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The Adrenergic Mechanism of the Haemodynamic Effects of Massive Doses of Hydrocortisone in Controlled Haemorrhagic Shock in the Dog
Author(s) -
HÄGGENDAL E.,
LINDFORS MARIA,
LUNDBERG D.
Publication year - 1978
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.1978.22.3.208
Subject(s) - phenoxybenzamine , medicine , propranolol , vasodilation , shock (circulatory) , hydrocortisone , adrenergic receptor , vascular resistance , hemodynamics , blood pressure , endocrinology , blockade , cardiac output , anesthesia , receptor
Haemorrhagic shock was induced in anaesthetized dogs by bleeding them into a blood reservoir system. By adjusting the blood level of the reservoir at a certain distance over the heart level the mean arterial blood pressure was kept at 6.7 kPa (50 mmHg). As has been found earlier, massive doses of hydrocortisone (80–560 mg·kg −1 body weight) caused a dose‐dependent decrease in the total peripheral resistance. The degree of vasodilation distinctly increased during concomitant alpha‐receptor blockade induced by phenoxybenzamine. The beta‐receptor blocking drug propranolol efficiently inhibited the vasodilation caused by hydrocortisone and phenoxybenzamine. The findings fit with the hypothesis that massive doses of hydrocortisone induce an increased stimulation of the adrenergic beta 2 ‐receptors of the vascular smooth muscles.