Acta physiologica Academiae Scientiarum Hungaricae最新文献

Effects of the prostaglandin synthesis inhibitor indomethacin (4 mg/kg) were studied on the intrarenal circulation of anaesthetised (pentothal 50 mg/kg i.p.) rats in normovolemia or subjected to acute extracellular volume expansion (intravenous infusion of 0.9% NaCl at a dose of 50 ml/kg) using Sapirstein's 86Rb indicator dilution technique. Circulatory parameters were determined one hour after indomethacin treatment. The following conclusions were drawn: 1. In normovolemic rats the renal, cortical and medullary blood flow remained unaltered. No changes occurred in regional vascular resistances of the kidney or in the distribution pattern of intrarenal blood flow. Water output was moderately reduced while sodium excretion remained unaffected. 2. In rats subjected to acute extracellular volume expansion renal cortical blood flow was slightly augmented, medullary perfusion rate declined; the intrarenal blood flow distribution was shifted towards the cortex. The vascular resistance in the cortex did not change whereas that in the medulla was slightly augmented. Under these conditions indomethacin did not influence salt and water excretion. Our results provide further evidence that unlike in anaesthetised dog, in the anaesthetised rat endogenous prostaglandins probably do not play a decisive role in the control of renal blood flow, intrarenal circulation and salt and water excretion.

The dimethylglyoxim cytochemical method was used for detecting endogenous nickel (Ni) in the canine and human myocardium. Electrondense deposits were observed in the myocardial cells and the wall and lumen of capillaries of the dog heart when after CO-intoxication the blood COHb level exceeded 30%. Energy-dispersive microanalysis proved the presence of Ni in the reaction product. Detection of the Ni-reaction product in the myocardium of human cadavers may be of forensic importance, since the reaction is resistant to post mortem autolysis and may help to identify the cause of death.

This paper reports on partial purification and characterization of a natural (endogenous) factor capable of inhibiting in vivo DNA synthesis in mouse pneumocytes in a tissue-specific manner. By using a combination of ultrafiltration and various chromatographic techniques, the active agent has been partially purified from aqueous extracts of both bovine and rat pulmonary tissue. The factor responsible for the observed effect was found to be a heat labile compound, most likely a protein of approx. 40 000 molecular weight. Its chemical and physicochemical properties determined so far, and also the manner of its biological action implies that this lung tissue derived agent might be an endogenous proliferation inhibitor with a chalone-like character operating in the pulmonary epithelial cells.

Arterial blood pressure (BP) and heart rate (HR) were continuously recorded during lateral hypothalamic self-stimulation with optimal stimulus parameters in rats. Hyper-hypotensive, hypertensive and hypotensive reactions were observed during separate self-stimulation, and the biphasic type considerably prevailed over other types of reactions. During the single cycles of self-stimulation hyper-hypotensive and hypertensive reactions with different heart rate reactions also occurred. In this case the biphasic type was seen in 75% of all reactions, whereas the hypotensive type occurred in 25% of the cases. The main type of BP reaction (92%) during continuous self-stimulation for 60-240 min was a gradual increase of the mean BP level from 15 to 40 mm Hg against initial values (p less than 0.001), that depended on the duration of self-stimulation. Changes of HR were more variable: tachycardia and bradycardia were seen approximately with the same frequency. Comparative analysis of cardiovascular reactions during hypothalamic SS and escape reactions provoked by ventromedial hypothalamus stimulation revealed some peculiarities of autonomic manifestations during positive and negative emotional reactions. The results of this comparison raises the question of a stress-reaction during self-stimulation behaviour.

The effects of intracerebroventricular administration of two different cholecystokinin antisera were tested on acquisition and extinction of active avoidance behaviour as well as on acquisition, maintenance and extinction of conditioned feeding behaviour of rats. Both antisera delayed the extinction of active avoidance and conditioned feeding response, while they were ineffective on acquisition and maintenance. These data suggest that the endogenous CCK of the brain might be a physiological modulator of extinction processes.

The effect of calcium chloride injected into the cerebral ventricles of group-housed unanaesthetized cats upon vocalization (rage, hissing and snarling), fighting (attack with paws and claws, defense with paws and claws and biting), mydriasis, tremor and clonic-tonic convulsions produced by carbachol and eserine injected similarly was investigated. Calcium chloride depressed or almost completely abolished the vocalization and fighting due to carbachol and eserine. On the other hand, mydriasis, tremor and clonic-tonic convulsions evoked by carbachol and eserine were not significantly changed by calcium chloride. It is apparent that calcium chloride can "dissociate" vocalization and fighting from autonomic and motor phenomena such as mydriasis, tremor and clonic-tonic convulsions caused by carbachol and eserine. Calcium chloride inhibited the vocalization and fighting produced by carbachol and eserine most probably by a nonspecific stabilizing action on central muscarinic cholinoceptive sites. These results further support the view that calcium ions in excess have an atropine-like action also in the central nervous system.

The possible interactions between the vasoactive trace metal nickel ion (Ni2+) and membrane Na-K-ATPase in the isolated perfused rat heart and in the isolated canine coronary artery have been studied. The characteristic features of 1 microM Ni2+-induced contractile response in the canine coronary artery strip were similar to those evoked by the inhibition of Na-K-ATPase. Inhibition of the pump activity by ouabain (10(-4)M) or by K+-deficient Krebs solution prevented Ni2+-action both in the canine coronary artery strip and in the perfused rat heart, indicating that when Ni2+ causes coronary vasoconstriction the Na, K-exchange is influenced. Further studies are needed to clarify whether Ni2+ acts directly on the enzyme, or the vascular action of this trace metal depends on the ionic gradients maintained by the electrogenic Na-K-pump.

Gastric ulcer was provoked by indomethacine (20 mg/kg s.c.) in rats. The ulcer protection by prostacyclin and cimetidine as well as the changes of tissue cAMP level in the gastric fundic mucosa--during ulcer-provocation and ulcer protection--were studied. The animals received prostacyclin (125, 250 and 500 micrograms/kg) and cimetidine (2.5 and 50 mg/kg) together with indomethacine. Evaluation of the results was undertaken 4 hours after the administration of the provoking agent. The number and severity of the ulcers as well as the cAMP level of the gastric fundic mucosa were measured. The following results were obtained: (1) cAMP level of the gastric fundic mucosa remained unaltered at the time of ulcer provocation; (2) cimetidine and prostacyclin reduced the number and severity of the ulcers in a dose-dependent manner; (3) cAMP level of the gastric fundic mucosa was reduced after cimetidine and prostacyclin treatment in a dose-dependent manner, the extent of which however did not show any correlation with the degree of ulcer-preventive action. The experimental results indicate that (1) the development of indomethacine-induced gastric ulcer is independent of the ATP--adenylate cyclase--cAMP system of the gastric fundic mucosa; (2) the ulcer protective action of cimetidine and prostacyclin is independent of tissue cAMP system of the gastric fundic mucosa in this model.