Pulmonary hypertension is a pathophysiologic process characterized by progressive elevation of pulmonary vascular resistance and right heart failure, which is a common complication of many diseases. Pulmonary hyperten...Pulmonary hypertension is a pathophysiologic process characterized by progressive elevation of pulmonary vascular resistance and right heart failure, which is a common complication of many diseases. Pulmonary hypertension with no apparent causes （unknown etiology） is termed primary pulmonary hypertension or, more recently, idiopathic pulmonary arterial hypertension （IPAH）. Before the availability of disease-specific （targeted） therapy （through the mid-1980s） the median life expectancy from the time of diagnosis in patients with this disease was 2.8 years. Modem treatment has markedly improved physical function and has extended survival, and the 5-year mortality is 50%. Although there is already more than 100 years of research history, the mechanisms of this disease are still not very clear. Recently, with the development of cell biology and molecular genetics, further research into the mechanisms responsible for pulmonary hypertension have been possible, which has helped in its diagnosis and treatment. It is believed that the mechanisms of pulmonary hypertension can not only be described by pathophysiology but involve multiple factors （pathways） like cellular, humoral and molecular genetics, etc.展开更多
Background The balance between vasodilation and vasoconstriction plays a major role in maintaining vascular homeostasis. However, the underlying mechanisms are unclear. More and more evidence suggested that there was ...Background The balance between vasodilation and vasoconstriction plays a major role in maintaining vascular homeostasis. However, the underlying mechanisms are unclear. More and more evidence suggested that there was an interaction in the regulation of vasorelaxation between nitric oxide （NO） and hydrogen sulfide （H2S）. We explored the interaction between and effects of NO and H2S on the relaxation of pulmonary arteries in rats. Methods Seven male Sprague-Dawley rats were anaesthetized with chloral hydrate and the pulmonary arteries of each rat separated for the study of vascular activities. The vasorelaxing activities of pulmonary artery rings in response to different doses of a NO donor, sodium nitroprusside （SNP）, or a H2S donor, sodium hydrogensulfide （NariS）, were measured in vitro. When pulmonary artery rings were treated with a cystathionine-y-lyase inhibitor, DL-propargylglycine, in the presence of SNP or a nitric oxide synthase inhibitor, Nω-nitro-L-arginine methyl ester, in the presence of NariS, the changes in relaxing activities were analyzed. Results The relaxation of pulmonary artery rings was in a dose dependent manner in response to either SNP or NariS. The relaxation rates of pulmonary artery rings increased from （30.90±4.62） % to （60.50±8.08） % when the concentration of SNP increased from 1 pmol/L to 3 pmol/L and from （26.13±4.12） % to （53.09±14.01） % when the concentration of NariS increased from 25 pmol/L to 100 μmol/L. However, when appropriate inhibitor was added, the relaxation responses to SNP and NariS decreased. Conclusions The results suggested that similarly to NO, H2S acted as a vasorelaxant either independently of, or synergistically with NO in the regulation of vasorelaxation. The interaction between NO and H2S played an important role in regulating relaxing activities of pulmonary arteries.展开更多
基金This work was supported by the grants from Changjiang Scholars Program （No. 985-2-087-111）, the National Science Foundation for Distinguished Young Scholars （No. 30425010）, the Major State Basic Research Development Program of China （No. 2006CB503807）, the Research Fund for the Doctoral Program of Ministry of Education of China （No. 20070001702 and No. 20070001770） and the National Natural Science Foundation of China （No. 30630031）.
文摘Pulmonary hypertension is a pathophysiologic process characterized by progressive elevation of pulmonary vascular resistance and right heart failure, which is a common complication of many diseases. Pulmonary hypertension with no apparent causes （unknown etiology） is termed primary pulmonary hypertension or, more recently, idiopathic pulmonary arterial hypertension （IPAH）. Before the availability of disease-specific （targeted） therapy （through the mid-1980s） the median life expectancy from the time of diagnosis in patients with this disease was 2.8 years. Modem treatment has markedly improved physical function and has extended survival, and the 5-year mortality is 50%. Although there is already more than 100 years of research history, the mechanisms of this disease are still not very clear. Recently, with the development of cell biology and molecular genetics, further research into the mechanisms responsible for pulmonary hypertension have been possible, which has helped in its diagnosis and treatment. It is believed that the mechanisms of pulmonary hypertension can not only be described by pathophysiology but involve multiple factors （pathways） like cellular, humoral and molecular genetics, etc.
基金This work was supported by the grants from the National Natural Science Foundation of China （No. 30425010, No. 30571971 ＆ No. 30630031）, the Major Basic Research Program of China （No. 2006CB503807）, the Natural Science Foundation of Beijing （No. 7072082） and the Changjiang Scholars Program.
文摘Background The balance between vasodilation and vasoconstriction plays a major role in maintaining vascular homeostasis. However, the underlying mechanisms are unclear. More and more evidence suggested that there was an interaction in the regulation of vasorelaxation between nitric oxide （NO） and hydrogen sulfide （H2S）. We explored the interaction between and effects of NO and H2S on the relaxation of pulmonary arteries in rats. Methods Seven male Sprague-Dawley rats were anaesthetized with chloral hydrate and the pulmonary arteries of each rat separated for the study of vascular activities. The vasorelaxing activities of pulmonary artery rings in response to different doses of a NO donor, sodium nitroprusside （SNP）, or a H2S donor, sodium hydrogensulfide （NariS）, were measured in vitro. When pulmonary artery rings were treated with a cystathionine-y-lyase inhibitor, DL-propargylglycine, in the presence of SNP or a nitric oxide synthase inhibitor, Nω-nitro-L-arginine methyl ester, in the presence of NariS, the changes in relaxing activities were analyzed. Results The relaxation of pulmonary artery rings was in a dose dependent manner in response to either SNP or NariS. The relaxation rates of pulmonary artery rings increased from （30.90±4.62） % to （60.50±8.08） % when the concentration of SNP increased from 1 pmol/L to 3 pmol/L and from （26.13±4.12） % to （53.09±14.01） % when the concentration of NariS increased from 25 pmol/L to 100 μmol/L. However, when appropriate inhibitor was added, the relaxation responses to SNP and NariS decreased. Conclusions The results suggested that similarly to NO, H2S acted as a vasorelaxant either independently of, or synergistically with NO in the regulation of vasorelaxation. The interaction between NO and H2S played an important role in regulating relaxing activities of pulmonary arteries.
