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At least two developmental responses necessary to prepare the fetal lung to serve as a gas-exchange organ, the release of surface-active material and the reabsorption of alveolar water, can be stimulated by beta-adrenergic agonists. The sensitivity of these responses increases dramatically in late gestation. beta-Adrenergic receptors can be identified by radioligand binding and are present in human fetal lung as early as 16 weeks of gestation. The temporal relationship of the increases in both pulmonary beta-receptors and plasma-free cortisol in the fetal rabbit during gestation suggests that endogenous glucocorticoids may cause increased concentration of pulmonary beta-receptors. Treatment of pregnant rabbits at 24 or 25 days of gestation results in precocious increases in both fetal lung beta-receptors and agonist-specific, high-affinity binding. The increase in receptor concentration with glucocorticoid is not dependent on other endocrine response inasmuch as 0.1 microM dexamethasone increases beta-receptor concentrations at 24 and 48 hours of incubation in cultures of fetal rabbit lung organ. This effect of glucocorticoid to increase beta-receptor concentration and high-affinity binding may explain the increased fetal pulmonary beta-adrenergic response at term and may be responsible in part for the reduction in neonatal respiratory syndrome seen after antenatal glucocorticoid therapy.
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In 14 patients undergoing cardiac catheterization for suspected coronary artery disease, alinidine, 0.6 mg/kg, was administered intravenously to determine its effects on left ventricular (LV) function, coronary blood flow and myocardial oxygen consumption. To assess effects independent of changes in heart rate (HR), measurements were made at spontaneous and matched pacing HRs. At spontaneous HR, alinidine decreased HR from 70 ± 2 to 61 ± 3 beats/min (p < 10−6). Peak rate of LV pressure decreased from 1,652 ± 92 to 1,371 ± 80 mm Hg/s (p < 10−5) and Vmax decreased from 47 ± 3 to 41 ± 2 s−1 (p < 10−4). Coronary sinus blood flow decreased from 109 ± 9 to 89 ± 7 ml/min (p < 0.01) and myocardial oxygen consumption from 10.9 ± 1.0 to 9.0 ± 0.8 ml O2/min (p < 0.05). At a matched pacing HR of 98 ± 3 beats/min before and after alinidine administration, peak rate of LV pressure decreased from 1,984 ± 124 to 1,793 ± 106 mm Hg/s (p < 10−4) and Vmax from 60 ± 5 to 56 ± 4 s−1 (p < 0.02). Coronary sinus blood flow and myocardial oxygen consumption were not significantly changed at matched pacing HRs. The time constant of the first 40 ms of LV isovolumic relaxation was prolonged by alinidine only during spontaneous HR. Thus, alinidine results in a bradycardia-dependent decrease in myocardial oxygen consumption. It has negative inotropic properties independent of changes in HR and so is not a pure bradycardia-specific agent.
