study on the effect of calcitonin administration on hypophyseal - testicular axis in rats

The present study was designated to clarify the effect of calcitonin [CT] on the hypophysial testicular axis. A total number of forty adult male albino rats were used and they were classified into three main groups. The first group [control group] consisted of 10 adult male albino rats, which were injected intramuscularly with saline allover the period of experiment. The second group: [sCT-, administered group] consisted of 10 adult male albino rats, which were injected with sCT intramuscularly on alternative days, in a dose of 10 U/kg body weight/days for 4 weeks at 10 AM. However the third group [orchidectomized group consisted of 20 adult male rats. This third group was subdivided into two equal groups: Orchidectomized control group which was injected intramuscularly with saline, two weeks after the operation, for four weeks and Orchidectomized CT-administered group which were injected intramuscularly with sCT, two weeks after the operation, on alternative days in a dose of 10 U/kg body weight day for 4 week at 10 AM. The plasma levels of FSH, LH and testosterone were estimated [by radioimmunoassay] and the Ca[2+] plasma levels were estimated [by Clorometric method] for all groups. Also, histopathological examination was performed for the testes of the first and second groups to evaluate the local effect of CT and also to identify the effect of change in plasma gonadotropin levels on the testes.The results of these investigations showed that, the testosterone plasma levels were significantly decreased in healthy group after sCT administration, the FSH and LH plasma levels were significantly decreased in both healthy and orchidectomized groups after sCT administration and sCT administration caused insignificant change in Ca[2+] plasma levels in both healthy and orchidectomized groups after sCT administration. The histopathological study revealed that sCT administration caused thickening of the basement membrane of the seminiferous tubules in 20% of the total number of rats treated with sCT, thickening of the basement membrane and replacement of the interstitial cells of Leydig by halonosis in 50% of the total number of rats treated with sCT and thickening of the basement membrane, replacement of the interstitial cells of Leydig by halonosis and spermatic arrest at the stage of secondary spermatocytes in 30% of the total number of rats treated with sCT. From the above results, it could be concluded that CT administration resulted in a significant reduction in testosterone plasma levels that may be through a reduction in pituitary gonadotropins secretion and through a direct effect on the testes

Possible protective role of nitric oxide in myocardial ischemia

Much interest has been focused on the role of endogenous and exogenous NO pathways as regulators of cardiovascular function in health and disease. Despite the great number of studies on the effect of nitric oxide on cardiac functions under basal and ischemic conditions, however their results remains highly controversial.So this study was designed to throw more light on the role of endogenous NO [synthesized of L-argenine] and exogenous NO [from sodium nitroprusside] in modulation of myocardial function in ischemic conditions A total number of 80 isolated hearts from adult male white New-Zeland rabbits weighing 1.5-2 Kg, grouped into 8 groups were used in this study. When administered before 25 min of global ischemia and early in reperfusion it was found the NO donors L. Arginine, SNP induced a significant cardioprotective effect expressed by a reduction in the percentage of post ischaemic cardiac damage. This was manifested by a lesser reduction in heart rate, amplitude of contraction, coronary flow rate and also lesser lactate dehydrogenase [LDH] release when compared with control group. While administration of NOS inhibitor L. NAME or guanylate cyclase inhibitor MB induced cardiac damage manifested by an increase in the percentage of post ischaemic reduction in heart rate, amplitude of contraction, coronary flow rate and an increased LDH release as compared to control group. Co-administration of NO donors with NO inhibitors abolished the cardio protective effect of NO donors. In conclusion it was found that NO has a significant cardio-depressant effect under basal conditions, however it increased coronary flow rate and moreover, NO donors have a significant cardio protective effect, following ischaemia and reperfusion. These findings may have clinical value as it illustrate the role of NO donors as potential therapeutic agents in the treatment and prevention of coronary artery disease

Relative arteriovenous potency of nitric oxide

Much interest has been focused on the role of endogenous and exogenous nitric oxide [NO] pathways as regulators of cardiovascular function in health and disease. Moreover, despite the well documented vasodilator effect of NO, the relative arteriovenous potency of nitric oxide donors and inhibitors and the role of NO in portal circulation remain unclear. So this study was designed to throw more light on the role of NO on different blood vessels in vitro. This work studied the effect of L-NAME, L-arginine,SNP and MB in 3 different doses on the contractile effect of submaximal dose of noradrenaline on isolated dog aortic,femoral artery,femoral vein and portal vein strips. L-NAME and MB induced a significant increase of noradrenaline induced contraction in all vascular strips with all tested doses. However the response of venous strips was significantly higher than arterial strips with the least effect on aortic strips and highest on portal vein strips indicating a higher sensitivity of veins especially portal vein and the importance of NO in maintenance of basal vascular tone in all tested strips. On the other hand L-arginine and SNP induced a significant reduction in the noradrenaline-induced contraction in all vascular strips with all tested doses. This effect was more in veins especially portal vein than arterial strips.This veno-selectivity illustrate a potential role for NO in control of venous tone and in turn preload which is a major risk factor in some cardiovascular diseases as heart failure.Also the high portal sensitivity under basal condition suggest a possible use of NO as therapeutic agents in portal hypertension, however further studies on portal hypertensive subjects are recommended to illustrate its effects under condition of increased portal pressure

Influence of angiotensin-converting enzyme inhibition on experimental portal hypertension in rabbits

In this study we evaluated the effect of angiotensin converting enzyme inhibitor [ACEi] [captopril] on the portal venous pressure and angiotensin II plasma level in normal and experimentally induced portal venous hypertension in rabbits [PHT] [by partial ligation of portal vein for 3 weeks]. It was found that captopril administration reduces the portal venous pressure insignificantly from 7.23 +/- 0.47 mmHg in control group to 6.96 +/- 0.32 [P > 0.05] and caused insignificant reduction of angiotensin II plasma level from 6.98 +/- 0.63 pg/ml in control group to 6.75 +/- 0.39 pg/ml [P> 0.05]. However, after partial ligation of portal veins the portal venous pressure rises to 13.53 +/- 0.51 mmHg and decreased significantly by captopril to 8.7 +/- 0.86 mmHg [p < 0.001] also angiotensin II level increased in PHT rabbits to 11.77 +/- 0.65 pg/ml [P < 0.001] and reduced significantly by captopril to 7.66 +/- 0.67 pg/ml. [P < 0.001]. We conclude that ACE inhibitors may be of great value in treatment of patients with portal hypertension and esophageal varices