�ber den Einflu� von metabolischer Alkalose und metabolischer Acidose auf die Kontraktilit�t des isolierten Herzens

Kohlhardt, M.; Wirth, K; Dudeck, Joachim

doi:10.1007/bf00362535

Cited by 14 publications

(3 citation statements)

References 24 publications

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“…Over the last decades, the influence of metabolic acidosis on cardiac contractility was intensively investigated in different animal models [1,2,4,5,9,11,12,33]. In the presence of an acidotic pH, a serious species-independent decrease in contractility was found [11].…”

Section: Discussionmentioning

confidence: 99%

“…In the presence of an acidotic pH, a serious species-independent decrease in contractility was found [11]. Therefore, acidosis influences EC coupling and the Ca 2+ -myofilament response [4,5,7-10].…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, acidosis has been shown to decrease the cellular Ca 2+ transient amplitude [1]. Kohlhardt and co-workers [11] showed a significantly decreased cardiac output induced by acidosis (pH 7.00) by almost 25% in nonfailing cat hearts. An additional number of studies verified the decrease in contractility in other species [12-18].…”

Section: Introductionmentioning

confidence: 99%

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Mild metabolic acidosis impairs the β-adrenergic response in isolated human failing myocardium

Schotola¹,

Toischer²,

Popov

et al. 2012

Crit Care

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IntroductionPronounced extracellular acidosis reduces both cardiac contractility and the β-adrenergic response. In the past, this was shown in some studies using animal models. However, few data exist regarding how the human end-stage failing myocardium, in which compensatory mechanisms are exhausted, reacts to acute mild metabolic acidosis. The aim of this study was to investigate the effect of mild metabolic acidosis on contractility and the β-adrenergic response of isolated trabeculae from human end-stage failing hearts.MethodsIntact isometrically twitching trabeculae isolated from patients with end-stage heart failure were exposed to mild metabolic acidosis (pH 7.20). Trabeculae were stimulated at increasing frequencies and finally exposed to increasing concentrations of isoproterenol (0 to 1 × 10-6 M).ResultsA mild metabolic acidosis caused a depression in twitch-force amplitude of 26% (12.1 ± 1.9 to 9.0 ± 1.5 mN/mm2; n = 12; P < 0.01) as compared with pH 7.40. Force-frequency relation measurements yielded no further significant differences of twitch force. At the maximal isoproterenol concentration, the force amplitude was comparable in each of the two groups (pH 7.40 versus pH 7.20). However, the half-maximal effective concentration (EC50) was significantly increased in the acidosis group, with an EC50 of 5.834 × 10-8 M (confidence interval (CI), 3.48 × 10-8 to 9.779 × 10-8; n = 9), compared with the control group, which had an EC50 of 1.056 × 10-8 M (CI, 2.626 × 10-9 to 4.243 × 10-8; n = 10; P < 0.05), indicating an impaired β-adrenergic force response.ConclusionsOur data show that mild metabolic acidosis reduces cardiac contractility and significantly impairs the β-adrenergic force response in human failing myocardium. Thus, our results could contribute to the still-controversial discussion about the therapy regimen of acidosis in patients with critical heart failure.

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