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At least 703 records · Page 39Linked to original sources
PubMed2001

Hormone metabolism in the pulmonary circulation.

We measured hormonal levels in blood samples from pulmonary and radial arteries in 117 patients undergoing aorto-coronary by-pass surgery with the aim of investigating the role of the pulmonary vessel endothelium in hormone metabolism. Insulin and glucagon concentrations were significantly higher in pulmonary artery blood with respect to radial artery blood (73 +/- 65 vs. 65 +/- 47 pmol/l, p < 0.005, and 80 +/- 49 vs. 73 +/- 51 ng/l, p < 0.01, respectively), while no difference was found for growth hormone, prolactin, C peptide, insulin-like growth factor I, follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone, parathyroid hormone, thyroglobulin, triiodothyronine, thyroxine, free triiodothyronine, and free thyroxine. Moreover, prolactin concentrations were more than twice the normal levels, this being an effect of propafol and the opiate fentanyl used for the general anesthesia. Assuming that the arteriovenous differences observed are a marker of peptide hormone degradation, our study has demonstrated that with similar kinetics insulin and glucagon secreted into portal circulation and escaping from hepatic extraction undergo further homeostatic removal of about 9-10 % in the pulmonary circulation before entering the general circulation.

Aged↗
PubMed1992

Neutrophil retention during a single transit through the pulmonary circulation.

Our laboratory has previously reported that 70-80% of polymorphonuclear cells (PMNs) are delayed with respect to erythrocytes (RBCs) in a single pass through the lungs of dogs, whereas only 5-15% of PMNs are delayed in a single pass through human lungs. Because these results were obtained using a direct blood sampling method in animals and an indirect gamma camera method in humans, the reported differences could be related to differences in measurement technique. The present study was designed to settle this question by comparing both techniques in a single species. The results show that the gamma camera technique previously used in humans underestimates the retention of PMNs with respect to RBCs during a single pass through the lung. They also show that this problem can be corrected by modifying the analysis of the data obtained using the gamma camera. We conclude that the pulmonary circulation retains PMNs with respect to RBCs to a comparable degree in animals and humans.

Animals↗
PubMed1997

Non-invasive assessment of technetium-99m albumin transit time distribution in the pulmonary circulation by first-pass angiocardiography.

This study describes a non-invasive method for assessment of the lung transit time distribution of a tracer, using first-pass technetium-99m albumin angiocardiography and a model-free method of deconvolution. Ten patients received a first injection of 1 MBq kg-1 in the external jugular vein to position a gamma camera in the left anterior oblique position and two additional injections (5 MBq kg-1) to record first-pass angiocardiographic data. Right and left ventricular time-activity curves were derived from regions of interest every 0.5 s over a 1-min period. The left ventricular curve was deconvoluted by the right ventricular curve to obtain the lung transport function. The deconvolution procedure was based on a modified version of the Kalman filtering technique. The procedure was repeated at an interval of 30 min in eight patients. Two patients were re-examined up to 2 years later. Skewness, kurtosis and relative dispersion of the distributions did not change over time. We also found that the distribution, once normalized by its first moment, was independent of isolated changes in heart rate or cardiac output. Comparison of curve shapes at an interval of 30 min by point by point analysis demonstrated the reproducibility of the technique. We conclude that computation of the pulmonary transit time distribution of 99mTc-albumin from a standard angiocardiography procedure by model-free deconvolution is reliable and reproducible over time. We suggest that it may be a valuable tool for the non-invasive follow-up of the pulmonary circulation.

Adult↗
PubMed1992

Bradykinin metabolism pathway in the rat pulmonary circulation.

OBJECTIVE: The contribution made by different enzymes to the degradation of bradykinin in physiological conditions was estimated by examining bradykinin metabolism in rat serum, in the in situ perfused lung and in vivo. METHODS: Dose-response curves for the hypotensive effect of intra-arterially and intravenously injected bradykinin were obtained in unanaesthetized rats. High-performance liquid chromatography was used to analyse the products of bradykinin breakdown after incubation with rat serum and perfusion through in situ lung preparations. RESULTS: In rat serum, kininase I degraded 34% and kininase II 11% of bradykinin, no evidence for other activities being detected. In the awake rat, D,L-2-mercaptomethyl-3-guanidino-ethylthiopropionic acid, an inhibitor of kininase I, did not reduce the percentage of bradykinin inactivation in the pulmonary circulation. In the in situ perfused lung 65% of bradykinin was metabolized and the main products were BK1-7, BK1-5 and BK4-9. Enalaprilat (an inhibitor of kininase II) blocked the formation of BK1-7 and BK1-5 and increased the recovery of BK4-9. beta-Mercapto-ethanol, which inhibits aminopeptidase P, and diprotin A, a specific inhibitor of dipeptidylaminopeptidase IV, both reduced the formation of BK4-9. Diprotin A also allowed the recovery of BK2-9. Bradykinin degradation and BK4-9 recovery were not affected by endopeptidase inhibitors. CONCLUSIONS: Our results show that the main degradation pathway of bradykinin in the lung is through the action of kininase II at the carboxyl terminus, and sequential cleavage by aminopeptidase P followed by dipeptidylaminopeptidase IV at the amino terminus. The amino-terminal degradation of bradykinin represents about 38% of the total lung kininase activity.

Aminopeptidases↗