Key result
Massive doses of hydrocortisone (80-560 mg/kg) caused a dose-dependent decrease in total peripheral resistance in dogs with haemorrhagic shock, likely via stimulation of vascular beta2-receptors.
Massive doses of hydrocortisone induce vasodilation in haemorrhagic shock likely via stimulation of adrenergic beta2-receptors of vascular smooth muscles.
Does not support hydrocortisone use in human haemorrhagic shock; leaves open beta2-mediated vasodilation in clinical settings.
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 beta2-receptors of the vascular smooth muscles.
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Häggendal et al. (1978) studied Haemorrhagic shock. Massive doses of hydrocortisone was evaluated on Total peripheral resistance. Massive doses of hydrocortisone (80-560 mg/kg) caused a dose-dependent decrease in total peripheral resistance in dogs with haemorrhagic shock, likely via stimulation of vascular beta2-receptors.
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