cyanide/hypoxia

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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