Effect of changes in nitric level oxide on myometrial contractility in pregnant and non-pregnant rats

Nitric oxide [NO] has been recognized as a molecule that shares in regulation of the reproductive system physiology. The present study aimed to investigate the effects of NO excess and NO deficiency on spontaneous myometrial contractions and on myometrial responsiveness to oxytocin as well, in both non-pregnant and late pregnant rats. Female adult rats were divided into two main groups: estrogen-primed non-pregnant model and time-mated late pregnant model. Rats in each model were divided into three groups: a control group, L-arginine-treated group and L-NAME-treated group. Myometrial strips taken from the different groups were suspended in organ bath containing Krebs' solution, gassed with 95% O2 and 5% CO2 for recording of isometric contractions. Spontaneous uterine motility was recorded, followed by oxytocin addition for recording of myometrial responsiveness to this hormone. Serum nitrate level was determined in all rats. L-arginine supplementation caused a significant increase in serum nitrate levels in both rat models, accompanied by decreased spontaneous myometrial contractility and attenuation of the stimulatory effect of oxytocin in both non-pregnant and pregnant rats, compared to the control values. The predominating effect in the non-pregnant model was on the average force, and in the pregnant model on the frequency of contraction. Following treatment with L-NAME. serum nitrate was significantly decreased, yet the spontaneous myometrial contractility and its responsiveness to oxytocin were non-significantly changed in both non-pregnant and pregnant rats, compared to the control group. The NO donor L-arginine has proved to have an inhibitory effect on both spontaneous and oxytocin-induced myometrial contractions, when administered in vivo, in both non-pregnant and late pregnant states, establishing the importance of the L-arginine/NO system as a uterine smooth muscle relaxant. L-arginine could, therefore, provide a useful therapeutic measure for conditions with pathological uterine contractility, like dysmenorrhea or preterm labor, taking into consideration that increased NO attenuates myometrial responsiveness to oxytocin

Enhanced coronary flow following experimental androgen deprivation by orchidectomy

Androgen deprivation is an effective treatment for patients with advanced prostate cancer. The present work was conducted to study the impact of testosterone deprivation on cardiac functions and coronary flow. Experimental androgen deprivation was induced in rats by orchidectomy, compared to sham-operated controls. Two weeks after operation, rats were subjected to measurements of body weight, plasma testosterone and ECG recording. Cardiac functions were studied on isolated perfused hearts in a Langendorff preparation, under basal conditions and following exposure to 30 minutes of global ischemia followed by another 30 minutes of reperfusion. The following parameters were assessed: heart rate [HR], peak tension [PT], time to peak tension [TPT], half relaxation time [HRT], and myocardial flow rate [MFR]. Absolute weights of different cardiac chambers and their relative weights were also determined. The orchidectoimzed [ORX] rats exhibited non significant changes in ECG parameters, significant increase in absolute weights of whole heart and left ventricle, associated with significant body weight gain. Hearts isolated from ORX rats displayed a significant increase in basal preischemic MFR compared to their matching controls. Upon isehemia reperfusion [I/R], MFR of hearts isolated from ORX rats was still higher compared to controls, After 30 minutes of reperfusion, hearts of control rats displayed non significant change in HR associated with significant decrease in MFR as compared to preisehemie values; while in hearts of ORX rats, HR was significantly decreased, and accompanied with non significant changes in MFR. The augmented MFR in response to I/R, in ORX rats,, was however associated with significant increase in TPT and HRT, indicating impaired ventricular contractility and delayed relaxation, respectively when compared to controls. Upon I/R, PT was preserved in ORX group, while it was deteriorated in the controls, as compared to the preischemia values. Expenmental androgen deprivation induced marked increase in coronary flow, possibly due to lack of the predominant vasoconstrietor effect of testosterone hormone