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Biomedical subjects

D X Wang

Publications and source records attributed to D X Wang.

At least 55 records · Page 3Linked to original sources
PubMed1993

Hypoxia increases cytosolic free calcium in porcine pulmonary arterial endothelial cells.

Alteration of cytosolic free calcium ([Ca2+]i) in hypoxia was studied with fluorescent probe, Fura-2 in cultured porcine pulmonary arterial endothelial cells. It was found that hypoxia caused by bubbling the cell suspension with 100% N2 increased [Ca2+]i in endothelial cells by 90 +/- 20% (n = 8, P < 0.05), but didn't affect that in a Ca(2+)-free buffer, La3+ (2 x 10(-5) mol/L) inhibited the hypoxia-induced increment in [Ca2+]i, whereas verapamil (10(-8) mol/L) didn't. These findings suggest that hypoxia could induce Ca2+ influx in pulmonary arterial endothelial cells, which might play an important role in vascular response to hypoxia.

Animals↗
PubMed1993

The regulatory effect of substances released from porcine bronchial epithelial cells on hypoxic pulmonary vasoconstriction.

In this study, porcine pulmonary artery segments (intact or denuded) and bronchial segments (with or without epithelium) were tested in organ bath. Hypoxia caused a bronchial epithelium dependent relaxation of intact or denuded pulmonary artery preconstricted with phenylephrine. Constriction in intact pulmonary artery coated with epithelium denuded bronchus was observed during hypoxia. The bronchial epithelium-dependent relaxation could be inhibited by indomethacin but not be blocked by the following agents: atropine, propranolol, gossypol, methylene blue and chlorpheniramine. The results suggested that HPV was endothelium-dependent. Hypoxia could cause the production of an epithelium-derived relaxing factor (EpDRF), which acted directly on smooth muscle. The effect of EpDRF was not mediated by pulmonary endothelium, but might be related to arachidonic acid cyclooxygenase pathway.

Animals↗
PubMed1993

Effect of hypoxia on release of vasoactive substances from cultured pulmonary arterial and aortic endothelial cells.

The effect of hypoxia on the production and release of vasoactive substances from endothelial cells of pulmonary artery (PAECs) and aorta (AECs) was studied. The results indicated that the overall effect of the long half-life vasoactive substances released from PAECs and AECs was vasoconstrictive. The long half-life lipid-soluble substances produced by PAECs and AECs were vasodilative, and did not change in hypoxia. However, the long half-life water-soluble heat-unstable and heat-stable ones were vasoconstrictive. Hypoxia could reduce the release of the former and promote that of the latter which might be peptides. The PAECs could release specific long half-life mediator which was pulmonary artery-constrictive, water-soluble, heat-unstable, and not related to hypoxia. Hypoxia inhibited the production of PGI2, a short half-life vasodilator, in PAECs, but not in AECs.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Role of sympathetic nerve and adrenal gland in the potentiation of hypoxic pulmonary vasoconstriction during cigarette smoking.

The aim of this study was to investigate the role of sympathetic nerve and adrenal gland in the changes in hemodynamics and hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking in Wistar rats. Data showed that an increment of pulmonary vascular resistance (PVR) induced by alveolar hypoxia was partially prevented by prazosin (alpha 1-receptor blocker) and prazosin combined with propranolol (beta-receptor blocker), but not significantly affected by propranolol or adrenalectomy. Cigarette smoking could increase PVR and potentiate HPV, whereas the potentiation of HPV was partially inhibited by prazosin and strengthened by propranolol, but not affected by adrenalectomy. It is suggested that the sympathetic nerve excitation caused by cigarette smoking may play a role in the strengthening of HPV.

Adrenal Glands↗
PubMed1992

[Influence of cigarette smoking on the hypoxic pulmonary vasoconstriction in isolated rat lungs--the role of prostaglandins and leukotrienes].

Isolated rat lungs perfused with blood were used to determine the effects of cigarette smoke, delivered into the lung by a ventilator, on the pulmonary vascular resistance (PVR), and on the hypoxic pulmonary vasoconstriction (HPV), and to explore the role the prostaglandins (PG) and leukotrienes (LT) play in that effect. The results showed that PVR did not change, while HPV was significantly enhanced by smoking. Indomethacin, an inhibitor of PG biosynthesis, administered in the perfusing blood (20 micrograms/ml) increased HPV in non-smoking lungs, but not in lungs after smoking. Diethylcarbamazine citrate (DEC; 1 mg/ml), an inhibitor of LT biosynthesis, decreased HPV before and after smoking. After perfusion with both indomethacin and DEC, HPV also decreased. It is suggested that LT act as mediators whereas PG as modulators in HPV, and PG and LT might play an important role in the increase of HPV by cigarette smoking.

Animals↗
PubMed1992

Effect of endotoxin on hypoxic pulmonary vasoconstriction--the role of prostaglandins and leukotrienes.

In this study, we observed the effect of endotoxemia on hypoxic pulmonary vasoconstriction (HPV) in dogs and explored roles played by prostaglandins and leukotrienes in this process. 5 micrograms/kg BW of E. coli endotoxin induced transient rise in pulmonary arterial pressure and pulmonary vascular resistance (PVR). 30 min after injection of endotoxin when PVR tended to decline, pulmonary vasoconstriction response to alveolar hypoxia was lost, and the ratio of TXB2 to 6-keto-PGF1 alpha decreased significantly. HPV was enhanced at 60-100 min and then returned to the control level at 2 h after injection of endotoxin. At these periods the ratio of TXB2 to 6-keto-PGF1 alpha was the same as before use of endotoxin, whereas plasma concentration of leukotrienes was markedly increased. Indomethacin could prevent the early loss of HPV, but no effect on the late increment of HPV was found. Diethylcarbamazine, which blocked the production of leukotrienes after use of endotoxin, could inhibit late increment of HPV. We concluded that the early loss of HPV was related to the vasodilator prostacyclin, and the late increment of HPV was mainly brought about by leukotrienes.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effect of cigarette smoking on hypoxic pulmonary vasoconstriction and its relation to animal species and period of smoking.

The alteration in hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking was studied in Wistar rats, piglets and in humans. The percentage change of pulmonary vascular resistance (delta PVR%) and the amplitude of the systolic wave in impedance pneumorheogram (delta H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats increased (delta PVR% from 55.0 +/- 15.6% to 102.3 +/- 12.4%), which is mainly mediated by leukotrienes (LTs); whereas HPV in piglets decreased (delta PVR% from 65.2 +/- 12.5% to 55.9 +/- 9.8%), which is mainly mediated by beta-adrenergic receptors, and HPV in humans also increased (delta H% from 20.6 +/- 2.6% to 31.1 +/- 4.1%), in which prostaglandins and leukotrienes may play the role of mediators. However, after one-month cigarette smoking, the HPV in rats fell significantly (delta PVR% 11.4 +/- 1.6%). An increase in synthesis of vasodilative prostaglandins and a decrease in leukotrienes synthesis may be the contributing factors to this alteration in HPV.

Adolescent↗
PubMed1992

Effects of dietary oils on pulmonary vascular reactivity and chronic hypoxic pulmonary hypertension in rats.

The effects of dietary oils on pulmonary vasoreactivity and chronic hypoxic pulmonary hypertension were assessed in rats fed on soybean oil (SO), pig oil (PO), soybean oil plus pig oil (SP) or a regular diet (HC) started two months before the onset of chronic normobaric hypoxia (10 +/- 0.5% O2 ventilation, 8 h per day, for 14 days). The mean pulmonary arterial pressure and pulmonary vasoreactivity to acute hypoxia were higher in the SO group than in the PO, SP and HC groups. Hypertrophy of the right ventricle in the SO group was more serious as well. Blood viscosity and hematocrit were augmented by chronic hypoxic in SO, PO, PS and HC groups, but no significant differences were found among them. The findings suggest that dietary soybean oil can potentiate hypoxic pulmonary vasoconstriction, and thereby promote the development of pulmonary hypertension and right ventricular hypertrophy.

Animals↗
PubMed1992

Alteration in hypoxic pulmonary vasoconstriction during hypothermia in dogs.

This study was performed to investigate the pulmonary vascular reactivity during hypothermia. It was found that the pulmonary vessels were more sensitive to alveolar hypoxia in hypothermic dogs, and that hypoxic pulmonary vasoconstriction (HPV) was enhanced, which could be inhibited by alpha 1-adrenoceptor blocker prazosin. The concentration of arterial plasma norepinephrine (NE) increased in dogs with hypothermia or in those with hypothermia plus hypoxia, but there was no significant difference between these two groups. The plasma level of 5-hydroxytryptamine (5-HT) was reduced during hypoxia in hypothermic dogs. Increase in plasma 6-keto-PGF1 alpha, which appeared in hypoxic dogs, was not observed during hypoxia in hypothermic dogs. These findings suggest that a potentiation in the sensitivity and reactivity of alpha-adrenoceptor in pulmonary vessels and a decrease in the modulation of PGI2 might be responsible for the enhancement of HPV. 5-HT seemed not to play a contributing role in the alteration of HPV.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of cigarette smoking on the function of metabolizing arachidonic acid and angiotensin I in the isolated perfused rat lungs.

The effects of acute and chronic cigarette smoking on the metabolism of exogenous arachidonic acid (AA) and angiotensin I (AI) in perfused isolated rat lungs were studied. The results showed that acute cigarette smoking did not alter the contents of 6-keto-PGF1 alpha (the stable metabolite of PGI2) and TXB2 (the stable metabolite of TXA2) in the effluent and the increment of pulmonary artery pressure (delta Ppa) caused by AA. The conversion of A I into A II was significantly increased (P < 0.01), while the delta Ppa induced by A I injection was obviously decreased as compared with controls (P < 0.05). After cigarette smoke exposure for 30 days, the delta Ppa caused by AA or A I did not differ from that of controls, but the contents of 6-keto-PGF1 alpha and A II increased more markedly than those in non-smoking rats (P < 0.05). It is suggested that acute and chronic cigarette smoking in rats can promote the lung function of converting A I into A II, chronic smoking can increase the lung function of metabolizing AA into PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of acute ingestion of ethanol on hemodynamics and hypoxic pulmonary vasoconstriction in dogs--role of leukotrienes.

The effects of acute intragastric administration of ethanol on hemodynamics and hypoxic pulmonary vasoconstriction were studied in spontaneously breathing dogs. The dogs were given 0.5 g/kg of 10% ethanol (v/v) in 5 min. Hemodynamic measurements were obtained before and 30 min after ingestion of ethanol. Mean pulmonary arterial pressure and pulmonary vascular resistance increased markedly after ingestion of ethanol, and hypoxic pulmonary vasoconstriction was augmented significantly by ethanol as well. Diethylcarbamazine citrate (DEC), a lipoxygenase inhibitor, inhibited these effects of ethanol in a dosage of 200 mg/kg. The above findings suggest that ethanol can induce pulmonary vasoconstriction, which may be predominantly mediated by leukotrienes (LTs).

Animals↗
PubMed1991

Effect of experimental acute hypertension of the biliary tract on hemodynamics and activity of the major splanchnic nerve in rabbits.

An experimental study of the effect of acute biliary hypertension on hemodynamics and activity of the major splanchnic nerve was conducted in Japanese big ear white rabbits. A catheter with an inflatable rubber bag fixed to its anterior end was inserted into the extrahepatic biliary duct via the duodenum, and a biliary high pressure of 20 kFa (150 mmHg) was created and maintained for 2 h by inflating the bag with water. The right major splanchnic nerve was isolated and the impulse frequencies of the nerve were recorded during the study. Arterial blood pressure was also dynamically monitored. A significant fall of the arterial blood pressure (P less than 0.01) and an increase in impulse frequency of the nerve (P less than 0.01) were found in this "simple type" acute biliary high pressure without infection. Biliary decompression immediately eliminated these abnormalities (P less than 0.01). The drop in blood pressure was much less prominent if the right splanchnic nerve was blocked prior to biliary high pressure.

Animals↗
PubMed1991

Effects of dietary magnesium on pulmonary vascular reactivity and chronic hypoxic pulmonary hypertension in rats.

The effects of dietary magnesium (Mg) on pulmonary vascular reactivity and chronic hypoxic pulmonary hypertension were assessed in rats. The rats were fed high magnesium (H-Mg) diet or a regular diet for two months before the start of hypoxia, 10 +/- 0.5% O2 ventilation, 8 h/day, for 14 days running. The plasma level of Mg was significantly increased in the H-Mg group as compared to the controls. Mean pulmonary arterial pressure, pulmonary vascular reactivity to hypoxia and pulmonary vascular resistance were significantly lower in the rats fed H-Mg diet than in those fed regular diet. The weight ratios of the right ventricle to the ending body weight (RV/EBW) and to the left ventricle plus interventricular septum (RV/LV + S) in the rats fed H-Mg diet were remarkably lower as well. No difference was observed in blood viscosity and hematocrit between the H-Mg group and the hypoxic control. The above findings suggest that dietary Mg can attenuate basic pulmonary resistance and hypoxic pulmonary vasoconstriction, thereby preventing the development of chronic hypoxic pulmonary hypertension and right ventricular hypertrophy.

Animals↗
PubMed1991

Effects of cigarette smoking, hypoxia and vasoactive mediators on the production of PGI2 and TXA2 in cultured pulmonary artery endothelial cells.

Effects of cigarette smoke extract (CSE) and some vasoactive mediators on the production of PGI2 and TXA2 in normoxic and hypoxic pulmonary artery endothelial cells (PAECs) in culture were studied. The production of PGI2 in PAECs was inhibited by hypoxia or verapamil, but promoted by angiotensin II (A II), noradrenaline (NE) or platelet activating factor (PAF), while that of TXA2 slightly increased except when treated with PAF. The effect of AII, NE, PAF and verapamil, however, was not influenced by hypoxia. CSE inhibited the production of PGI2 in normoxic PAECs but did not further reduce 6-keto-PGF1 alpha in hypoxic PAECs medium. The results suggest that a) the production of PGI2 during hypoxia might be stimulated by vasoactive mediators produced during hypoxia, not by hypoxia directly; b) the production and release of PGI2 were related to intracellular calcium; c) the augmented production of PGI2 might be one of the mechanisms in the pulmonary vasodilating role of PAF; and d) prostaglandin production might be associated with the alteration of hypoxic pulmonary vasoreactivity after cigarette smoking.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Mapping the receptor-recognition site of human transforming growth factor-alpha.

The receptor-recognition site human transforming growth factor-alpha (TGF alpha), a 50-residue tricyclic peptide with three disulfide bonds, was mapped by a set of 46 peptide analogs consisting of linear, monocyclic, bicyclic, and tricyclic structures representing individual and overlapping subdomains of human TGF alpha. Linear overlapping fragments ranging from 7 to 18 residues and spanning the entire length of TGF alpha as well as monocyclic analogs with one disulfide linkage were found to be inactive in both receptor-binding and mitogenic assays. Bicyclic analogs with two disulfide linkage and representing either the amino or carboxyl two-thirds of TGF alpha showed low activity at 0.1-0.9 mM concentrations. Tricyclic analogs containing all three disulfide linkages but lacking either the amino or carboxyl terminal heptapeptide was, respectively, 3% and 0.1% as active as TGF alpha. These results show that determinants for the receptor binding cannot be represented by a short continuous fragment or a single subdomain, but are located on a discontinuous surface on a folded structure with disulfide restraints. Furthermore, these results when combined with our previous results which shows that the middle subdomain (second disulfide loop) is not involved in the receptor binding suggest that the receptor-binding residues are constituted of three fragments located at the first and third subdomains as well as the external carboxyl peptide.

Amino Acid Sequence↗
PubMed1991

[Effect of dihydroetorphine on contraction response of guinea pig ileum, mouse, and rabbit vas deferens induced by electric field stimulation in vitro].

Dihydroetorphine (DHE) inhibited contraction response of isolated guinea pig ileum and mouse vas deferens induced by electric field stimulation with IC50 values of (4.4 +/- 4.3) x 10(-16) mol.L-1 and (1.1 +/- 1.4) x 10(-18) mol.L-1 respectively. These effects of DHE were antagonized by naloxone (Nal). On guinea pig ileum, the antagonistic effect of Nal against DHE was similar to those against morphine and etorphine. However, on mouse vas deferens, the antagonistic effect of Nal against DHE was more potent than those against morphine and etorphine. Besides, DHE showed antagonistic effect on k-receptors in isolated rabbit vas deferens.

Analgesics, Opioid↗
PubMed1991

[Effects of cigarette smoking on pulmonary vasoreactivity].

The effects of cigarette smoking on hemodynamics and hypoxic pulmonary vasoconstriction were studied in intact rats, in isolated rat lungs and in humans. The results show that smoking increases the vascular tone of pulmonary arterioles and venules, and increases their reactivity to alveolar hypoxia; leukotrienes, prostaglandins and sympathetic nerve mediate the smoking--induced pulmonary vasoconstriction; and the augmentation of pulmonary vasoreactivity to hypoxia is mainly mediated by leukotrienes and sympathetic nerve, possibly by prostaglandins as well in humans.

Animals↗