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Page 1 from 129 results
Meat quality and rigor mortis development in broiler chickens with gas-induced anoxia and postmortem electrical stimulation.
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This study was conducted to evaluate the combined rigor-accelerating effects of postmortem electrical stimulation (ES) and argon-induced anoxia (Ar) of broiler chickens. One hundred broilers were processed in the following treatments: untreated controls, ES, Ar, or Ar with ES (Ar + ES). Breast
The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster.
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Carbon dioxide gas is used as an insect anesthetic in many laboratories, despite recent studies which have shown that CO(2) can alter behavior and fitness. We examine the effects of CO(2) and anoxia (N(2)) on cold tolerance, measuring the rapid cold-hardening (RCH) response and chill coma recovery
Mechanics of guinea pig taenia coli smooth muscle during anoxia and rigor.
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Potassium-contracted guinea pig taenia coli relaxed when exposed to hypoxic glucose-free conditions, and this was followed by a second contraction. During this second contraction, which was not inhibited by ethylene glycol-his-(beta-aminoethylether)-N,N'-tetracetic acid (EGTA) the muscle was in
Understanding the temporal relationship of ATP loss, calcium loading, and rigor contracture during anoxia, and hypercontracture after anoxia in cardiac myocytes.
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[Intrauterine rigor mortis in fetal death due to anoxia].
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Cold hardening modulates K+ homeostasis in the brain of Drosophila melanogaster during chill coma.
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Environmental temperature is one of the most important abiotic factors affecting insect behaviour; virtually all physiological processes, including those which regulate nervous system function, are affected. At both low and high temperature extremes insects enter a coma during which individuals do
Resting Ca2+ influx does not contribute to anoxia-induced cell death in adult rat cardiac myocytes.
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Calcium has been proposed as a primary influence on cell death during ischemic episodes in myocardial cells. One component of calcium entry into a cell is resting calcium influx. This basal movement of calcium is blocked by 100 micromol/L gadolinium chloride (GdCl3) in cardiac myocytes. Therefore,
Facilitating effect of cold shock on recovery from anoxia-induced contractile depression in isolated rat heart and heart muscle.
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The effect of rapid cooling on the recovery process from anoxia-induced hypodynamic state was studied in isolated rat ventricular muscle and ventricle. Following 10-15 minutes' perfusion of N2-saturated Krebs solution, the muscle was reoxygenated. When the muscle was rapidly cooled for 10-30 seconds
Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence.
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The stiffness of rat cardiac trabeculae was measured in vitro to distinguish between an increase in unstimulated force (Fu) caused by rapid cycling of cross bridges or caused by rigor bridges during hypoxia. The force was measured with a strain gauge, the sarcomere length was determined by laser
Glutamate-loading stimulates metabolic flux and improves cell recovery following chemical hypoxia in isolated cardiomyocytes.
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The amino acid glutamate is used in cardioplegic solutions, yet evidence is conflicting as to whether or not exogenous glutamate is indeed cardioprotective. This controversy may be because increasing extracellular glutamate does not necessarily lead to an increase in intracellular glutamate. In this
Cytosolic free Ca2+ in single rat heart cells during anoxia and reoxygenation.
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Free Ca2+ in the cytosol ([Ca2+]i) of individual rat ventricle cells injected with aequorin was measured under anoxia. In glucose-free medium myocytes spontaneously shortened after about 60 min, although [Ca2+]i was still at or near resting levels. However, within minutes a net inward movement of
Cytosolic [Ca2+], [Na+], and pH in guinea pig ventricular myocytes exposed to anoxia and reoxygenation.
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The aim of this study was to evaluate whether the magnitude and time course of the intracellular acidification observed in anoxic cardiac myocytes was sufficient to protect against reoxygenation-induced hypercontracture. Cytosolic [Ca2+], [Na+], and pH were measured using fluorescent indicators in
Relation of mitochondrial and cytosolic free calcium to cardiac myocyte recovery after exposure to anoxia.
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Mitochondrial calcium overload has been suggested as a marker for irreversible injury in the ischemic heart. A new technique is used to measure dynamic changes in mitochondrial free calcium concentration ([Ca2+]m) in electrically stimulated (0.2 Hz) adult rat cardiac myocytes during exposure to
Reoxygenation-induced rigor-type contracture.
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The hypothesis tested was that reoxygenation-induced contracture of myocardial cells, a form of reperfusion injury, can be due to a rigor-type mechanism. Isolated adult cardiomyocytes were exposed to 30- or 60-min anoxia (pH 6.4) and reoxygenation (pH 7.4). In cardiomyocytes, cytosolic Ca(2+) and
Myocardial elasticity and left ventricular distensibility as related to oxygen deficiency and right ventricular filling. Analysis in a rat heart model.
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Hypoxia-induced changes in diastolic left ventricular (LV) pressure volume (P-V) relationships and myocardial elasticity as well as the extent to which diastolic right ventricular (RV) interactions are involved under hypoxia were analysed in male open-chest Wistar rats under isovolumetric
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