effect of hydroalcoholic extract of olive leaves on blood pressure in rat model of two-kidney, one-clip goldblatt hypertension

In Iran's traditional medicine, the leaves of olive tree are of value for the treatment of hypertension. This study was designed to examine the effects of hydroalcoholic extract of olive leaves in rat model of two-kidney, one-clip hypertension and to further explore whether its hypotensive activity was mediated by enhancing the basal release of endothelium-derived nitric oxide. Animals were divided into two main groups including sham-operated and renal artery-clipped ones. The latter was further divided into 5 groups of untreated rats, vehicle-treated rats, which received daily oral administrations of one ml distilled water, and extract-treated rats receiving olive leaves extract at 50, 150 or 500 mg/kg in the same volume of vehicle starting the next day after the operation. Four weeks later, mean blood pressure and heart rate were measured under anesthesia before and after the administration of NG-nitro-L-arginine methyl ester [L-NAME]. Mean arterial pressures, and right kidney and heart weights of untreated and vehicle-treated renal artery-clipped rats were significantly higher but left kidney weights were significantly lower than those of shamoperated animals. However, there was no significant difference between the heart rates of these groups. Compared to vehicle-treated renal artery-clipped rats, treatment with hydroalcoholic extracts of olive leaves at 50, 150 or 500 mg/kg/day was associated with significantly lower mean arterial pressure, right kidney and heart weights but did not affect heart rate or left kidney weights. The intravenous administration of L-NAME resulted in a significant increase in mean arterial pressure in sham-operated and extract-treated rats whereas there was no change in renal artery clipped or vehicle-treated groups. The findings of the study show that hydroalcoholic extract of olive leaves prevents the clipinduced increase in mean arterial pressure, which might be partly mediated by enhancing the basal release of nitric oxide

[Vanadyl sulphate and its regenerative and trophic effects on beta cells of pancreas of STZ-induced diabetic mellitus rats]

Vanadyl sulfate [vanadium] has insulin like activity and trophic effects on the pancreatic beta cells of experimental-induced partial diabetic mellitus rats. In this study we investigated the trophic and regenerative effects of vanadium on pancreatic beta cells in conjunction with its insulin like actions in moderate diabetic rats. Moderate diabetic hyperglycemia was induced by IV injection of 40 mg/kg streptozotocin [STZ]. Diabetic animals with blood glucose levels [BG] of 500-600 mg/dl were randomly divided into three groups and treated as follows: group I [n=9], remained untreated [diabetic] whereas normoglycemia was induced in group II by daily IP injection of NPH insulin [n=11]; and group III [n=10] used fluid containing 1mg/ml vanadium. Blood samples were taken at specified times during the two months of treatment by nicking the tip of the tail to measure BG. Finally the rats were deeply anesthetized and sacrificed for histological evaluation of their pancreas. BG remained high in group I [552 +/- 7mg/dl], whereas group II were euglycemic and in group III, vanadium reduced BG level to 320 +/- 33mg/dl. Comparison of histological slides obtained from the pancreases of the three groups, with the exception of group III, revealed small and scarce islets of the pancreas, whereas, in group III, vanadium increased the size and the number of these islets looking like of normal rats. Amelioration of hyperglycemia in conjunction with increases in the size and the number of beta cells of group III seems to indicate that vanadium has regenerative and trophic effects on degenerated beta cells of moderate diabetic rats, and therefore, seems to cure diabetes by improving the activity beta cells of diabetic rats when degeneration of beta cells was not complete

Effects of noise exposure on the volume of adrenal gland and serum levels of cortisol in rat

Noise pollution is considered as a stressful factor in every day's life of the industrial world. The present study was designed to investigate the probable effects of different time exposure of noise stress on histomorphometric changes of adrenal gland, plasma cortisol and body weight of the rat. Sixty adult male Wistar rats were divided into two series of short time noise or STNE exposure [n=20] for one day and long time noise exposure or LTNE [n=40] for 30 days with a sound intensity of 100 dBA. LTNE series were further divided into five groups of control, sham, 4, 8 and 12-hrs noise exposure and STNE series were divided into four groups of the same as LTNE except sham group. The cortisol assay was performed on blood samples of pre and post treatment with noise in two series and Cavalieri methods in a stereological study for determination of adrenal volume changes only in LTNE series. The results showed that the mean plasma cortisol level [5.4 +/- 3.2 micro g/dl in LNTE-8 hrs and 4.9 +/- 1.8 micro g/dl in LNTE- 12 hrs], the volumes of cortex [7.08 +/- 1.31 mm[3] in LNTE-8h and 7.12 +/- 1.31 mm[3] in LNTE-12h], medulla [0.68 +/- 0.19 mm[3] in LNTE-8 h] of adrenal gland increased. The mean animal weight did not show any significant changes. Sound pollutions can increase the stress hormone level and cause increasing the volume of adrenal gland that may be related to the effect of noise on the hypothalamuspituitary- adrenal axis. These results may be important to increasing of many disorders such as cardiovascular diseases in industrial societies

Pre-ischemic treatment of pentoxifylline reduces infarct volumes in transient focal cerebral ischemia in the rat

Pentoxifylline [PTX] is used in human for intermittent claudication and cerebral vascular disorders including cerebrovascular dementia. It also inhibits the synthesis of tumor necrosis factor-

Effects of vanadyl sulphate on spermatogenesis in male rats

It is known that vanadyl compounds are capable of alleviating hyperglycemia in streptozotocin induced diabetic rats. To examine the effect of vanadyl sulphate [VS] on spermatogenesis of male rats. Male rats [n=10] were administered 32 mg/kg/day of VS orally and 50 mEq/l NaCl [as drinking water] for one month. Meanwhile, 11 male rats, the control group, received vehicle only; 50 mEq/l NaCl as drinking water. At the end of the study, blood testosterone level as well as spermatogram of rats in both groups were determined. The animals were sacrificed and their testes and epididimes were then studied under light microscope. In VS treated group, blood testosterone level, and sperm count were significantly decreased by 51% [normal = 2.83 0.7 ng/ml, p<0.001], and 80% [normal = 565 106/ml, p<0.05], respectively, as compared to the control group. However, sperm motility, shape, and histology of testes and epididymides were not different from those of the control group. Vanadyl sulphate has detrimental effects on spermatogenesis

Cardiovascular responses to hypercapnia and varying levels of arterial pH in the anesthetized cat

Effects of acute hypercapnia on the cardiovascular system [CVS] were studied in the anesthetized cat. After surgery the animal was exposed to a gas mixture of 12% CO2 and 25% o2 in nitrogen, and hypercapnia with low levels of arterial pH [pHa] was produced for 20 minutes. In the second run the same level of hypercapnia was induced by ventilating the same cat from the above gas mixture but pHa was kept normal by a slow and continuous infusion of THAM [0.5 mM/ kg/min]. Results of this study showed that hypercapnia increased aortic flow and induced peripheral vasodilation. Hypercapnia produced tachycardia in the presence of arterial acidosis whereas in its absence this response reversed to bradycardia. Hypercapnia increased mean arterial blood pressure [Pa] by 20% during low pHa, whereas this increase was only 10% in the absence of arterial acidosis. Therefore, it is concluded that hypercapnia in conjunction with arterial acidosis has a much stronger stimulatory influence on the CVS via different arterial chemoreceptors

Metabolic acidosis and severe hypotension: influence on survival time and shock period during hemorrhage in the cat

Metabolic acidosis and severe hypotension are the main causes of irreversibility during hemorrhagic shock. The influence of these two factors on durations of shock period and survival time were studied in four groups of anesthetized cats. In group I the animals were made hypotensive by reducing mean arterial blood pressure [Pa] to 45 mmHg with concurrent metabolic acidosis. In group II the same level of hypotension was produced, along with an intravenous infusion of 12% sodium bicarbonate solution [0.25 ml/kg/min.]; thus metabolic acidosis was prevented and arterial blood pH [pHa] was kept within its normal range- In group III the Pa was kept at 50 mmHg in the presence of metabolic acidosis, and in group IV, the Pa was kept at 50 mmHg [the same as group III] but acidosis was prevented. Durations of shock period and survival times of all groups were compared. The results of this study show that 1] preventing metabolic acidosis increased survival time by 400%, 2] keeping the Pa at 50 mmHg increased survival time by 800%, and 3] prevention of metabolic acidosis at a Pa of 50 mmHg still augmented survival time by more than 250%. We therefore conclude that control of pHa and prevention of severe hypotension may increase survival rates in patients suffering from hemorrhage

Hypoxia and its influences on the cardiovascular and respiratory systems of spontaneously breathing cats

Effects of acute systemic hypoxia on the cardiovascular system [CVS] and respiration of spontaneously breathing cats were studied in two conditions. 1]: Hypoxic air [6-8% 02 in N2] was given to the animal to induce systemic hypoxia for 20 minutes. Hyperventilation at this condition lowered arterial C02 tension [PaC02; hypocapnia]. 2]: In the second run, induction of hypocapnia was prevented by adding 3-5% C02 to hypoxic air. Comparison of the results of this study indicated that hypoxia, independent of the presence of hypocapnia, caused a significant increase in respiratory rate, aortic flow and arterial blood pressure. However, in the presence of hypocapnia, the increased respiratory rate was 10% less and a general arterial vasconstriction was observed

Trophic effects of Vanadyl sulphate on pancreatic Beta cells of chronic partially streptozotocin-induced diabetic rats

Rats were made partially diabetic by intravenous injection of 40 mg/kg body weight streptozotocin [STZ]. Diabetic rats received 50 mEq/l sodium chloride [base solution] as drinking water for one month and then divided into two groups. Group I rats only received base solution for another month whereas group II were switched to 0.5-1 mg/ml vanadyl sulphate [VS] in base solution. Two months after induction of diabetes another blood sample was taken and all rats were killed to save their pancreases for histopathologic evaluations. Blood glucose levels and fluid intake of group I rats were 550 +/- 15 mg/dl and 210 +/- 8 ml/day respectively. Their plasma insulin, however, decreased to 50% of normal control rats [27 +/- 3 microU/ml]. Blood glucose and water intake of group II rats declined to 185 +/- 7 mg/dl, 25 +/- 4 ml/day but plasma insulin rose to 47 +/- 5 microU/ml which were significantly different from the results obtained in group I. Although the central cells of Islets of Langerhans of untreated diabetic rats were shrunken or missing in the VS treated rats of group II these islets showed almost normal islets with some proliferation and hypertrophy of their beta cells. In conclusion it appears that VS ameliorates diabetes in STZ-induced chronic partially diabetic rats by proliferating the remaining viable beta cells and normalizing the serum insulin level

Hypoxia and its influences on the cardiovascular system of self breathing cats

Effects of acute hypoxia with/without the presence of hypocapnia on the cardiovascular system [CVS] were studied in anesthetized spontaneously breathing cats. After preparation, hypoxic air [8% O[2] and 92% N[2]] was given to the animal to reduce arterial O[2] tension to 45 +/- 3 mmHg. Stimulation of carotid chemoreceptors by hypoxic blood induced hyperventilation and the outcome was hypocapnia and alkalosis. It is shown that these two parameters reduce carotid chemoreceptor sensitivity to hypoxia. Hence, we tried to determine if this combination would hamper the influences of hypoxia on the CVS. Therefore, in a second run in the same cat induction of hypocapnia and alkalosis was prevented by adding 5% C0[2] to hypoxic air. The results of this study indicated that, hypoxia alone did not change vascular tone and heart rate; but it did increase respiratory rate, aortic flow, and mean arterial blood pressure [Pa]. The combination of hypoxia with hypocapnia diminished the stimulatory influences of carotid chemoreceptors on respiration. Despite the presence of bradycardia, aortic flow, Pa, and vessel tone did not change. From this observation we conclude that the reflex effect of hypoxia on vascular tone is not affected by hypocapnia; whereas, its negative chronotropic effect on the heart is potentiated

influence of vanadyl sulphate on islet cells, blood glucose and insulin levels of normal and STZ-induced diabetic rats

We have studied the influence of vanadyl sulphate [VS] on islet cells, blood glucose and insulin levels of normal and STZ-induced diabetic rats. Normal rats were given daily VS solution for one month and their blood glucose level was found not to differ from normal control rats, whereas their plasma insulin level was significantly lower and histological sections of pancreas showed that islets were larger in size and more abundant in number. The beta cells were hypertrophic and hyperplastic. In STZ-induced diabetic rats with blood glucose levels of more than 500 mg/dl and insulin levels of less than 30 micro U/ml. we found that one month after administration of VS, blood glucose and insulin levels became normal. Islets, which were shrunken and their beta cells almost destroyed at three days after STZ- injection, showed hyperplasia and hypertrophy. We conclude that: oral administration of VS can induce the proliferation of beta cells of normal rats while preserving their sensitivity to blood glucose level. VS, in STZ-induced diabetic rats, seems either to protect the beta cells from destruction or possibly induce their regeneration from undisturbed beta cells. Furthermore,we did not notice toxic effects of VS on any organ when histologically compared to normal ones