Anaesthesia

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