Acta physiologica latino americana最新文献

A perfused preparation of the hind limb of normal and diabetic rats was used to study the effects of lactic acidosis, alone or associated with hypoinsulinemic diabetes, on the incorporation of glucose and inorganic orthophosphate (Pi) into the skeletal muscle. A well oxygenated perfusate was recirculated for ninety minutes during which the lactic acid accumulated into the medium with the ensuing pH drop. The perfusions were practiced in the hind limb of alloxanized diabetic rats, in the hind limb of diabetic rats with perfusate containing 200 microU of insulin/ml, in the hind limb of 24 hour fasted rats, and on the hind limb of fed rats, and they were compared to similar groups with normalized pH perfusate with a sodium bicarbonate infusion. In the diabetic perfusions with lactic acidemia, it was observed that the addition of insulin increased the uptake of Pi and of glucose, and reduced the release of Pi by the muscular tissues. A smaller release of Pi by the preparations obtained from fed rats was observed when compared to the hind limb preparations of fasted rats. The diabetic preparations showed an increased glucose uptake when the pH was normalized, and a decrease of Pi released by the muscles, even in the absence of insulin, and at the same time, the administration of insulin associated with the normalization of pH increased the uptake of Pi and of glucose, and decreased the Pi released by the muscles. In all the groups, the administration of sodium bicarbonate significantly increased the lactate release into the medium. It was also found that the lactic acidosis reduced the uptake of Pi by the preparations inducing hyperphosphatemia. According to these results, muscular tissue plays a role in the hypophosphatemia that has been reported in the insulin treated diabetic ketoacidosis by increasing the incorporation of Pi and reducing its release by the same tissue.

Pancreatic content of lipase, amylase, trypsinogen, chymotrypsinogen and protein was studied in suckling and weaned mice at different ages. Protein content in pancreatic tissue was low at 15 days when compared with 30, 45 and 60 days of age. Specific activities of lipase and chymotrypsinogen were higher at 15 days of age, but chymotrypsinogen was not different at the studied ages post weaning. Amylase exhibited the highest value at 15 days and a marked depression at 30 days, and trypsinogen specific activity was not different between the studied groups. The present study demonstrates an age dependent enzyme pattern in mouse pancreas and reflects an active biosynthetic mechanism in suckling mice.

The authors confirmed the presence of monoamines and 5-hydroxy-indolacetic acid (5-HIAA) in the cephalic region of Diloboderus abderus larvae employing a high pressure liquid chromatography (HPLC) with electrochemical detector. An anticholinesterase insecticide produced an increase in the serotonin and 5-HIAA endogenous levels, and did not modify the catecholamines. Monoamine-oxidase activity was undetectable with a radioactive method using 3H-tyramine as substrate.

The amount of ouabain bound to an enriched fraction of heart or kidney medulla is reduced by propranolol. The inhibitory effect is greater under conditions in which complex II formation is promoted. Similar concentrations of propranolol are able to produce a reduction in Na+, K+-ATPase activity, by reduction of the number of active sites without changes in ionic affinity. The lack of stereospecificity and the high concentrations (greater than 10(-4)M) required indicate that this effect is independent of beta adrenergic blockade. Effectiveness reduction of cardiac glycosides in the presence of propranolol could be due to inhibition of drug interaction with its receptor.

A melanoma cell line (Bowes) was found to produce plasminogen activator even on its growing phase, and the rate of plasminogen activator production was rather constant. The production of plasminogen activator was proportional to the cell number. Morphologically, no specific features for plasminogen activator production were seen. Plasminogen activator was observed in the lysate of this cell line only when the cell number was large. The extracellular plasminogen activator activity was higher than the intracellular plasminogen activator activity, suggesting the existence of a secretion mechanism for the plasminogen activator.

Urinary steroidal profiles were studied in five women with Cushing's syndrome and in two normal women that were chosen as controls, by means of gas chromatography and gas chromatography-mass spectrometry. Four patients presented ACTH-dependent adrenal hyperplasia and the last patient had an adrenocortical carcinoma. Steroids were analyzed in urinary extracts, as their respective trimethylsilyloximes and/or trimethylsilylderivatives. Qualitative and quantitative data about 36 urinary steroids were obtained. Three pituitary patients showed a well defined picture of "5-ene pathway" in adrenal function. The fourth patient depicted some primary deficiencies of corticosteroid biosynthesis that overshadowed most biochemical expressions of Cushing's disease. The patient with adrenal carcinoma developed a steroidal pattern resembling autonomous functioning of adrenal cortex inner zones, showing both "5-ene pathway" and "4-ene pathway" increase. This patient also had an unexpected excretion of a major metabolite of 18-hydroxycorticosterone, that did not correlate with parameters of aldosterone production. Tetrahydro-6-hydroxy-cortisol was determined in urine of two patients and original data about urinary cortoic acids in Cushing's syndrome are given. Peripheral reductive metabolism played the most important role in almost all patients. In turn, some oxidative metabolic pathways for cortisol were not specifically favoured in the cases of Cushing's disease here reported.

The role of plasminogen activator in ovulation was investigated using the inhibitor, trans-aminomethylcyclohexane carboxylic acid (t-AMCHA). In the regular cycle rat, the plasminogen activator activity of the follicles increased from the diestrus to the estrus phase. In the latter phase, a proteolytic enzyme which was not inhibited by t-AMCHA appeared. After ovulation, the plasminogen activator activity decreased. When ovulation was induced in immature rats by pregnant mare serum gonadotrophin and human chorionic gonadotrophin, remarkable fibrinolytic activity appeared in the ovaries immediately before ovulation. When t-AMCHA was given in the ovulation-induced rats, the fibrinolytic activity of the ovaries was suppressed, the number of ovulated ova decreased and the timing of ovulation was delayed. When t-AMCHA solution was given to rats in the proestrus phase, ovulation was almost completely suppressed, but aprotinin solution exerted no effect on ovulation. These results suggest that plasminogen activator is a key enzyme in ovulation, and that the chain reaction from plasminogen activator to proteolytic enzyme (including collagenase) is of greater importance than that of plasminogen activator to plasmin.

Serum circulating immune complexes (CIC) were measured in 27 patients with non insulin dependent diabetes (NIDD). This was done by measuring the degree of binding to human red blood cells by the C3b complement fraction. At the same time, the percentage of B lymphocytes in peripheral blood was evaluated by means of the direct immunofluorescence technique for surface IgG and EAC rosettes for cells with receptors to C3b complement fraction. Twenty normal control subjects were simultaneously studied by the same methodology. An increase in serum CIC was observed in NIDD patients, as compared to healthy subjects. Values were 35.8 +/- 3.2 and 25.6 +/- 2.1 micrograms/ml, respectively. The percentage of cells with surface IgG was 10.2 +/- 0.8 in diabetic patients; this value was significantly higher than that found in the control group (6.0 +/- 0.8). No significant quantitative difference in the percentage of EAC binding cells was found between NIDD patients and the control group. When NIDD patients were divided into two groups, those with and those without microvascular complications, neither differences in CIC levels nor in the percentage of B lymphocytes were found. Nor any correlation could be found between the highest individual CIC levels and the highest percentage of lymphocytes with surface IgG. These data show an increase of CIC levels and of cells with surface IgG in NIDD patients who had not received insulin at least not in a constant or prolonged therapy. This could allow us to suspect the existence of antigen-antibody complexes different to insulin-antiinsulin CIC found in insulin dependent diabetes.

The superior cervical ganglia (SCG) provide sympathetic innervation to the pineal gland, cephalic blood vessels, the choroid plexus, the eye, carotid body and the salivary and thyroid glands. Removal of the ganglia brings about several neuroendocrine changes in mammals, including the disruption of water balance in pituitary stalk-sectioned rats and the alteration of normal photoperiodic control of reproduction and thyroid function in hamsters, ferrets, voles, rams and goats. These effects are commonly attributed to pineal denervation. However, pinealectomy does not always mimic ganglionectomy in its neuroendocrine sequelae. This paper discusses several examples illustrating the differences in ganglia and pineal removal, including the acute and chronic effects of ganglionectomy on the control of thyroid response to TSH in rats. A functionally relevant link between SCG and the hypothalamus occurs in rats, inasmuch as ganglionectomy depresses norepinephrine uptake and increases the number and responses of alpha-adrenoceptors in medial basal hypothalamus. Lastly the SCG are active points of concurrency for hormone signals, as revealed by the metabolic changes induced by steroid and anterior pituitary hormones in these structures, even in the absence of intact preganglionic connections, as well as by the existence of putative receptors for some of the hormones, namely estradiol, testosterone and corticosteroids. The SCG appear to constitute a peripheral neuroendocrine center.