Shivering endurance and fatigue during cold water immersion in humans.

An important component of survival time during cold exposure is shivering endurance. Nine male and three female healthy and fit subjects [mean (SD) age 24.8 (6.

Measurement and prediction of peak shivering intensity in humans.

Prediction equations of shivering metabolism are critical to the development of models of thermoregulation during cold exposure. Although the intensity of maximal shivering has not yet been predicted, a peak shivering metabolic rate (Shivpeak) of five times the resting metabolic rate has been reported. A group of 15 subjects (including 4 women) [mean age 24.

Immersion of distal arms and legs in warm water (AVA rewarming) effectively rewarms mildly hypothermic humans.

Introduction: Active rewarming of hypothermic victims for field use, and where transport to medical facilities is impossible, might be the only way to restore deep body temperature. In active rewarming in warm water, there has been a controversy concerning whether arms and legs should be immersed in the water or left out. Further, it has been suggested in the Royal Danish Navy treatment regime, that immersion of hands, forearms, feet, and lower legs alone might accomplish rapid rates of rewarming (AVA rewarming).

Interaction of some antiarrhythmic drugs with the heart sarcolemmal Na+-Ca2+ exchange system.

The effects of some Class I antiarrhythmics (quinidine, procainamide and lidocaine) and some Class II antiarrhythmics (propranolol, atenolol and acebutolol) on canine cardiac sarcolemmal Na+-Ca2+ exchange activity were studied. Both quinidine (5-100 microM) and procainamide (1-100 microM), unlike lidocaine, inhibited Na+-dependent Ca2+ uptake in sarcolemmal vesicles. The effective concentrations of these agents were well within their respective therapeutic ranges; about 30% inhibition was seen by 10 microM quinidine or procainamide.

Alterations in heart membrane calcium transport during the development of ischemia-reperfusion injury.

Global ischemia in guinea-pig hearts for 60 to 90 min depressed microsomal and mitochondrial Ca2+ uptake activities. Reperfusion of the 60 min ischemic hearts resulted in incomplete recovery of contractile function and calcium uptake activities of both mitochondrial and microsomal fractions. On the other hand, reperfusion of the 90 min ischemic hearts further depressed the microsomal Ca2+ uptake activity.