Acta physiologica Academiae Scientiarum Hungaricae最新文献

The possible involvement of adrenergic receptors in nickel ion (Ni2+)-induced coronary vasoconstriction was studied on isolated perfused rat hearts and on isolated canine coronary artery strips. The experiments on both models showed that (i) alfa-adrenergic blockade by phenoxybenzamine or phentholamine caused only partial depression of Ni2+-induced coronary vasoconstriction: (ii) beta-adrenergic receptor blockade by propranolol totally prevented Ni2+-action, and (iii) Ni2+ (1 microM) caused significant inhibition of coronary vasodilatation induced by isoproterenol. The experimental results indicate that alfa-adrenoceptors play minor role (if any) in the coronary action mechanism of Ni2+ but it may be mediated by beta-adrenergic mechanisms. Nickel was found to alter the reactivity of coronary beta-adrenoceptors suggesting a possible modulatory role of this trace metal in coronary adrenergic mechanisms.

In previous experiments a considerable interstitial oedema developed after myocardial infarction followed by the infusion of 6 mmol/kg/min norepinephrine lasting for 10 min in the 2nd and 48th hours as well as after a 60 min period of ventricular fibrillation during cardiopulmonary bypass. On the other hand myocardial dehydration was induced by hyperosmolality of 320-470 mOsm/l caused by mannitol or glucose after pancreatectomy. A close bilinear correlation was found between the myocardial water content and the increase of ventricular diastolic stiffness. It was further established that the increase of ventricular stiffness is followed by a decrease of the cardiac output index measured during left ventricular afterload. The cardiac output index was lower after myocardial infarction and pancreatectomy than during cardiopulmonary bypass or mannitol-treatment. Of clinical importance is the fact that ventricular performance decreases when myocardial water content exceeds or does not reach the value of 760-790 g water per 1000 g myocardium.

KCl-, and NaCl-myosins were prepared from different parts of the central nervous system (CNS). Throughout these experiments P and lipid contents were higher in NaCl-myosins than in KCl-preparations. Both KCl-, and NaCl-myosins have increased lipid and P contents compared with skeletal muscle myosins. When the specimens were separated by a molecular sieve, it was found by chromatographic technique on Sepharose 4B column that the cerebral and cerebellar myosins were composed of two fractions of different molecular mass while the brain stem and spinal cord myosins revealed only a single peak. The myosin fractions' Ca-ATPase activity could be augmented by rabbit muscle actin. The myosin preparations developed filamentous systems and aggregates which could be shown by scanning electron microscopy. All the CNS-myosin preparations could be phosphorylated; however, they were saturated to a different degree and were influenced by the presence or absence of serotonin. The kinetic studies revealed that the phosphate saturation of the brain stem, cerebellar and cerebral myosins depended on the ATP concentration and incubation time. The alkaline hydrolysates of lipid-free human brain myosin preparations contained amino acid phosphates, P-Arg, P-Lys and P-His in different amounts depending on their sources. In response to a phosphorylating mixture only the amount of P-Arg was elevated in the cerebral myosins, P-Arg and P-His in the brain stem preparations, and P-Arg, P-His and the amounts of unidentified compounds in the cerebellar ones.

The relaxant effects of prostacyclin (PGI2) and its stable 7-oxo-analogue, a product of Chinoin Pharmaceutical Works, were compared on isolated canine cerebral, bovine coronary, rabbit coeliac and human mesenteric arterial strips. The resting tone of the coronary, cerebral and human mesenteric arteries as well as the stimulation- or noradrenaline-evoked tone of coeliac vessels were reduced by both prostanoids. The relaxant action of 7-oxo-PGI2 was slow in onset and lasted until it was washed out. The IC50 values were 4 to 40 X 10(-9) mol/l for PGI2 and 1 to 6 X 10(-7) mol/L for 7-oxo-PGI2. Compared to PGI2, 7-oxo-PGI2 was more potent in relaxing coronary arteries than the other vessels studied. Isolated tracheae from guinea-pigs were contracted by PGI2 while relaxed by 7-oxo-PGI2.

The effect of the Ca-chelators EDTA and EGTA on sinoatrial activity and heart irritability was studied in dog experiments by perfusing the artery supplying the sinoatrial node. Beside the usual ECG recordings left and right atrial and left and right ventricular epicardial electrograms, His-bundle electrogram and the early activity of the sinoatrial node were recorded. In addition action potentials were recorded from the left auricle and right ventricle of the dog hearts. Local application around the sinoatrial and atrio-ventricular nodes of EDTA and EGTA caused sinus bradycardia and later sinus arrest within 1 min after introduction of the drugs. For substitution of the sinus rhythm junctional (seldom lower atrial) escape rhythm developed. One to two minutes later it was followed by atrial premature beats and even later atrial flutter and fibrillation could be recorded. In one third of the cases atrial fibrillation was followed by secondary ventricular fibrillation. Atrio-ventricular impulse conduction was prolonged in the av node by EDTA and EGTA. Atrial action potentials and the slow (Ca dependent) ventricular action potentials were depressed by EDTA and EGTA.

An increase in gastric mucus production was observed after PGF2 alpha administration and low dose argon-laser irradiation in human patients. The effect of PGF2 alpha on functioning of the gastric mucosa is opposite to that of the PGE group. The observed increase in mucus production is a new aspect of the bio-stimulatory effect of laser irradiation.

The aim of the present study was to reexamine the effect of antidiuretic hormone on intrarenal blood flow distribution by the microsphere technique in anaesthetized rats. The administration of 3, 6 or 60 mU/kg/h of arginine-vasopressin (VP) was accompanied by a dose-dependent antidiuresis. Glomerular filtration rate increased only at the dose level of 60 mU/kg/h and was not significantly altered by the lower doses. Total renal blood flow was not significantly influenced by any of the doses of VP. The two small doses caused no change in intracortical microsphere distribution but there was a significant decrease in the ratio of outer to inner cortical blood flow when 60 mU/kg/h of VP was infused. The results indicate that physiological doses of VP do not alter the distribution of intrarenal blood flow and show that the antidiuretic effect of VP is independent of changes in renal haemodynamics.

Nickel chloride (NiCl2) at low concentration (1 microM) induced isometric force development in isolated canine coronary artery strips. The Ni2+-action was linearly dependent on extracellular Ca2+-concentration in the range of 0 to 5.0 mM. Verapamil (10(-6) - 10(-3) M) did not prevent or abolish Ni2+-induced coronary contraction, but nitroprusside sodium even at low concentration (10(-8) M) antagonized the tonic force development. The results indicate that the stimulation of force development by trace amounts of NiCl2 in isolated canine coronary artery strips is dependent on transmembrane Ca2+-influx which is mediated by the T-system of Ca2+-activation.

The effect of low concentrations (1-10 microM) of nickel (Ni2+) was studied on the spontaneous contractile activity of isolated rat portal vein preparations. To distinguish between presynaptic and postsynaptic actions, Ni2+-induced changes of isometric force development evoked either by electrical field stimulation (80V/5 cm; 1 msec; 1-32 Hz) or by exogenous norepinephrine (NE) were compared. Ni2+ inhibited spontaneous isometric force development, decreased basal tone but significantly increased the frequency of contractions. The experimental findings that inhibition of the effect of selective stimulation of adrenergic nerves was significantly more pronounced than the depression of contractions evoked by exogenous norepinephrine indicate that in addition to postsynaptic actions, Ni2+ influences presynaptic mechanisms (i.e. NE-release) in this vessel preparation.