Acta physiologica Scandinavica最新文献

The release of prostaglandin E elicited by sympathomimetic amines was studied in the isolated rabbit heart. The hearts were prepared according to Langendorff, with conventional recording of stroke frequency and contractile force. Assays were made of the outflow of PGE during exposition to equimolar concentrations of methoxamine, noradrenaline, adrenaline and isoprenaline, in the absence and in the presence of phentolamine or propranolol. Noradrenaline caused an almost four-fold increase in the basal outflow of PGE from the heart, while methoxamine (an alpha-adrenoceptor agonist) and isoprenaline (a beta-adrenoceptor agonist) were both ineffective in this respect. Thus, the PGE-releasing capacity of the drugs was not correlated to their ability to activate alpha- or or beta-adrenoceptors. Furthermore, no relation was obtained between the PGE release induced by the drugs and the increase in heart rate and contractile force elicited by them. It is suggested that sympathomimetic drugs trigger PGE synthesis and release in the rabbit myocardium following activation of a hitherto unobserved adrenoceptive mechanism, optimally stimulated by NA.

In each of ten healthy young subjects breathing different concentrations of CO2 in O2, four alveolar CO2-tension levels were obtained, ranging from about 20 mmHg when hyperventilating in O2 to 50 mmHg. Maximum expiratory flows at 60% total lung capacity were measured at each level and corrected for the influence of the expired gas on the flow. The corrected maximum flow decreased significantly when the alveolar CO2 tension was below 30-35 mmHg, while there was only slight or no influence of CO2 on the maximal flow when the tension was above 35 mmHg. The decrease is taken as evidence of a constrictor effect on peripheral bronchi of hypocapnia.

Pulmonary microembolization secondary to platelet aggregation has been suggested to be a pathogenetic component of the shock lung syndrome. In vitro experiments have also shown that platelets can release factors with a permeability-enhancing activity. We studied the effect of collagen-induced platelet aggregation on the hydraulic conductivity of thexchange vessels in isolated, blood-perfused rabbit lungs. The net rate of fluid filtration in each pair of lungs was determined during standardized elevations of left atrial pressure before and after platelet aggregation induced by intraarterial collagen infusions. Such infusions were followed by a significant, but transient increase in the net rate of fluid filtration. These lungs were papaverinized so that collagen infusions caused only minor increases in inflow pressure. Separate experiments indicated that the observed increase in pulmonary arterial pressure could not explain the increase in net filtration rate after collagen infusion. When platelet-poor plasma was used as a perfusate no change in the net rate of fluid filtration was observed after collagen infusion. The conclusion from these experiments is then that intravascular platelet aggregation induced by collagen infusion caused a transient increase in the permeability of the pulmonary exchange vessels.

The choline acetyltranferase activity underwent marked changes during the life span: in the submaxillaries, the total enzyme activity increased 70-fold from birth up to the age of 3 months and it then remained constant throughout the rest of the observation period, i.e. up to 28-29 months; in the parotids, in contrast, it continued to rise beyond the age of 3 months and the highest value was reached at 24 months. The weights of the glands increased markedly up to 3 months. The gain in weight was less pronounced thereafter.