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Abstract
Adult female rabbits were injected with phenoxybenzamine (α-adrenoceptor blocker) (Group 1), propranolol (β-adrenoceptor blocker) (Group II), and Isocarboxazid (MAOI) (Group III). Physiological saline was injected in the controls. Treatment started one day before mating and continued until autopsy. At 3, 12, and 24 hr postcoitum (PC), utero-oviductal contractions were recorded in vivo using micro-balloon-ended, fluid-filled catheters as pressure receptors. At 24 hr PC, all groups were autopsied and flushings of the contralateral oviducts were evaluated for both sperm count and number of sperm attached and/or penetrating the eggs. Phenoxybenzamine induced reduction in the amplitude and frequency of both active contractions and resting pressure fluctuations. This suppressive effect was more remarkable at 12 and 24 hr PC than at 3 hr PC. Propranolol induced incoordination and instability in the utero-oviductal resting pressure and increased the amplitude of isthmic contraction, and in frequency of uterine and ampullary contractions. Such excitatory effects were more pronounced at 3 hr PC than at 12 and 24 hr PC. More effective α-adrenergic blockade seemed to coincide with postovulatory progesterone dominance, increase in concentration, and response to genital tract PGE. More effective β-adrenoceptor blockade coincided with preovulatory estrogen dominance and increased concentration and response to genital tissue PGF. At 24 hr PC, sperm count was reduced in the oviduct and fewer numbers of sperm were attached to the eggs in phenoxybenzamine- and propranolol-treated females. Phenoxybenzamine -induced suppression of utero-oviductal contractions facilitated oviductal sperm ascent. Propranolol caused irregular sperm transport with rapid loss in the peritoneal cavity. At 24 hr PC, oviductal sperm count increased and an excessive number of sperm were attached to the eggs in isocarboxazid-treated rabbits. The pharmacology of sperm transport is discussed in relation to infertility and contraception.