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Biomedical subjects

C Steinmann

Publications and source records attributed to C Steinmann.

27 records · Page 2Linked to original sources
PubMed1988

[Stress reaction in boars of the German Landrace and Piétrain breeds during semen collection from the phantom].

The effect of the semen collection procedure at the phantom on heart and circulatory system, on blood values of the acid-base-equilibrium and on plasma enzyme values was investigated in four boars of the German Landrace and four boars of the Piétrain race. In most of the boars tachycardia (heart rate above 239/min), an increase of plasma lactate concentration (above 10.0 mmol/l) and of plasma creatine kinase (CK) concentration (plasma CK above 1,000 U/l) were the consequences of the exertion by semen collection. The extent of the exertional reactions on heart and vasculatory parameters strongly depended on the individual disposition while in most of the metabolic blood values the two different races varied evidently. The values of CK 24 hours after semen collection were related to the plasma lactate concentration as well as to the heart rate during semen collection.

Acid-Base Equilibrium↗
PubMed1987

Mitochondrial Ca2+ fluxes and levels during ischaemia and reperfusion: possible mechanisms.

It has been shown that myocardial ischaemia depresses the uptake and enhances the release of Ca2+ by mitochondria. Reperfusion of the ischaemic areas may result in a further deterioration of the above processes. Despite these marked changes in Ca2+ fluxes, reperfusion has been shown always to be associated with a marked increase in mitochondrial Ca2+ content. To explain the latter observation, it has been proposed that reperfusion promotes respiration-supported mitochondrial Ca2+ uptake in preference to ADP phosphorylation. To evaluate this hypothesis, the effect of exogenous ADP on mitochondrial respiration-linked Ca2+ uptake was investigated in control, ischaemic and ischaemic-reperfused hearts. The results show that ADP significantly depresses mitochondrial Ca2+ uptake in all three preparations, indicating that Ca2+ is not taken up preferentially to ADP phosphorylation in reperfused tissue. It is suggested that reperfusion-induced increased mitochondrial Ca2+ levels are probably not due to increased respiration-linked Ca2+ uptake, but rather to augmented conversion of ionized Ca2+ to calcium phosphate which does not participate in ionic fluxes.

Adenosine Diphosphate↗
PubMed1983

Normothermic ischemic cardiac arrest of the isolated working rat heart. Effects of time and reperfusion on myocardial ultrastructure, mitochondrial oxidative function, and mechanical recovery.

The ischemic state of the myocardium of the isolated working rat heart after induction of normothermic ischemic cardiac arrest was assessed by the interrelationship among changes in myocardial ultrastructure, mitochondrial oxidative phosphorylation, and tissue high energy phosphate contents. At all time intervals (10-40 minutes) studied, the ultrastructural changes were more severe in the subendocardium than in the subepicardium. After 25-40 minutes of normothermic ischemic cardiac arrest, the mitochondrial oxygen uptake (state 3) became increasingly depressed, particularly in mitochondria isolated from the subendocardium. Mitochondrial oxidative function, as measured in vitro, did not correlate well with mitochondrial ultrastructural damage. In addition, the effects of coronary reperfusion on the ability of the ischemic heart to recover in terms of ultrastructure, mechanical, and metabolic function were evaluated. Hearts subjected to 10-40 minutes of normothermic ischemic cardiac arrest showed almost complete ultrastructural recovery of the subepicardium upon reperfusion; regression of ultrastructural changes occurred to a lesser extent in the subendocardium. Reperfusion for 30 minutes did not alleviate the depression in mitochondrial oxidative function, while tissue ATP levels did not return to control, preischemic levels. After 20 minutes of normothermic ischemic cardiac arrest, the mechanical performance of the working heart during reperfusion was significantly depressed, compared with pre-ischemic control values. Normal ultrastructure of the subendocardium always accompanied mechanical recovery, while improvement of mitochondrial oxidative function was not essential.

Adenosine Triphosphate↗
PubMed1978

[A improved demonstration of ischemic myocard injuries with a combined method for evidence of the succine dehydrogenase and the acridin-fluorchrome-technique (MS-AO-technique) (author's transl)].

A method is described for combined enzyme histochemical and fluorescence microscopical investigation of ischemic injuries. This new method allows to distinguish between 1 reversible and 3 irreversible zones at the experimental ligature infarct of 48 h duration. Heterolysis is discussed as reason for the 3 outer zones and autolytic processes for the central area.

Animals↗