STUDIES ON THE MECHANISMS INVOLVED IN THE CARDIOVASCULAR-RESPONSE OF THE RAT TO HEMORRHAGE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 254  (1) , 58-69
Abstract
Acute reductions in blood volume and in arterial pressure produced by hemorrhage in the rat resulted in significant changes in heart rate. Generally when bleeding lowered mean arterial blood pressure to 90 mm Hg or less, heart rate fell in proportion to the depth of hypotension, but when arterial pressure remained > 100 mm Hg, regardless of the volume of shed blood, heart rate increased. The bradycardia observed when the animals were bled to low pressures (40 mm Hg) could be prevented by vagotomy or with a combination of atropine and propranolol. This suggests the effect is a reflex action centrally mediated. Propranolol alone had only small effects on the heart rate response, indicating that the reflex is predominantly under vagal influence. Phenoxybenzamine or adrenal demedullation had no effect on heart rate or blood pressure changes during or after hemorrhage. Pargyline, at a dose which significantly inhibited MAO [monoamine oxidase] and increased brain stem norepinephrine and dopamine levels, reduced the magnitude of the shock bradycardia. These results are discussed in relation to an earlier report, which indicates that the potent inhibitor of epinephrine synthesis, SKF 64139 [7,8-dichloro-1,2,3,4-tetrahydro-isoquinaline], will prolong the bradycardia and hypotension associated with hemorrhage in this model.