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Biomedical subjects

Y N Cai

Publications and source records attributed to Y N Cai.

At least 19 recordsLinked to original sources
PubMed1993

[Effect of hypoxia on the conversion of angiotensin I to A II in pulmonary vascular endothelial cells].

The effect of hypoxia on intrapulmonary conversion of angiotensin I (A I) to angiotensin II (A II) was examined by using an isolated rat lung preparation perfused at constant flow and cultured calf pulmonary artery endothelial cells. The conversion rate of A I in endothelial cells of pulmonary vascular bed was found to be decreased in both acute hypoxic and chronic hypoxic (CH-5000, CH-8000) rats. The conversion rate of A I to A II was significantly higher in acute hypoxic rat lungs than that in denuded endothelial cells rat lungs. There was no significant difference between chronic hypoxic and denuded endothelial cells rat lungs. In cultured calf pulmonary artery endothelial cells (PAEC) exposed to hypoxia (3% O2) for 30 minutes the conversion of A I to A II was significantly reduced. In the time course of hypoxic exposure the conversion of A I to A II in cultured calf PAEC showed significant difference between hypoxia and normoxia. The results indicated that (1) Acute and chronic hypoxia impaired pulmonary conversion of A I to A II. (2) Effect of hypoxia on the pulmonary conversion of A I to A II is associated with the degree and the time of hypoxia.

Angiotensin I↗
PubMed1992

[Preliminary study on the effect of endothelin on the contraction of isolated rat pulmonary artery and its mechanism].

Experiment was performed on the rings of right pulmonary artery (PA) taken from male Wistar rats. Each ring was suspended in an organ bath (37 degrees C) containing Krebs solution, gassed with 95% O2-5% CO2 (pH7.40). The changes of vascular tension were measured. The contraction of PA to endothelin (ET) (10(-9) mol/L) and the effects of 764-3 (50, 100, 200, 300 micrograms/ml as a scavenger of superoxide anion), verapamil (3 x 10(-6) mol/L) NDGA, indomethacin, atropine, phentolamine, propranolol, ketanserin tartrate and diethylcarbamazine on the ET-induced contraction were investigated. The results indicated that ET can induce a potent and sustained contraction of PA, inhibited by verapamil and 764-3, but unaffected by inhibitors of cyclooxygenase, lipoxygenase, leukotrienes systhetase or adrenergic, serotonergic, cholinergic receptors. It is suggested that the influx of extracellular Ca2+ and the production of superoxide anion might be involved in the ET-induced contraction. Arachidonate metabolism and receptors mentioned above probably didn't participate in the responses.

Animals↗
PubMed1992

[Reduction of genotoxic damage in oral mucosa with myasthenia gravis by traditional Chinese medicine].

Micronucleated exfoliated cell (MEC) of oral mucosa of 40 patients with myasthenia gravis (MG) and 54 normal controls were observed by means of micronucleus test. The frequency of MEC of two groups were 9.56/1000 and 2.55/1000 respectively, and their difference was remarkably significant (P < 0.001). 22 cases were treated by TCM Qiang Ji Jian Li Capsule. The frequency of MEC after treatment fell from 14.38/1000 to 6.00/1000. The difference was significant (P < 0.002). The frequency of Spleen-asthenia group higher than that of non-Spleen-asthenia (P < 0.05). The results revealed that. The patients with MG had genotoxic damage. (2) The constitution with the Spleen-asthenia and the genotoxic damage was related. (3) Qiang Ji Jian Li Capsule of invigorating the Spleen and benefiting Qi could reduce the genotoxic damage.

Adolescent↗
PubMed1991

[Effect of chronic hypoxia on endothelium-dependent relaxation and the content of cGMP in rat pulmonary artery].

This experiment was designed to investigate whether chronic hypoxia affect rat pulmonary artery (PA) endothelium-dependent relaxation and the content of cGMP in PA. Both ACh and ATP could induce endothelium-dependent relaxation of PA, not prevented by indomethacin, but completely abolished by methylene blue. These results indicated that vasodilatation of PA induced by both ACh and ATP is mediated by EDRF (endothelium-derived relaxing factor). Chronic hypoxia significantly depressed PA endothelium-dependent relaxation. The percent relaxation of IPPA and EPPA by 10(-6) mol/L ACh was 61.3% and 59.2% of those in control, and the percent relaxation of IPPA and EPPA by 1.8 x 10(-5) mol/L ATP was 64.9% and 55.3% respectively of the control. Chronic hypoxia also depressed SNP-induced endothelium-independent relaxation. Chronic hypoxia significantly decreased the content of cGMP in PA. The basic level of cGMP was 51.9 +/- 5.7 (n = 14) in hypoxia group and 84.9 +/- 9.7 (n = 14) pmol/g wet wt. in control group (P less than 0.01). After treatment of PA with ACh (10(-7) mol/L), the content of cGMP was 91.4 +/- 7.3 (n = 5) pmol/g wet wt. in hypoxic group and 240.8 +/- 30.6 (n = 5) pmol/g wet wt. in control group (P less than 0.01). Our data suggest that chronic hypoxia might depress rat pulmonary artery endothelium-dependent relaxation through the inhibition of soluble guanylate cyclase in vascular smooth muscle cells.

Animals↗
PubMed1990

Ligustrazine is a vasodilator of human pulmonary and bronchial arteries.

We have investigated the dilator effect of ligustrazine, the semisynthetic principle of a traditional Chinese herbal remedy, on human pulmonary and bronchial arteries in vitro. Ligustrazine caused a concentration-dependent relaxation of human small pulmonary arteries, which was independent of endothelium. Although ligustrazine was equally potent in inducing dilatation of pulmonary and bronchial arteries, it was about 10 times more potent in relaxing small pulmonary arteries (300-500 microns i.d.) compared with lobar pulmonary arteries (7-8 mm i.d.). By contrast, the relaxant responses of small and lobar pulmonary arteries to sodium nitroprusside was not significantly different. Ligustrazine was equally potent in relaxing prostaglandin F2 alpha- or 5-hydroxytryptamine-precontracted pulmonary arteries, suggesting that it is not a prostaglandin F2 alpha or 5-hydroxytryptamine antagonist. Preincubating the vessels with propranolol (1 microM) or indomethacin (10 microM) had no significant effect on the ligustrazine-induced vasodilatation. However, ligustrazine caused concentration-dependent inhibition of calcium-evoked contraction when applied to rat aorta in calcium-free K(+)-depolarizing medium. We conclude that ligustrazine is a dilator of human pulmonary and bronchial arteries, which is endothelium-independent and that ligustrazine preferentially relaxes pulmonary resistance vessels rather than large conduit pulmonary arteries.

Animals↗
PubMed1990

Enhanced reactivity to bradykinin, angiotensin I and the effect of captopril in the pulmonary vasculature of chronically hypoxic rats.

We compared the reactivity of pulmonary vessels to bradykinin (BK) and angiotensin I (AI) in normal and chronically hypoxic rats; the latter have pulmonary hypertension and muscularized pulmonary arterioles. These peptides are respectively inactivated and activated by the angiotensin converting-enzyme (ACE) on pulmonary endothelium. Isolated lungs were perfused at a constant flow rate when changes in pulmonary artery pressure (Ppa) reflect changes in vascular resistance. Dose-response curves to BK (1 ng-10 micrograms) were derived during normoxia and pre-constriction by hypoxia; BK both decreased and increased vascular resistance, i.e. vasodilation and vasoconstriction. In normal rats only constriction was seen in normoxia, which reflected low basal vascular tone, whereas in chronically hypoxic rats there was only dilatation which reflected high basal vascular tone. In hypoxia in normal rats, low doses caused dilatation, high doses constriction; in chronically hypoxic rats there was again only dilatation which was larger than in controls. After the ACE-inhibitor captopril, constriction was exaggerated in control rats in both normoxia and hypoxia and took place in chronically hypoxic rats after high doses in both normoxia and hypoxia; oedema often followed. Dose-response curves to AI (1 ng-micrograms) in normoxia showed greatly enhanced pressor responses in chronically hypoxic compared with normal rats, probably attributable to increased sensitivity to angiotensin II (AII) rather than enhanced conversion of AI to AII. Captopril caused a proportionate reduction in responses in both groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1989

Effect of ligustrazine on pulmonary vascular changes induced by chronic hypoxia in rats.

1. Acute and chronic effects on the pulmonary circulation of ligustrazine, a chemically identified and synthesized principle of a Chinese herb, were studied in rats. It dilated lung vessels and reversed hypoxic pulmonary vasoconstriction. 2. In rats kept 2 weeks in 10% O2 in a normobaric chamber and simultaneously treated with ligustrazine, right ventricular hypertrophy and muscularization of pulmonary arterioles were attenuated compared with saline-treated rats. Pulmonary artery pressure, measured in isolated lungs perfused at a constant flow rate, was also less in ligustrazine-treated rats. 3. In isolated blood-perfused lungs of chronically hypoxic and control rats, the relation between pressure and flow was measured during normoxia (ventilation with air plus 5% CO2), hypoxia (2% O2 plus 5% CO2) and after ligustrazine during continued hypoxia. Alveolar pressure was always greater than left atrial pressure; thus flow was determined by the pulmonary artery minus alveolar pressure difference. 4. Pressure/flow lines were measured during normoxia in four groups of rats: (1) control, saline-treated; (2) control, ligustrazine-treated; (3) chronically hypoxic, saline-treated; (4) chronically hypoxic, ligustrazine-treated. Both chronically hypoxic groups had steeper lines (higher resistance) than the control groups, which were similar in all respects. However, in chronically hypoxic rats, the extrapolated intercept of the line on the pressure axis, probably attributable to small newly muscularized arterioles in a state of tone, was much increased in the saline-treated group but did not differ from controls in the ligustrazine-treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Reactivity and site of vasomotion in pulmonary vessels of chronically hypoxic rats: relation to structural changes.

The high pressure muscular pulmonary circulation of chronically hypoxic (CH) rats was compared with the low pressure circuit in control (C) rats; differences were found in the effects of lung inflation, in pressure/flow relations during lung inflation, in reactivity to autocoids, and in responses to pulmonary dilator drugs. Isolated blood-perfused lungs of CH rats (2 to 3 wk in 10% O2) were compared with those of C rats kept in air. High inflation (alveolar) pressure (Palv) caused a rise in pulmonary artery pressure (Ppa) close to delta Palv in both groups; in CH rats, Ppa continued to rise, whereas it adapted to a lower level in C rats. Pressure-flow (P/Q) lines were measured at high and low Palv, all in Zone 2 state. In normoxia, high Palv caused a parallel shift in the P/Q line close to delta Palv in both C and CH rats. However, during hypoxic pulmonary vasoconstriction (HPV), high Palv caused a shift in the P/Q line less than delta Palv in C rats and greater than delta Palv in CH rats. Similar differences between C and CH rats were seen during constriction caused by almitrine, a drug that simulates HPV. Thus, these stimuli affect vessels that are functionally "extra-alveolar" in C rats but functionally "alveolar" in CH rats. We consider whether vasoconstriction by hypoxia and almitrine moves peripherally to the newly muscularized alveolar arterioles that are found in CH rats. Reactivity of lung vessels to bradykinin, angiotensin-1, and platelet-activating factor was greater in CH than in C rats, possibly also associated with muscularization of arterioles in the former.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Effects of chronic hypoxia and verapamil on cAMP content in tissues and blood plasma.

Changes in cAMP content of tissues of lung, heart and aorta and in blood plasma of rats during chronic hypoxia and administration of verapamil were determined and investigated. The results showed that chronic hypoxia (15 days) obviously increased cAMP content of blood plasma, lung and myocardiac tissues. Verapamil, a calcium agonist, attenuated the increase of cAMP content in blood plasma and lung but did not affect cAMP content of the myocardium. It is suggested that a calcium influx is responsible for the increase in cAMP content.

Animals↗
PubMed1989

Pulmonary vasodilator action of ligustrazine, active principle of a traditional Chinese remedy, in rats and ferrets.

The action of ligustrazine on the pulmonary circulation was tested in isolated perfused rat lung in vitro and autoperfused ferret lower left lobe preparation in vivo. Ligustrazine reduced hypoxic pulmonary vasoconstriction in a dose-dependent manner. It had a lesser dilator effect on KCl-induced vasoconstriction than verapamil and a relatively small inhibitory effect on the pressor response to angiotensin II. Ligustrazine preferentially inhibited the vasoconstriction caused by hypoxia and almitrine. The increased slope and intercept of the pressure-flow line caused by hypoxic vasoconstriction was reduced to the normal range after administration of ligustrazine (4 mg). Thus ligustrazine proved to be a powerful pulmonary vasodilator; it had a relatively small depressor effect on systemic blood pressure.

Animals↗
PubMed1989

Changes in cardiac and respiratory function of Antarctic Research Expedition members--preliminary report.

Cardiac and respiratory functions were estimated in 16 Chinese Antarctic Research Expedition members (Third expedition) before and after spending three months in the Antarctic. No significant changes were found in ECG examination. In cardiac function test, prolonged LVET and abbreviated PEP were found. PEP/LVET decreased significantly. Respiratory ventilation function examination showed an increase in FEV1 and FEV25 and a decrease in ERC. Results showed that cardiac and respiratory functions remained almost unchanged in the Expedition members. It is also suggested that a physiological compensation may have occurred in these members' cardiac functions either in the Antarctic or during the return sea voyage.

Antarctic Regions↗
PubMed1985

Responses of blood volume and red cell mass in two strains of rats acclimatized to high altitude.

Two strains of rats, one that adapts successfully to high altitude (HA) (Madison = M) and the other that adapts poorly and suffers a high mortality rate at high altitude (Hilltop = H) were studied during 40 days of exposure to a simulated altitude of 18 000 ft (5450 m; PB = 175). The time rate of change of blood volume (TBV), red cell volume (RBCV), plasma volume (PV) and hematocrit (Hct), and the interrelationships of these variables, particularly emphasizing TBV, PV and Hct as functions of RBCV, were compared in the M and H strains. Sea level control values in the two strains were not different, but by the 5th day at HA RBCV and TBV had expanded to a greater extent in H than M - a difference that was maintained throughout the 40 days - but PV decreased similarly in the two strains. By 30 days the inter-strain differences of RBCV, TBV, and Hct became more pronounced but still no difference of PV was noted. The most significant feature was the greater polycythemic response of H, which at the extreme range was not associated with any further decrease of PV and therefore resulted in rapid expansion of TBV. The probable effects of these responses on cardiovascular function and oxygen transport are discussed, comparing the differences of H and M strains, which became maladaptive in H. The similarity of the responses in H to those of man with chronic mountain sickness is noted.

Adaptation, Physiological↗