possible role for testosterone hormone on lipid peroxidation and some parameters of oxidant-antioxidant balance in rat myocardial tissue

The link between androgens and coronary artery disease remains elusive and the possible mechanisms that may relate testosterone to the development of cardiovascular diseases have not been well established yet. This study was designed to clarify the effect of testosterone hormone on lipid peroxidation and oxidants-antioxidant balance in rat myocardial tissue. Forty male albino rats included in this study were divided into 4 equal groups. Group [1] served as control rats and the other three groups were subjected to castration. One week after castration, group [2] rats were injected with solvent, group [3] rats received i.m. testosterone enanthate 10 mg/kg once weekly and group [4] received i.m.daily injections of vitamin E [alpha-tocopherol] in a dose of 20 mg/kg/day. All injections were continued for 4 weeks then all rats were sacrificed by decapitation and the hearts were obtained and prepared for the estimation of lipid peroxides as thiobarbituric acid reactive substance [TBARS], nitrite concentration, glutathione [GSH], glutathione peroxidase [GSH-PX] activity and vitamin E [alpha tocopherol]. TBARS and nitrites concentrations were significantly higher in the myocardial tissue extract of group [2] than group [1] rats while GSH and GSH-PX were sign lower, indicating that castration put the rat myocardial tissue under oxidative stress. However, in group [3] and group [4], TBARS and nitrites were sign lower and GSH and GSH-PX activity were sign higher than group [2], indicating that testosterone replacement therapy as well as vitamin E therapy protected the castrated rats from the oxidative stress and restored the oxidant- antioxidant balance in rat myocardial tissue. It could be concluded that testosterone may have a role in preserving oxidant- antioxidant balance in myocardial tissue of albino rats and this may be one of the mechanisms that could explain a suggested cardioprotective role of testosterone

Effect of Ca++ channel blockers and H2 receptor blockers on Modulation of pain threshold and analgesic activity of morphine in rats

This work was carried out on 42 albino rate to study the effect of the C.C.B [verapamil] and. H2 receptor antagonist [ranitidine] on modulation of pain threshold and morphine antinociceptive action. Our study demonstrated that C.C.B [verapamil] has antinociceptive action to thermal stimulation indicating that Ca+ is an important mediator in pain pathway. However pretreatment of rats with a single Intraperitoneal dose [I.P] of C. C.B neither potentiates nor inhibited the analgesic activity of morphine. On the other h and C.C.B [verapamil] decreased the antinociceptive action of morphine when it was given in a single [I.P] dose after morphine injection. The H2 receptor antagonist [rantidine] induced antinociceptive activity which may be through its binding to opiate receptors as the opiate antagonist naloxone blocked this effect. Pretreatment of rats with ranitidine greatly potentiated the analgesic activity of morphine, a result which may be of value in reducing the dose of morphine and hence its side effects

experimental study of the interaction between opioid and adrenergic receptors in suprarenal function and lipid metabolism

The effect of chronic administration of butorphanol. a totally synthetic opioid with agonistic-antagonistic activity, on lipid metabolism and suprarenal function and its interaction with adrenergic receptors was investigated 40 mice were divided into four groups; the first group served as a control group, the second group received daily butorphanol injections for six weeks with gradual increase in dose every week. The third group received butorphanol and Co-dergocrine Mesylate [hydergine], an alphaadrenergic blocker, and the forth group received butorphanol and propranolol [Inderal], a beta adrenergic-blocker, for the same period. Animals were weighed at the beginning and at the end of the experiment and the following parameters were estimated at the end of the experiment: serum cholesterol, phospholipid-s triglycerides, liver triglycerides, serum Na+, K+ and cortisol. We found that butorphanol tartarate caused a significant decrease in body weight gain% and a significant increase in serum lipids [cholesterol, triqlycerides and phospholipids] with a significant decrease in liver triglycerides indicating an apparent inhibitory effect on lipid metabolism. Also, serum K+ increased with a significant decrease in serum sodium and serum cortisol indicating a possible suppressive effect of butorphanol on suprarenal function. We found also that the use of alpha or beta adrenergic receptor blockers could improve the body weight gain and ameliorate the effects of butorphanol on serum cholesterol, serum triglyceides, serum phospholipids. liver triglycerides, serum Na+. K+ and cortisol. We conclude that repeated administration of increasing doses of the synthetic opioid butorphanol could affect the lipid metabolism and the suprarenal function and that blocking of adrenergic activity by alpha or beta-adrenergic blockers may have a role in ameliorating these effects