Summary
The effect of prostaglandin E2 on the activity of the pregnant human uterus in vivo has been studied in 50 women at or near term and in need of induction. Labour was successfully induced in all cases with a continuous infusion of 0·5 μg./min. The uterine activity produced by prostaglandin infusion resembled that of normal spontaneous labour. No unphysiological increase in uterine tonus was observed. The average infusion time was 5·5 hours and the average infusion‐delivery interval was 10 hours.
Summary1. The antagonism of the smooth muscle stimulating actions of PGF2a and PGE2 by polyphloretin phosphate (PPP) was studied on several isolated smooth muscle preparations and on the blood pressure of the anaesthetized rabbit. 2. PPP (2'5-20 ,ug/ml) reversibly inhibited contractions of the jird colon produced by PGE2 or PGF2a; PGF2a was more readily antagonized than PGE2. 3. PPP (2S5-30 jug/ml) reversibly antagonized contractions produced by PGE2 and PGF2a on the isolated rabbit jejunum and uterus. In these preparations PPP antagonized PGE2 as readily as PGF2a. 4. It is concluded that PPP is a selective antagonist to the prostaglandins on these tissues, for contractions produced by other agonists, such as acetylcholine, angiotensin, 5-hydroxytryptamine and bradykinin were not reduced by concentrations of PPP which markedly antagonized responses to the prostaglandins. 5. Intravenous injections of PPP (25-200 mg/ kg) resulted in a variable antagonism to the fall in blood pressure produced by intravenous injections of PGF2a in the anaesthetized rabbit; vasodepressor responses produced by PGE2 and acetylcholine were not antagonized. 6. The mechanism of this antagonism by PPP is not clear and must await further investigation.
1. Adrenaline, noradrenaline and phenylephrine caused contraction of the corpus cavernosum muscle of the human penis. These sympathomimetic amines did not product inhibitory effects even in the presence of the alpha-adrenoreceptor blocker, phentolamine. The effect of dopamine was similar to that produced by these three sympathomimetic amines. Higher doses of isoprenaline and salbutamol also contracted this preparation. 2. Cocaine and guanethidine enhanced the motor response to adrenaline, noradrenaline and phenylephrine while the action of dopamine was blocked by these two drugs. 3. The motor response to adrenaline, noradrenaline and phenylephrine was antagonized by phentolamine and often potentiated by the beta-adrenoreceptors blocking drug, propranolol. The contractions produced by high doses of salbutamol and isoprenaline were also abolished by phentolamine. These findings indicate that the motor response to sympathomimetic amines is the result of activation of alpha-adrenoreceptors in the corpus cavernosum muscle. 4. At low doses, isoprenaline and salbutamol relaxed the corpus cavernosum muscle strip. The inhibitory action was blocked by low concentrations of the beta-adrenoreceptor antagonist, propranolol but not by practolol (beta 1-adrenoreceptor antagonist) and butoxamine (beta 2-adrenoreceptor antagonist). beta-adrenoreceptors are present in the corpus cavernosum muscle but these are unlikely to be either of the beta 1 or beta 2 type. The possible existence of a third type of beta-adrenoreceptor is suggested.
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