OBJECTIVETo study the effect of Simulated Microgravity and its Associated Mechanism on Pulmonary Circulation in Rats).

METHODSRat tail-suspension model was used to simulate the physiological effects of microgravity and changes in pulmonary blood vessel morphology, pulmonary arterial and venous blood pressure, pulmonary vascular resistance, pulmonary vasomotoricity, as well as the regulation of pulmonary circulation by cytokines produced and released by the lung of rats were measured.

RESULTSThe walls of pulmonary blood vessels of rats were thickened, and the pulmonary artery was reconstructed with increased pulmonary vascular resistance. The pulmonary blood vessels of rats became more prone to dilation as contractions increased. Rat epithelial Adrenomedulin gene transcription and protein expression were upregulated. The level of basic fibroblast growth Factor of rat was also elevated.

CONCLUSIONFindings from the present study on rats revealed that the microgravity can affect pulmonary blood vessel structure, pulmonary arterial pressure, and pulmonary blood vessel self-regulation and cytokine production.

Animals ; Hemodynamics ; Male ; Pulmonary Artery ; physiology ; Pulmonary Circulation ; physiology ; Rats ; Rats, Wistar ; Weightlessness

AIM AND METHODSTo study the roles of carbon monoxide on hypoxic pulmonary vasoconstriction (HPV) by investigating the effects of exogenous carbon monoxide and heme oxygenase inhibitor ZnPPIX on hypoxic vasoconstriction reaction of isolated rat pulmonary arterial rings (PAR).

RESULTSHypoxia caused constriction in PAR preconstricted by PE. Both ZnPPIX and carbon monoxide inhibited hypoxic pulmonary constriction significantly by increasing the cGMP level after hypoxia.

CONCLUSIONZnPPIX and exogenous carbon monoxide can inhibit HPV. The reduction of cGMP induced by the decreased of CO may be one of reasons of HPV.

Animals ; Carbon Monoxide ; physiology ; Hypoxia ; In Vitro Techniques ; Male ; Pulmonary Artery ; physiology ; Rats ; Rats, Wistar ; Vasoconstriction ; physiology

Humans ; Ion Channels ; Myocytes, Smooth Muscle ; metabolism ; physiology ; Pulmonary Artery ; metabolism ; physiology

BACKGROUNDNon-heart-beating donor lung has been a promising source of lung transplantation. Many studies on non-heart-beating donor lungs are based on animal lung transplantation. In this study, we assessed by organ bath the effect of one-hour warm ischemia on the non-heart-beating donor lung in terms of the integrity of contractile and relaxant functions and tissue structures of pulmonic arteries and bronchi.

METHODSSixteen Swedish pigs were randomly classified into two groups: heart-beating donor group and 1-hour warm ischemia non-heart-beating donor group. Pulmonic and bronchial rings were taken from the isolated left lungs of the pigs. The pulmonic rings were stimulated by U-46619 (5.7 mol/L) and acetylcholine (10(-4) mmol/L) to assess the contractile abilities of smooth muscle and the endothelium-dependent relaxation response, respectively. As such, acetylcholine (10(-5) mmol/L) and natrium arachidonic acid (0.01%) were used to detect the contraction of bronchial smooth muscle and epithelium-dependent relaxation response. Meanwhile, the variances of precontraction tension of control groups were recorded to measure whether there was spontaneous relaxation during endothelium/epithelium-dependent relaxation course. Finally, papaverine solution (10(-4) mmol/L) was used to detect the non-endothelium/epithelium-dependent relaxant abilities of pulmonic and bronchial smooth muscles.

RESULTSThere was no significant difference in the tension values of precontraction of pulmonic rings (P > 0.05), endothelium-dependent relaxation (P > 0.05), precontraction of bronchial rings (P > 0.05) and epithelium-dependent relaxation (P > 0.05) between the heart-beating donor group and the 1-hour warm ischemia non-heart-beating donor group. And the pulmonic and bronchial rings of each subgroup B had no spontaneous relaxation. Finally, papaverine solution relaxed the smooth muscle of all the rings completely.

CONCLUSIONSThe results of this experiment suggest that the contractile and relaxant functions and tissue structures of pulmonic arteries and bronchi are not damaged after warm ischemia for 1 hour, and support the further study of non-heart-beating donor lung.

Animals ; Bronchi ; physiology ; Endothelium, Vascular ; physiology ; Lung Transplantation ; Pulmonary Artery ; physiology ; Swine ; Tissue Donors ; Vasodilation ; Warm Ischemia ; methods

Animals ; Calcium ; physiology ; Chloride Channels ; physiology ; Electrophysiological Phenomena ; Male ; Muscle, Smooth, Vascular ; cytology ; physiology ; Myocytes, Smooth Muscle ; physiology ; Pulmonary Artery ; cytology ; physiology ; Rats ; Rats, Wistar

OBJECTIVETo explore the alterations in pulmonary arterial reactivity during pulmonary arterial hypertension at the early-stage of pulmonary fibrosis in rats.

METHODSSixty-six male Sprague-Dawley rats were randomly divided into 2 groups: bleomycin (BLM) group and sham group. The rats in BLM group were received single intratracheal instillation of BLM (5 mg/kg), and the rats in sham group received equal volume of 0.9% normal saline (NS). The alterations in pulmonary arterial reactivity were measured by vascular tension detected technique, the pathomorphological changes in the wall of pulmonary arteries were displayed with Hematoxylin-Eosin (HE) staining, the degree of fibrosis in lung was revealed with Masson staining, and the mean pulmonary arterial pressure was detected via a catheter in the pulmonary artery.

RESULTS(1) The contractile response to a- adrenoceptor agonist phenylephrine (PE), of pulmonary arteries both with remaining endothelium and with removing endothelium, from BLM-treated rats , was reduced significantly, compared with sham rats (P both < 0.05). (2) The relaxant response to the endothelially dependent vasodilator acetylcholine (Ach), of pulmonary arteries with remaining endothelium, from BLM-treated rats, was also reduced, compared with sham rats (P < 0.01). (3) In sham rats, the contractile response to (omega) -nitro-L-arginine methyl ester (L-NAME) plus PE, of pulmonary arteries with remaining endothelium, was enhanced, compared with that to PE alone (P < 0.01), while in BLM group, the contractile responses to L-NAME plus PE, of pulmonary arteries with remaining endothelium, was not different from that to PE alone (P > 0.05). (4) In BLM group, vascular endothelial cells lost. (5) In BLM group, the initial stage of fibrogenesis was observed in lungs, and the mean pulmonary arterial pressure increased, compared with that in sham group (P < 0.05).

CONCLUSIONThe abnormal responsibility of pulmonary arteries occurred during pulmonary arterial hypertension at the early-stage of pulmonary fibrosis in rats.

Animals ; Familial Primary Pulmonary Hypertension ; Hypertension, Pulmonary ; complications ; physiopathology ; Male ; Pulmonary Artery ; physiopathology ; Pulmonary Fibrosis ; complications ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Vasomotor System ; physiology

OBJECT: To evaluate changes in the diameter of bronchi and pulmonary arteries during respiration. MATERIALS AND METHODS: The ratio of the diameter of matched inner bronchi and accompanying pulmonary arteries was calculated from full inspiration and expiration HRCT of healthy men. RESULTS: In 106 pairs of matched bronchi and pulmonary arteries, the brohchial-arterial ratios were 0.61+/-0.18(upper lung), 0.72+/-0.21(lower lung), and0.65+/-0.20(total) at full inspiration and 0.51+/-0.32(upper lung), 0.52+/-0.15(lower lung), and 0.51+/-0.26(total) atfull expiration HRCT, denoting a statistically significant increase in bronchial diameter of the entire lung atfull inspiration. The inner diameter of the bronchus was larger than the diameter of the accompanying pulmonary artery by 0.1% at full expiration and 8.5% at full inspiration. CONCLUSION: The result of this study would be helpful in understanding the physiology of the lung during respiration.
Adult* ; Arteries ; Bronchi ; Bronchiectasis ; Humans ; Lung ; Male ; Physiology ; Pulmonary Artery ; Respiration*

AIMThrough studying local regulatory mechanisms in pulmonary arteries (PA) and thoracic aortae (TA) under simulated microgravity (SM), to collect some data for the researches of adaptive mechanisms in pulmonary and systemic arteries and for the mechanisms accounting for orthostatic intolerance after SM.

METHODSCardiopulmonary circulatory function during 7-day 6 degrees head down bed rest (HDT) in male young volunteers was measured with a XXH-2000 pulmonary circulation and cardiac function instrument. - 30 degrees C tail suspended (TS) rats were used as the model to simulate the physiological effects of M. The PA and TA changes of vasoreactivity were respectively observed by vitro vessel rings perfusion.

RESULTSThe changes in volume of PA and pulmonary vein during a cardiac cycle and the preload in left cardiac ventricle in men increased significantly in the initial HDT. The super-regulatory phenomena appeared in both pulmonary and systemic circulation, but earlier and more obviously in pulmonary circulation than systemic circulation during 96-144 h. The dilatory reactivity in TS7 PA increased significantly, tended to decrease in TS14. The dilatory reactivity of TA in TS7 had a significant increase, had a slight increase in TS14. The contractile reactivity of PA decreased slightly in TS7 from CON, and were attenuated significantly in TS14. The contractile reactivity of TA in TS14 decreased significantly. The responsiveness to KCl, phenylephrine and sodium nitroprusside in VEC- removed PA had no differences among all groups.

CONCLUSIONThe differences in changes between pulmonary and systemic arteries under SM could be an important sign of depressed local regulatory function, which might be mainly due to dilatory function in VEC and contribute to the occurrence of orthostatic intolerance after SM.

Animals ; Aorta, Thoracic ; physiology ; Humans ; Male ; Pulmonary Artery ; physiology ; Rats ; Rats, Wistar ; Vascular Resistance ; Weightlessness ; Weightlessness Simulation ; Young Adult

To investigate the effect of peroxynitrite (ONOO(-)) on the reactivity of rabbit pulmonary artery, the responses of rabbit pulmonary artery rings (PARs) pre-incubated with ONOO(-) to endothelium-dependent and receptor-dependent relaxants ACh and ADP, endothelium-dependent and receptor-independent relaxant calcium ionophore A23187, endothelium-independent relaxant sodium nitroprusside (SNP) and alpha(1)-adrenoceptor agonist phenylephrine (PE) were observed in vitro in an accumulative manner. (1) Relaxations of PARs to ACh, calcium ionophore A23187 and ADP were markedly impaired with shift of accumulative dose-response curve of each agonist to the right. Inhibition of endothelium-dependent and receptor-dependent or independent relaxation by ONOO(-) was dose-dependent. (2) ONOO(-) incubation inhibited SNP-induced relaxation in a dose-dependent manner. (3) Contractile response of PARs to PE varied with the different doses of ONOO(-). In PARs pre-incubated with 0.5 mmol/L ONOO(-), contractile response was significantly enhanced with shift of PE accumulative dose-response curve to the left, whereas in PARs pre-incubated with 1.0 mmol/L or 2.0 mmol/L ONOO(-), it was markedly reduced with right shift of PE accumulative dose-response curve. (4) Vehicle of ONOO(-) had no effect on responses to each agonist.Decomposed ONOO(-) had minimal effect on the response to PE and ADP, in contrast, relaxation of PARs to ACh, A23187 and SNP were enhanced. These results indicate that ONOO(-) may contribute to regulatory disorder of pulmonary artery reactivity.
Animals ; Dose-Response Relationship, Drug ; In Vitro Techniques ; Peroxynitrous Acid ; physiology ; Pulmonary Artery ; physiology ; Rabbits ; Vasodilation ; drug effects

AIMTo investigate the role of calcium-activated chloride channels and the Cl- channel blockers niflumic acid (NFA) and indanyloxyacetic acid (IAA-94) in the regulation of vascular contraction induced by phenylephrine (PE).

METHODSThe PE-induced contraction in rat pulmonary artery was observed by using routine blood vascular perfusion in vitro. The fluorescence Ca2+ indicator Fura-2/AM was used to observe intracellular free Ca2+ concentration ([Ca2+]i) of rat pulmonary artery smooth muscle cells (PASMCs) which were obtained by the acute enzyme separation method (collagenase I plus papain) on NFA and IAA-94 effects on PE-induced contraction. Changes of [Ca2+]i in PASMCs were measured by spectrofluorometry.

RESULTSThe anion channel blockers NFA and IAA-94 produced inhibitory effects on PE-induced contractions in the pulmonary artery. NFA and IAA-94 negligibly affected the KCl-induced pulmonary artery contractions. PE could increase [Ca2+]i but NFA and IAA-94 negligibly affected it.

CONCLUSIONCalcium-activated chloride channels contribute to the agonist-induced pulmonary artery contractions under physiological conditions, which may be a new clue to investigate the hypoxic pulmonary vasoconstriction.

Animals ; Calcium ; physiology ; Chloride Channels ; physiology ; Glycolates ; pharmacology ; Male ; Muscle, Smooth, Vascular ; physiology ; Niflumic Acid ; pharmacology ; Phenylephrine ; pharmacology ; Pulmonary Artery ; physiology ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction