Studies on the mechanisms involved in the cardiovascular response of the rat to hemorrhage.
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| Abstract |
Acute reductions in blood volume and in arterial pressure produced by hemorrhage in the rat resulted in significant changes in heart rate. In general, when bleeding lowered mean arterial blood pressure to 90 mmHg or less, heart rate fell in proportion to the depth of hypotension, but when arterial pressure remained above 100 mmHg, regardless of the volume of shed blood, heart rate increased. The bradycardia observed when the animals were bled to low pressures (40 mmHg) could be prevented by vagotomy or with a combination of atropine and propranolol. This suggests the effect is 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 and increased brain stem norepinephrine and dopamine levels, reduced the magnitude of the shock bradycardia. These results are discussed in relation to our earlier report (Pendleton et al., 1980a) which indicates that the potent inhibitor of epinephrine synthesis, SK & F 64139, will prolong the bradycardia and hypotension associated with hemorrhage in this model.
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| Authors | J P McCafferty, J M Roesler, R G Pendleton |
| Journal | Archives internationales de pharmacodynamie et de therapie (Arch Int Pharmacodyn Ther) Vol. 254 Issue 1 Pg. 58-69 (Nov 1981) ISSN: 0003-9780 [Print] Belgium |
| PMID | 7337495 (Publication Type: Journal Article) |
| Chemical References |
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