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Страница 1 от 740 полученные результаты
Response of cytosolic calcium to anoxia and cyanide in cultured glomus cells of newborn rabbit carotid body.
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Microscopic fluorometry was used to examine the effects of anoxia and cyanide (CN-) on cytosolic calcium [Ca2+]i of cultured carotid body (CB) glomus cells from newborn rabbits. Applications of high K+ and veratridine (VRT), a sodium channel activator, induced rapid and marked increases in [Ca2+]i.
Effects of Cyanide Ion and Hypoxia on the Volumes of Second-Stage Juveniles of Meloidogyne incognita in Polyethylene Glycol Solutions.
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Changes in the volumes of second-stage juveniles of Meloidogyne incognita were monitored in aqueous solutions of polyethylene glycol supplemented with dilute balanced salts. At key points within a 48-hour cycle of fluctuating water potential, nematodes were placed under hypoxic conditions or exposed
Drosophila neurons respond differently to hypoxia and cyanide than rat neurons.
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Compared with mammalian species, Drosophila melanogaster exhibits marked tolerance to hypoxia or anoxia. However, the underlying cellular mechanisms of tolerance are still largely unknown. In order to assess the electrophysiologic response to O(2) lack in Drosophila neurons and compare them to those
Corticosterone accelerates hypoxia- and cyanide-induced ATP loss in cultured hippocampal astrocytes.
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Glucocorticoids potentiate injury to the rodent hippocampus following a variety of metabolic insults, including hypoxia/ischemia, both in vitro and in vivo. We have examined whether corticosterone (CORT), the principal glucocorticoid in the rat, could exacerbate hypoxic energy failure in cultured
Force development of isoproterenol-damaged frog heart muscle in cyanide anoxia.
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From recent experiments it is indicated that in frogs living at +25 degrees C the abnormal response to cyanide anoxia appears as soon as 4-5 hr after the first isoproterenol (IPR) injection, but the aneurysm does not appear until a few hours after the second injection of IPR. There is evidently a
Effect of time on the response to cyanide anoxia of frog heart damaged by isoproterenol.
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Isoproterenol (IPR) induces damage to the heart of frogs living at 25 degrees. The resistance of an isometric ventricular strip to histotoxic anoxia induced by cyanide is significantly reduced 4 hours after one injection of IPR and still more after repeated injections. Macroscopically visible heart
On the mechanism of hepatic glycogenolysis induced by anoxia or cyanide.
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Addition of glucagon to isolated hepatocytes increased glycogenolysis and phosphorylase a in a proportional manner. KCN caused slightly more glycogenolysis at considerably lower levels of phosphorylase a; the discrepancy was most pronounced after pretreatment of the hepatocytes with EGTA. When
Mechanisms regulating the cardiac output response to cyanide infusion, a model of hypoxia.
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When tissue metabolic changes like those of hypoxia were induced by intra-aortic infusion of cyanide in dogs, cardiac output began to increase after 3 to 5 min, reached a peak (220% of the control value) at 15 min, and returned to control in 40 min. This pattern of cardiac output rise was not
The blood acid-base changes in acute cyanide poisoning in the rat in comparison with those in acute anoxic anoxia: with special reference to the relation with the time to death.
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Rats were given orally various doses of NaCN (20,15,10, and 7 mg of CN per kg). When respiration stopped, the chest was opened and heart blood was taken anaerobically, and blood acid-base, lactate, and glucose determinations were made. As a control to chemical anoxia by cyanide, indentical
Severe hypoxia produced by concomitant intoxication with sublethal doses of carbon monoxide and cyanide.
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It has long been known that a number of tissue hypoxicants are generated in the fire scenario. However, until recently few investigators have undertaken to correlate smoke inhalation deaths with the simultaneous exposure to histotoxic hypoxicants. Carbon monoxide and hydrogen cyanide are two
Light absorbance changes in the mouse carotid body during hypoxia and cyanide poisoning.
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The isolated carotid body (CB) of the mouse was bathed with modified Tyrode's solution (pO2, 170 Torr) and transilluminated at different wave-lengths (500-620 nm). Difference spectra (normoxia vs hypoxia--pO2, 10 Torr) showed peaks of increased light transmittance (LT) at 500 and especially at 540
A comparison of some effects of phosphine, hydrogen cyanide and anoxia in the lesser grain borer, Rhyzopertha dominica (F.) (Coleoptera: Bostrychidae).
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The effects of phosphine, hydrogen cyanide and anoxia on levels of ATP, pyruvate and lactate in Rhyzopertha dominica are compared. The effect of phosphine on anaerobiosis is not directly comparable either with HCN or anoxia. Reduction of catalase by feeding 3 amino 1,2,4 triazole does not enhance
Cardiovascular responses to chemoreflex activation with potassium cyanide or hypoxic hypoxia in awake rats.
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Although intravenous (iv) injection of potassium cyanide (KCN) activates the arterial chemoreflex, it has been questioned whether cytotoxic hypoxia reproduces a physiological stimulus such as hypoxic hypoxia (low inspired O2 tension). Thus, the goal of the present study was to compare the
Effects of hypoxia, cyanide, and ischaemia on myocardial contraction: observations in isolated muscle and intact heart.
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Using potassium cyanide (KCN) to stimulate hypoxia, the effects of intracoronary injections of KCN were compared with total occlusions of the same vessel. Imparied contraction as measured by segment length gauges was of equally abrupt onset following both interventions. The magnitude of systolic
Influence of carbon monoxide, hypoxic hypoxia or potassium cyanide pretreatment on acute carbon monoxide and hypoxic hypoxia lethality.
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Pre-exposure of mice to 500 or 1000 ppm of carbon monoxide (CO) for 4 hours resulted in a significant decrease in lethality induced by exposure to 2500 ppm of CO 24 hours later. Pre-exposure to CO had no effect on lethality induced by hypoxic hypoxia (low inspired O2 tension) or potassium cyanide
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