Yang Guang-tian

Effects of L-tetrahydropalmatine on energy metabolism, endothelin-1 and NO during acute cerebral ischemia-reperfusion of rats.

SummaryTo investigate the effects of L-tetrahydropalmatine (L-THP) on energy metabolism, endothelin-1 (ET-1) and NO during acute cerebral ischemiareperfusion of rats, 24 Wistar rats were randomly divided into four groups, with 6 rats in each group: sham-operation group, simple ischemia group, ischemiareperfusion group and treatment group (L-THP group). Cerebral ATP, lactate, ET-1 and NO levels were measured in all groups. Our results showed that treatment with L-THP could increase cerebral ATP levels, but decrease cerebral lactate, ET-1 and NO concentrations during ischemia-reperfusion in the treatment group. It is concluded that L-THP could improve cerebral energy metabolism and protect the injured brain tissue, the mechanism of which might be related to suppression of overproduction of ET-1 and NO.

Strain difference in pulmonary vascular responsiveness to hypoxia in rats

SummaryThe difference in pulmonary vascular response to hypoxia between Hilltop Sprague-Dawley (HT) rats and Wistar (W) rats was studied. Effects of inhibitor of leukotriene (LT) synthesis or prostaglandin (PG) synthesis on hypoxic pulmonary vasoconstriction (HPV) and chronic pulmonary hypertension were observed, and variations in plasma TXB2 and 6-keto-PGF1a during hypoxia were determined. The results showed that in rats of both strains LTs are the major mediator of HPV, which is also mediated by vasoconstrictive PGs in HT rats, while modulated by vasodilative PGs in W rats. This might be the crucial mechanism responsible for the higher pulmonary vascular responsiveness in HT rats. Differences in the modulating effect of histamine and in the structural feature of pulmonary arteriole might be contributing factors as well.

Effects of L-Tetrahydropalmatine on neuron apoptosis during acute cerebral ischemia-reperfusion of rats

SummaryTo investigate the effects of L-Tetrahydropalmatine (L-THP) on neuron apoptosis during acute cerebral ischemiareperfusion of rats and explore the effects of heat shock protein (HSP) on neuron apoptosis, Wistar rats were randomly divided into 3 groups; normal group, ischemia-reperfusion group and treatment group. The condition of neuron apoptosis, the survival state of neuron, pathological changes under an electron microscope and the number of HSP70 positive cells were measured in all groups. Results showed that the apoptosis neuron number was increased obviously at the 24th h during reperfusion and was further increased at the 48th h, the 72th h. While the number of survival neurons was decreased gradually with the prolongation of reperfusion time. Treatment with L-THP could decrease the apoptosis neuron number but increase the survival neuron number and the HSP70 positive cell number. Our study suggested that L-THP could decrease apoptosis and necrosis of neuron, up-regulate the expression of HSP70 and protect the cerebral ischemic injury.

Der Einfluß des Rauchens auf die hypoxische pulmonale Vasokonstriktion in der isolierten Lunge der Ratte — die Rolle der Prostaglandine und Leukotriene

ZusammenfassungAn isolierten perfundierten Rattenlungen wurde der Einfluß des Rauchens auf die pulmonale vaskuläre Resistenz (PVR) und auf die hypoxische pulmonale Vasokonstriktion (HPV), sowie die Rolle der Prostaglandine (PG) und Leukotriene (LT) bei diesem Effekt geprüft. Es zeigte sich, daß Rauchen den Basisgefäßtonus der Lunge nicht veränderte, während HPV durch Zigarettenrauchen signifikant erhöht wurde. Nach der Applikation von Indomethacin, einem Cyclooxygenaseinhibitor, in das Perfusionsblut (20 μg/ml) wurde HPV stärker, aber nach Rauchen verstärkte sich HPV nicht mehr weiter. Diethylcarbamazine citrate (DEC, 1 mg/ml), ein Lipidoxygenaseinhibitor, verminderte HPV vor und nach dem Rauchen. Nach Applikation der beiden Agentien war HPV sowohl vor als auch nach dem Rauchen vermindert. Das läßt darauf schließen, daß bei der HPV die LT als Mediatoren und die FG als Modulatoren wirken. Die beiden könnten auch eine wichtige Rolle spielen bei der durch Rauchen induzierten Erhöhung von HPV.AbstractIsolated 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 prostsglandines (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 μg/ml) increased HPV in non-smoking lungs, but not in lungs after smoking. Diethylcarbamazine citrate (DEC, l 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.: 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.

Investigation of the distribution and changes of VLDLR Subtype in fibrotic cardiac muscles

SummaryVery low-density lipoprotein receptor (VLDLR) is the major receptor with which cells can uptake the triacylglycerol from blood. It is divided into two subtypes according to presence of O-linked sugar domain located in the VLDLR receptor immediately outside of the membrane. Type I VLDLR contains the O-link domain, while type II has no such domain. The type I VLDLR are mainly found on the surface of human myocardial cells. The result of our quantitative polymerase chain reaction on the normal and fibrotic cardiac muscles showed that both subtypes and expression level of VLDLR on the myocardial cell surface did not vary significantly between the normal and the fibrotic cardiac muscles despite the presence of malfunction due to fibrosis. This finding suggests that fibrosis doesn’t exert significant influence on the subtype and the expression of VLDLR on the surface of myocardial cells. Such inconsistence with the changes found in other fibrotic tissues is awaiting further studies.

Effects of Prostaglandins and Leukotrienes on Hypoxic Pulmonary Vasoconstriction in Rats

SummaryTo investigate the effects of prostaglandins (PGs) and leukotrienes (LTs) on hypoxic pulmonary vasoconstriction (HPV),in vivo rats experiment andin vitro perfused lung experiment were conducted. The effect of hypoxia on hemodynamics, concentrations of TXB2 and 6-keto-PGF14 in serum and lung tissue during hypoxia and effects of PGs and LTs on HPV were observed. The results showed that pulmonary arterial pressure (Ppa) and pulmonary vascular resistance were increased during hypoxia, but cardiac output and systemic arterial pressure were decreased. There were increases of the concentrations of TXB2 and 6-keto-PGF14 and their ratio in serum and lung tissue during hypoxia. After use of cyclooxygenase inhibitor (indomethacin)in vivo andin vitro, HPV was augmented respectively, but after use of lipoxygenase inhibitor (diethylcorbamazine) or leukotriene receptor blocker (LY-171883), HPV was attenuated. It was suggested that LTs mediated pulmonary vasoconstriction, PGs inhibited pulmonary vasoconstriction and they played a modulating role during hypoxia.

The role of histamine in acute hypoxic pulmonary hypertension in dogs

SummaryThe role of histamine in acute hypoxic pulmonary hypertension was studied in dogs, and the correlation between the effect of histamine and the characteristics of hypoxic pulmonary response was examined. Acute hypoxic pulmonary vasoconstrictive response was not blocked by H1-receptor antagonist, but was potentiated by H2-receptor antagonist. Combined H1- and H2-receptor blockade failed to modify the hypoxic pulmonary vasoconstriction. It seems that H1-receptor antagonist could abolish the potentiating effect of H2-receptor antagonist. Exogenous histamine dilated lung vessels when pulmonary vascular tone was increased. This is in contrast to its vasoconstrictive effect when pulmonary vascular tone was normal. The vasodilating effect of histamine was blocked by H2-receptor antagonist. It is deduced that histamine probably plays the role of a modulator in hypoxic pulmonary vascular response. The dominant effect of H2-receptor caused by increasing pulmonary vascular tone might be implicated in the modulating effect. Infusion of histamine not only suppressed the pulmonary response to hypoxia, but also attenuated the progressive increase in pulmonary vascular resistance in repeated hypoxia. The reduction of the modulating effect of histamine probably contributes to the progressive increase in pulmonary vascular response to repeated hypoxia.

Wirkung von Strophanthin, Digoxin und Isoproterenol auf die Herzkontraktilität während Hypoxie und hyperkapnischer Azidose

ZusammenfassungAm isoliert perfundierten Meerschweinchenherzen wurde bei unterschiedlichen Gasbedingungen (Perfusate mit 5% CO2 und 95% O2; 8% CO2 und 90% O2; 10% CO2 und 90% O2; 5% CO2 und 21% O2 begast) die Wirkung von k-Strophanthin, Digoxin und Isoproterenol geprüft. Es wurden die Drücke und dP/dt max im re. und li. Ventrikel, und der Koronardruck gemessen. Unter Normalbedingung (5% CO2 und 95% O2) und bei Azidose (8% CO2 und 90% O2, bzw. 10% CO2 und 90% O2) zeigten sich keine signifikanten Unterschiede, dagegen wies der Effekt der Medikamente auf das Meerschweinchenherz unter Normalbedingung und bei Hypoxie (5% CO2 und 21% O2) wesentliche Unterschiede auf. Das bedeutet, daß die inotrope Wirkung dieser Medikamente auf das isolierte Herz unter Hypoxie vermindert ist.Perfusate, die mit 5% CO2 und 21% O2 begast werden, bedeuten für das Herzpräparat eine Hypoxie.

Herzkontraktilität während der akuten respiratorischen Azidose und während der akuten Hypoxie

Die Akutanderung des CO2-Druckes und des Sauerstoffdruckes des Perfusats beeinflust deutlich die Kontraktilitat des isolierten Meerschweinchenherzens in dem modifizierten Langendorff-Praparat. Die respiratorische Azidose mindert statistisch signifikant die Kontraktilitat der rechten sowie auch der linken Kammer. Die Steigerung der Azidose (CO2 von 8 auf 10%, pH von 7,297 auf 7,246) bringt keine statistisch signifikante Verschlechterung. Die Hypoxie (21 und 11% O2) mit oder ohne Azidose verursacht statistisch signifikante Abnahme der Druckwerte und von dP/dt max wie im linken so auch im rechten Ventrikel.ZusammenfassungDie Akutänderung des CO2-Druckes und des Sauerstoffdruckes des Perfusats beeinflußt deutlich die Kontraktilität des isolierten Meerschweinchenherzens in dem modifizierten Langendorff-Präparat. Die respiratorische Azidose mindert statistisch signifikant die Kontraktilität der rechten sowie auch der linken Kammer. Die Steigerung der Azidose (CO2 von 8 auf 10%, pH von 7,297 auf 7,246) bringt keine statistisch signifikante Verschlechterung. Die Hypoxie (21 und 11% O2) mit oder ohne Azidose verursacht statistisch signifikante Abnahme der Druckwerte und von dP/dt max wie im linken so auch im rechten Ventrikel.Für die Myokardkontraktilität scheint die Hy oxie entscheidend zu sein. Die respiratorische Azidose und auch die Hypoxie wurden den klinischen, häufigen Zuständen angepaßt. Es ist möglich, daß eine extreme respiratorische Azidose (pCO2 über 80 mmHg), auch ohne Hypoxie ebenso zu deutlichen Einschränkungen der Herzkontraktilität führen würde