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Biomedical subjects

T Tveita

Publications and source records attributed to T Tveita.

21 records · Page 2Linked to original sources

Hemodynamic and metabolic effects of hypothermia and rewarming.

There is a lack of detailed knowledge of the pathophysiologic mechanisms initiated during and after rewarming. To study cardiac function after rewarming from hypothermia sodium pentobarbital anesthetized open chest-dogs were cooled to 25 degrees C and rewarmed. Myocardial blood flow was measured at different temperatures, and blood samples were drawn from the aorta and the coronary sinus for metabolic measurements. Mean aortic blood pressure (AOP) and aortic blood flow were recorded. Compared to precooling, AOP and heart rate were both significantly reduced during hypothermia. During rewarming stroke volume (SV) decreased significantly. At the end of rewarming AOP and SV were significantly lower than before cooling and myocardial blood flow, as well as oxygen and lactate uptake were only 50% of precooling levels. The present study demonstrated that hypothermia and rewarming depress cardiovascular function. Changes in peripheral vascular function, myocardial metabolism and contractility, may lead to the observed reduction in recovery upon rewarming.

Animals↗

Lack of effect of indomethacin on ordered growth of the femur in rats.

The effect of indomethacin on ordered growth in length and width of the femur was studied in 48 adolescent rats given 2 mg/kg/day of the drug, a regimen previously shown to inhibit fracture healing. The animals were given either indomethacin suspension, or the vehicle alone, orally for 6 weeks. All the animals tolerated the treatment well. During drug treatment the femur distal to the intertrochanteric crest grew about 7 mm in length. Indomethacin plasma levels were about 1 microgram/ml in the indomethacin-treated animals. Indomethacin did not inhibit ordered growth in either length or width. This indicates that indomethacin does not inhibit the normal homeostasis of the skeletal system in adolescent rats.

Animals↗

Changes in ventricular fibrillation threshold during acute hypothermia. A model for future studies.

Hypothermia and rewarming are associated with an increased incidence of lethal arrhythmias in man. The relationship between reduction in body temperature and ventricular fibrillation threshold was studied in 7 pentobarbital anaesthetized dogs using programmable electrical stimulation while cooling and rewarming between 37 degrees C and 25 degrees C in steps of 3 degrees C. Fibrillation threshold was defined as the number of extrastimuli required to evoke ventricular fibrillation. QRS-durations and corrected QT-intervals (QTc) were measured from surface electrocardiograms. Monophasic action potential durations were recorded from the base and apex of the heart. Fibrillation threshold decreased with decreasing temperatures; e.g., at 37 degrees C ventricular fibrillation was not inducible after 5 extrastimuli, while at 25 degrees C only 2 extrastimuli were required. From 37 degrees C to 25 degrees C QRS-width, monophasic action potential durations and QTc increased while conduction velocity decreased. The differential effects on conduction and monophasic action potential duration provide a basis for induction of ventricular fibrillation during acute hypothermia. This model of hypothermia-induced ventricular fibrillation should prove useful for future studies aimed at understanding the mechanisms responsible for hypothermia-related deaths.

Action Potentials↗