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chills/hypoxia

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Página 1 a partir de 129 resultados
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
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

[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,
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
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
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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