The Effect of Intravenous Infusion of Salbutamol on Heart Rate, Plasma Potassium and the Ventilatory Response to Carbon Dioxide and Hypoxia in Normal Man

Abstract

cut (n = 5, for each group). The aortic receptors are not chemosensitive in the rabbit (Bouverot et al., 1973, Respiration Physiology, 17, 209).No significant difference in HBF was observed between the two groups of rabbits during the control period or after 15 or 120 min of hypoxia, nor was there any difference in Pa,o, or Pa,co,. In a further group of three rabbits the ventilatory response to the inhalation of 10% 0, was measured before and after carotid sinus nerve section. Before carotid sinus nerve section ventilation increased by 66.65 13.7% (meanksm), after carotid sinus nerve section inhalation of 10% O2 decreased ventilation by 9.5 5 5.4%. This confirms that there is no contribution from aortic receptors to the respiratory response to hypoxia in the rabbit. It is concluded that the changes in HBF observed during hypoxia in the anaesthetized rabbit cannot be attributed to stimulation of the peripheral chemoreceptors by hypoxia. 24. Prolonged hypoxia causes selective hypertrophy of the right ventricle (RV) in animals and man. Hypertrophy of the left ventricle (LV) in hypertensive rats is accompanied by an increase in intracellular pH (pH,) and in intracellular buffering capacity (Saborowski et al., 1973, Respiratory Physiology, 18, 171). There has been no comparison of the effect of chronic hypoxia on pHi in muscle from RV and LV. Groups of up to twenty male rats (Cummins Sprague Europe) were maintained at a constant Po, of either 19.9 5 0.4 kPa or 12.0 k 0.27 kPa (meant SD) in an environmental chamber for 28 days. The mean chamber Pco,was 0.1450.14 kPa for both groups and the average chamber temperatures were similar. Food and water were freely provided. After 28 days the rats were removed from the chamber and anaesthetized with ether. Aortic blood was then sampled while the animal breathed a gas mixture similar to that in the chamber through a mask and muscle was removed from the atria, RV and LV. The extracellular fluid volume (ECFV) was calculated from the distribution volume of [51Cr]EDTA and the pHi measured using the [14C]DM0 technique. The hypoxic rats weighed 386+11 g as opposed to 411 & 25 g for controls (P<O.OOl). The weight of the LV muscle was 701 ?C 35 mg in control rats and 648 5 48 mg after hypoxia ( P < 0-001) whereas RV muscle weight increased from 168521 mg to 241528 mg (P<0401). These findings agree with Hunter et al. (1974, Clinical Science and Molecular Medicine, 46, 375) who used a similar chamber. The ECFV of the RV did not change significantly (23 rt 3.4% control, 21.3 rt 3.2% after hypoxia; P>O.1) nor was there any change in the ECFV of the LV, or atria. The pHI of muscle from each of the heart chambers did not change despite a significant difference in arterial pH (7.47 k0.04 hypoxic group, 7.39 5 0.05 control ; P < 0.001) and arterial Pco, (3.50 ik EXTRACELLULAR SPACE AND INTRACELLU-0-33 kPa hypoxic group, 5.73k0.86 kPa control, P < 0.001) between the groups.These results show that in spite of hypertrophy of the right ventricle in chronic hypoxia, there is no change in ECFV o...

Characterization of beta‐adrenoceptor subtype mediating the metabolic actions of salbutamol.

“…This insulin release appears to be mediated by direct stimulation of pancreatic 13-adrenoceptors rather than being secondary to blood glucose elevation which was relatively less in magnitude and slower in onset. These results with salbutamol are similar to those with isoprenaline, a non-selective P-adrenoceptor agonist, and are in agreement with those of other workers (Goldberg et al, 1975;Massara et al, 1975;Leitch et al, 1976;Taylor et al, 1976). The pronounced fall in serum potassium during the salbutamol intravenous infusion results from a movement of potassium from extracellular to intracellular compartments secondary to stimulation of insulin release and glycolysis.…”

“…salbutamol, by intravenous administration are currently used in the treatment of severe asthma (Fitchett, McNicol & Riordan, 1975;Marlin & Turner, 1975a & b;Williams, Parrish & Seaton, 1975), cardiovascular shock (Wyse, Gibson & Branthwaite, 1974) and premature labour (Liggins & Vaughan, 1973;Korda, Lineham & Jones, 1974). Numerous metabolic effects including insulin release, hypokalaemia, lipolysis and glycogenolysis, which have important clinical implications, have been reported with salbutamol in animals (Loubatieres, Mariani, Sorel & Savi, 1971) and man (Goldberg, van As, Joffe, Krut, Bersohn & Seftel, 1975;Massara, Fassio, Camanni & Molinatti, 1975;Leitch, Clancy, Costello & Flenley, 1976;Taylor, Gaddie, Murchison & Palmer, 1976;Wang & Clansen, 1976). Although insulin release is mediated by stimulation of pancreatic 3-adrenoceptors (Porte, 1967;Imura, Kato, Ikeda, Morimoto & Yawata, 1971;Loubatieres et al, 1971;Goldberg et al, 1975), the subtype of f-adrenoceptor, i.e.…”

Effects of the beta 2‐adrenoceptor antagonist ICI 118,551 on exercise tachycardia and isoprenaline‐induced beta‐adrenoceptor responses in man.

“…The effects of ICI 118,551 on finger tremor were similar to propranolol but different from atenolol which, nonetheless, resulted in some attenuation of tremor responses. The metabolic tests used were chosen because they are influenced by stimulation of 12adrenoceptors (Leitch et al, 1976;Holgate et al, 1980). Isoprenaline induced significant changes in each metabolic parameter, though the effect on free fatty acid was not sensitive to the degree of antagonism studied, a finding which has been observed previously (Harms et al, 1978).…”

Bronchial Hyperresponsiveness and Anesthesia

“…If albuterol is given intravenously or if excessive doses are inhaled, the resultant high plasma concentrations can effectively abolish P2 selectivity such that bronchodilation and tachycardia may occur to the same extent (19). These drugs are highly effective for prophylaxis of bronchoconstriction and vital for acute therapy to reverse it.…”