Regulation of cardiovascular functions during acute blood loss.
Sudden blood loss of moderate degree causes fall in blood pressure, which is compensated to certain extent by baroreceptor mediated rise in heart rate and vasoconstriction. In case of severe haemorrhage fall in blood pressure is accompanied by bradycardia indicating failure of baroreceptor mediated recovery in blood pressure. In such conditions partial recovery in the blood pressure with time is possible due to mechanisms other than baroreflex. Therefore, in the present study the regulation of cardiovascular functions on increasing severity of blood loss in the absence of any therapeutic intervention was examined to elucidate the mechanisms involved in the recovery of blood pressure under such conditions. Two groups of animals were studied: (a) In the first group (n = 10) 20% of the total blood volume loss was induced, (b) In the second group (n = 10) 35% of the total blood volume loss was induced. In both the groups cardiovascular parameters were evaluated for one hour after the induction of haemorrhage to record any recovery due to natural compensatory mechanisms. In both the groups there was a significant fall in mean arterial pressure, cardiac output, stroke volume, right atrial pressure and base deficit. A significant increase in heart rate and total peripheral resistance was produced after 1 min of haemorrhage in 20% blood loss while a fall in total peripheral resistance and no rise in heart rate was produced after 35% blood loss. There was a recovery in cardiac output and mean arterial pressure with time in both the cases of blood loss. While a rise in heart rate and stroke volume was produced in 20% blood loss however an initial increase in stroke volume alone and later rise in heart rate alone was produced during recovery phase in 35% blood loss. These finding suggest that 20% blood loss is compensated by baroreflex while 35% blood loss is not accompanied by tachycardia so mechanisms other than the baroreflex, like increase in the vagal tone, contribute to the initial recovery in blood pressure and cardiac output.
Gupta
Rajinder K
RK
Department of Physiology, Vallabhbhai Patel Chest Institute, University of Delhi, P.O. Box 2101, Delhi110 007, India. vpciphysiology@yahoo.com
Fahim
Mohammad
M
D000818:Animals; D016280:Atrial Function, Right; D001794:Blood Pressure; D002302:Cardiac Output; D002320:Cardiovascular Physiological Phenomena; D004285:Dogs; D005260:Female; D006339:Heart Rate; D006470:Hemorrhage / Q000503:physiopathology*; D008297:Male; D011311:Pressoreceptors; D013318:Stroke Volume; D014655:Vascular Resistance