Influence of lactic acidosis on cardiovascular response to sympathomimetic amines

Gd, Ford; Wh, Cline; Fleming, W H

doi:10.1152/ajplegacy.1968.215.5.1123

Cited by 34 publications

(7 citation statements)

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“…Thus acidaemia may affect the efferent pathway of the reflex. Further, the chronotropic effects of injected sympathomimetic amines are reduced by systemic acidaemia in the dog (Bendixen, Laver & Flacke, 1963;Manley, Woodbury & Nash, 1966;Ford, Cline & Fleming, 1968). Thus the effect of acidaemia on sympathetic nerve stimulation may be a modification of the action of the released sympathetic transmitter; it is possible that the depression of the reflex response of tachycardia by stimulation of the left atrial receptors during acidaemia is at the same site.…”

Section: Discussionmentioning

confidence: 99%

Depression of the reflex tachycardia from the left atrial receptors by acidaemia

Harry¹,

Kappagoda²,

Snow³

1971

The Journal of Physiology

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SUMMARY1. The effects are described of an acidaemia, produced either by the inhalation of carbon dioxide or by an intravenous infusion of hydrochloric acid, on the reflex increase in heart rate which results from stimulation of the left atrial receptors in the anaesthetized dog.2. The results show that during acidaemia the reflex increase in heart rate from stimulation of the left atrial receptors is reduced. The extent of the reduction is related to the degree of the acidaemia.3. It is suggested that it is necessary to monitor and correct changes in the pH of arterial blood in experiments which involve reflex changes in heart rate, especially if the efferent pathway involves the sympathetic nerves.4. It is also suggested that the occurrence of such an acidaemia in anaesthetized surgically traumatized animals may be a factor contributing to the variability in results from investigations involving reflex changes in heart rate in response to stimulation of the left side of the heart.

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Section: Discussionmentioning

confidence: 99%

Depression of the reflex tachycardia from the left atrial receptors by acidaemia

Harry¹,

Kappagoda²,

Snow³

1971

The Journal of Physiology

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“…Underlining this, Kohlhardt et al described already in the 1960s a significant, moderateacidosisinduced cardiac output decrease in nonfailing cats by 25% (pH = 7.00) (13). Further investigations on acidosis-induced decrease of myocardial contractility and its effect on catecholamine response were performed using different approaches and models (14)(15)(16)(17)(18)(19)(20)(21)(22); however, there still exist no experimental data describing the specific effect of metabolic acidosis in isolated ovine hearts even though sheep are widely used as animal models (23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41).…”

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confidence: 99%

Influence of Mild Metabolic Acidosis on Cardiac Contractility and Isoprenaline Response in Isolated Ovine Myocardium

Schotola¹,

Sossalla²,

Rajab

et al. 2011

Artificial Organs

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The postoperative course after major surgical procedures such as cardiothoracic operations is often accompanied by acute metabolic abnormalities due to large volume and temperature shifts. In general, those intervention-induced trauma might cause the use of catecholamines to stabilize hemodynamics. Within the cardiac community, there are still controversial discussions about standardized medical therapy to treat postoperative acidosis, for example, buffering versus nonbuffering for improving catecholaminergic response of myocardial contractility. The aim of this study was to investigate the influence of mild (and thus clinically relevant) acidosis on myocardial contractility and catecholamine response in explanted trabeculae of ovine hearts. Intact trabeculae (n = 24) were isolated from the right ventricle of healthy sheep hearts. Two different groups (group 1: pH = 7.40, n = 9 and group 2: pH = 7.20, n = 13) were investigated, and force amplitudes were measured at frequencies between 30 and 180 beats per minute and increasing catecholamine concentrations (isoprenaline 0-3 × 10(-6) mM). Force-frequency relation experiments in the presence of a physiological and/or mild acidotic pH solution showed no significant differences. Mean force amplitudes normalized to the lowest frequency showing no significant differences in force development between 0.5 and 3 Hz (n = 9 vs. 13, P = n.s.) (0.5 Hz absolute values 3.1 ± 2.6 for pH = 7.40 vs. 3.8 ± 2.6 mN/mm(2) for pH = 7.20, P = n.s.). Moreover, there was no significant difference in relaxation kinetics between the two groups. Furthermore, the experiments showed similar catecholamine responses in both groups. Force amplitudes normalized to baseline and maximum force showed no significant differences in force development between baseline and maximum isoprenaline concentrations (n = 6 vs. 9, P = n.s.) (baseline absolute values 4.3 ± 4.0 for pH = 7.40 vs. 3.9 ± 1.2 mN/mm(2) for pH = 7.20, P = n.s.). Additionally, relaxation kinetics did not show differences after catecholamine stimulation. The presented experiments revealed no significant negative inotropic effects on isometrically contracting ovine trabeculae with mild metabolic acidosis (pH = 7.2) compared with physiological pH (7.4). Additionally, similar catecholamine responses were seen in both groups. Further investigations (e.g., in vivo and/or in failing hearts with reduced compensatory reserves) will be necessary to examine optimal medical treatment for metabolic abnormalities after cardiac surgery.

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“…Previous studies of the effect of acidosis on the response of cardiac muscle to catecholamines have shown that acidosis either decreases (Mantley, Woodbury & Nash, 1966;Nakanishi, Okuda, Kamata, Seguchi, Nakazawa & Takao, 1987) or does not change the response to catecholamines (Ford, Cline & Fleming, 1968). The depressant effect of acidosis was shown to be accompanied by a decrease in receptor numbers at pH 6 0 (but not at pH 6'8) in newborn rabbit hearts, while adenylate cyclase activity was depressed at both pH levels (Nakanishi et al 1987).…”

Section: Introductionmentioning

confidence: 80%

The effect of acidosis on beta‐adrenergic receptors in ferret cardiac muscle

Nimmo¹,

Than²,

Orchard³

et al. 1993

Experimental Physiology

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SUMMARYAcidosis decreases the force of contraction of cardiac muscle in response to noradrenaline. The role of ,l-adrenergic receptors in this response to acidosis was investigated. Radioligand techniques were used to determine ,3-adrenergic receptor number and the degree of G-protein coupling, and to see whether these were altered in tissues subject to acidosis. The effect of pH on agonist and antagonist binding to these receptors was also investigated. Tissue pre-exposure to acidic conditions had no effect on numbers of 8-adrenergic receptors and no effect on the affinity of [l251]iodocyanopindolol (ICYP) for the receptors. Agonist competition experiments indicated that there was no change in the affinity of isoprenaline for these receptors, and there was no change in the relative proportions of high and low affinity binding sites. When radioligand experiments were performed under acidic conditions, however, the total number of ,3-adrenergic receptors increased, and the affinity of these receptors for isoprenaline increased.This increase in agonist affinity might, therefore, minimize the shift to the right seen in the dose-response curve to noradrenaline during acidosis.

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Influence of lactic acidosis on cardiovascular response to sympathomimetic amines

Cited by 34 publications

References 0 publications

Depression of the reflex tachycardia from the left atrial receptors by acidaemia

Depression of the reflex tachycardia from the left atrial receptors by acidaemia

Influence of Mild Metabolic Acidosis on Cardiac Contractility and Isoprenaline Response in Isolated Ovine Myocardium

The effect of acidosis on beta‐adrenergic receptors in ferret cardiac muscle

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