A Comparison of the Effects of Salbutamol, Etilefrine and Dextran During Hypotension and Low Cardiac Output States in Rabbit

Abstract

The effects of salbutamol (25 and 50 micrograms/kg), etilefrine (50 and 200 micrograms/kg) and dextran (8 ml/kg) on cardiovascular function have been studied in the rabbit. The three drugs raised the resting cardiac output (with salbutamol producing delta max 52%, P less than 0.001, n = 5) and right heart filling pressure (RHFP, delta max from dextran 3.5 cmH2O; P less than 0.001, n = 6) and lowered total peripheral resistance (TPR, delta max from salbutamol 46%, P less than 0.001, n = 5). However, TPR rose with the 200 micrograms/kg etilefrine (P less than 0.05, n = 5). Pulse pressure rose with salbutamol (P less than 0.001, n = 6) and etilefrine (P less than 0.05, n = 6). Etilefrine raised resting BP (delta max, P less than 0.001, n = 6); salbutamol lowered resting BP (delta max, P less than 0.001, n = 6) while dextran (n = 6) had little effect on resting BP. The actions of salbutamol are mediated mainly through beta 2-adrenoceptors although the drug also has some minor beta 1-adrenoceptor action. With etilefrine, the increase in cardiac output and the reduction in TPR are mediated through beta-adrenoceptors while the increases in RHFP, blood pressure and TPR are a direct action on the alpha-adrenoceptors. However, during haemorrhage the fall in diastolic pressure produced by salbutamol was considerably reduced while the reduction in mean BP and systolic pressure (which sometimes rose) was abolished. Dextran raised BP during hypotension produced by either sympathectomy or haemorrhage but not during normotension. The reflex recovery in RHFP and the reflex tachycardia were slightly attenuated during lower body negative pressure (LBNP) after salbutamol or dextran. The reflex recovery in blood pressure was complete and the pressure sometimes exceeded the resting level by up to 10 mmHg during LBNP after salbutamol, etilefrine (50 micrograms/kg only) and dextran. The reduced TPR (presumably due to vasodilation) and the increases in cardiac output and RHFP at an adequately maintained blood pressure produced by suitable doses of the three drugs may be useful in the management of circulatory shock and related states.

The hypotensive mechanisms for the aqueous stem bark extract of Musanga cecropioides in Sprague-Dawley rats

“…The possibility that the extract could be inducing its hypotensive effect via a sympatholytic mechanism was examined in this study using bilateral carotid artery occlusion. Occlusion of the two common carotid arteries below their bifurcations stimulates the sympathetic nervous system thereby increasing blood pressure (Adigun and Fentam, 1984). Therefore, if the extract interferes with sympathetic activities, the increase in mean arterial pressure induced by bilateral carotid artery occlusion is attenuated by MCW injection.…”

“…Bilateral carotid artery occlu- sion was performed as described by Adigun and Fentam (1984). The rats were first exposed to BCO three times of 10 min interval with each occlusion lasting 1 min.…”

Pharmacology of stimulants prohibited by the World Anti‐Doping Agency (WADA)

“…A direct‐acting β1‐adrenoceptor agonist ( Karasawa et al ., 1992 ) with some α‐ and β2‐adrenoceptor actions ( Coleman et al ., 1975 ; Adigun and Fentem, 1984 ; Lippert et al ., 1987 ; Sweetman, 2007 ). It has been used for treatment of hypotensive states by cardiac and pressor actions, and as a nasal decongestant ( Sweetman, 2007 ).…”