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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hearts from 32 male Sprague-Dawley rats were studied to determine effects of anoxia on ventricular contractility. Maximum rate of ventricular pressure changes with time (Pmax) were obtained from simultaneous recordings of right and left ventricular pressure curves. Peak aortic flow and heart rate were measured. Anoxia was produced by 100% N2 respiration. Statistical models were repeated-measures analysis of variance and randomized block factorial analysis of variance. Alpha was 0.05. Heart rate during anoxia was significantly lower than during the 1st min of recovery. Heart rate during both these periods was significantly lower than in preanoxia or the remainder of recovery. Peak aortic flow was not significantly altered. In left ventricles positive Pmax was significantly higher than negative Pmax. In right ventricles positive and negative Pmax were not significantly different. Left ventricular Pmax was significantly depressed during anoxia, whereas right ventricular Pmax was not. Significant differences in pressure developed per mass of tissue was a possible source of variation in right (0.12 +/- 0.002 mmHg/mg) and left (0.16 +/- 0.009 mmHg/mg) ventricular contractile maintenance.
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PMID:Statistical analysis of effect of anoxia on rate of change of ventricular pressure. 712 96

Unlike in adult heart, embryonic myocardium works at low PO2 and depends preferentially on glucose. Therefore, activity of the embryonic heart during anoxia and reoxygenation should be particularly affected by changes in glucose availability. Hearts excised from 4-d-old chick embryos were submitted in vitro to strictly controlled anoxia-reoxygenation transitions at glucose concentrations varying from 0 to 20 mmol/L. Spontaneous and regular heart contractions were detected optically as movements of the ventricle wall and instantaneous heart rate, amplitude of contraction, and velocities of contraction and relaxation were determined. Anoxia induced transient tachycardia and rapidly depressed contractile activity, whereas reoxygenation provoked a temporary and complete cardioplegia (oxygen paradox). In the presence of glucose, atrial rhythm became irregular during anoxia and chaotic-periodic during reoxygenation. The incidence of these arrhythmias depended on duration of anoxia, and no ventricular ectopic beats were observed. Removal of glucose or blockade of glycolysis suppressed arrhythmias. These results show similarities but also differences with respect to the adult heart. Indeed, glucose 1) delayed and anoxic contractile failure, shortened the reoxygenation-induced cardiac arrest, and improved the recovery of contractile activity; 2) attenuated stunning at 20 mmol/L but worsened it at 8 mmol/L; and 3) paradoxically, was arrhythmogenic during anoxia and reoxygenation, especially when present at the physiologic concentration of 8 mmol/L. The last named phenomenon seems to be characteristic of the young embryonic heart, and our findings underscore that fluctuations of glycolytic activity may play a role in the reactivity of the embryonic myocardium to anoxiareoxygenation transitions.
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PMID:Glucose is arrhythmogenic in the anoxic-reoxygenated embryonic chick heart. 872 26