An in vitro perfused rat ovary model was characterized with respect to ovulation rate, oocyte maturation and steroidogenesis after priming with various doses of pregnant mare's serum gonadotrophin (PMSG) (10, 20 or 30 IU PMSG s.c. in the morning of day 28). In ovaries stimulated with LH 0.1 microgram ml-1 after 1 h of perfusion the number of ovulations was significantly higher in the 20 IU PMSG group than in the to IU PMSG group (6.8 +/- 1.0 ovulations per treated ovary versus 2.4 +/- 1.2, P less than 0.01). Priming with 30 IU PMSG did not result in significantly more or fewer ovulations than did 10 or 20 IU PMSG. No ovaries in the non-stimulated control groups ovulated. Oocytes retrieved directly at ovulation were mature (GVB or PB stage). Among oocytes retrieved from pre-ovulatory follicles punctured at 0, 2, 4, 6 and 8 h after stimulation with LH 0.1 microgram ml-1 there was an increasing number of oocytes with GVB (0/10 at 0 h and 10/10 at 8 h). Stimulation with LH resulted in a rapid release of progesterone, testosterone and oestradiol into the medium, whereas non-stimulated control ovaries exhibited a slow rise of all steroids throughout the perfusion period. It is concluded that priming with 20 IU PMSG in this model results in an optimal number of ovulations and that this model provides a useful tool in studies of various kinds of modifying influences on the ovulatory process.

Effects of norepinephrine (NE) and isoproterenol on simultaneously recorded electrical and contractile activity in rat portal vein were studied using a sucrose-gap technique. This vascular smooth muscle shows spontaneous phasic contractions correlated with bursts of action potentials. Norepinephrine (10" 9 to 10" 7 w/v) increases the duration of the bursts and shortens the interval between bursts after an initial period of continuous spike discharge. The tension response is greater than can be accounted for by the increase in electrical activity. High NE concentrations (10~3) produce depolarization, decrease of spike amplitude, or even abolition of spikes and maintained contractions. Norepinephrine increases contracture tension of K + -depolarized portal vein without changing membrane potential. Electrical and mechanical activity is reinitiated in preparations inactivated by elimination of Ca 2 + ; this may be due to release of bound calcium. Phenoxybenzamine abolishes the above NE responses. The typical response to isoproterenol (10" 9 to 10~7) in a normal ionic environment consists of moderate depolarization, decreased burst duration, but increased frequency of bursts and inhibition of tension development which is not simply correlated with the change in electrical activity. This pattern resembles that produced by lowering [Ca agent used and on the vascular bed studied. The cellular mechanisms responsible for these opposite reactions of vascular smooth muscle to adrenergic agents are insufficiently understood. A better understanding of these excitatory and inhibitory actions would require, among o:her things, a more complete knowledge of the electrophysiological events associated with the mechanical changes.In the previous article in this issue (4), we have described the technique used here for simultaneous recording of electrical and mechanical activity of the isolated rat portal vein and the responses of this preparation to changes in ionic composition of extracellular fluid. The present paper describes the electrical and mechanical responses to norepineph-