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Hypoxia in the pulmonary vein increases pulmonary vascular resistance independently of oxygen in the pulmonary artery
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作者 Sigridur Olga Magnusdottir Carsten Simonsen +2 位作者 Dan Stieper Karbing Bodil Steen Rasmussen Benedict Kjaergaard 《Animal Models and Experimental Medicine》 CAS CSCD 2024年第2期156-165,共10页
Introduction:Hypoxic pulmonary vasoconstriction(HPV)can be a challenging clinical problem.It is not fully elucidated where in the circulation the regulation of resistance takes place.It is often referred to as if it i... Introduction:Hypoxic pulmonary vasoconstriction(HPV)can be a challenging clinical problem.It is not fully elucidated where in the circulation the regulation of resistance takes place.It is often referred to as if it is in the arteries,but we hypothesized that it is in the venous side of the pulmonary circulation.Methods:In an open thorax model,pigs were treated with a veno-venous extra corporeal membrane oxygenator to either oxygenate or deoxygenate blood passing through the pulmonary vessels.At the same time the lungs were ventilated with extreme variations of inspired air from 5%to 100%oxygen,making it possible to make combinations of high and low oxygen content through the pulmonary circulation.A flow probe was inserted around the main pulmonary artery and catheters in the pulmonary artery and in the left atrium were used for pressure monitoring and blood tests.Under different combinations of oxygenation,pulmonary vascular resistance(PVR)was calculated.Results:With unchanged level of oxygen in the pulmonary artery and reduced inspired oxygen fraction lowering oxygen tension from 29 to 6.7 kPa in the pulmonary vein,PVR was doubled.With more extreme hypoxia PVR suddenly decreased.Combinations with low oxygenation in the pulmonary artery did not systematic influence PVR if there was enough oxygen in the inspired air and in the pulmonary veins.Discussion:The impact of hypoxia occurs from the alveolar level and forward with the blood flow.The experiments indicated that the regulation of PVR is mediated from the venous side. 展开更多
关键词 animal models cardiopulmonary support Hypoxic pulmonary vasoconstriction pulmonary circulation
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Role of Voltage-gated Potassium Channels in Pathogenesis of Chronic Pulmonary Heart Disease 被引量:6
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作者 柯琴梅 吴霁 +2 位作者 田莉 李伟 杜以梅 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2013年第5期644-649,共6页
The influence of hypoxia on the activity of voltage-gated potassium channel in pulmonary artery smooth muscle cells (PASMCs) of rats and its roles in the pathogenesis of chronic pulmonary heart disease were investig... The influence of hypoxia on the activity of voltage-gated potassium channel in pulmonary artery smooth muscle cells (PASMCs) of rats and its roles in the pathogenesis of chronic pulmonary heart disease were investigated. Eighty male Sprague-Dawley rats were randomly allocated into control group (n=10), acute hypoxic group (n=10), and chronic hypoxic groups (n=60). The chronic hypoxic groups were randomly divided into 6 subgroups (n=10 each) according to the chronic hypoxic periods. The rats in the control group were kept in room air and those in acute hypoxic group in hypoxia envi- ronmental chamber for 8 h. The rats in chronic hypoxic subgroups were kept in hypoxia environmental chamber for 8 h per day for 5, 10, 15, 20, 25, and 30 days, respectively. The mean pulmonary arterial pressure (mPAP), right ventricular hypertrophy index (RVHI), and the current of voltage-gated potas- sium channel (IK) in PASMCs were measured. Results showed that both acute and chronic hypoxia could decrease the IK in PASMCs of rats and the I-V relationship downward shifted to the right. And the peak Ir density at +60mV decreased with prolongation of hypoxia exposure. No significant difference was noted in the density oflK (at +60 mV) and I-V relationship between control group and chronic hy- poxic subgroup exposed to hypoxia for 5 days (P〉0.05), but there was a significant difference between control group and chronic hypoxic subgroup exposed to hypoxia for 10 days (P〈0.05). Significant dif- ferences were noted in the IK density (at +60 mV) and I-V relationships between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days (P〈0.01). Compared with con- trol rats, the mPAP and RVHI were significantly increased after chronic exposure to hypoxia for 10 days (P〈0.05), which were further increased with prolongation of hypoxia exposure, and there were signifi- cant differences between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days (P〈0.01). Both the mPAP and the RVHI were negatively correlated with the density OflK (r---0.89769 and -0.94476, respectively, both P〈0.01). It is concluded that exposure to hypoxia may cause decreased activity of voltage-gated potassium channel, leading to hypoxia pulmonary vasocon- striction (HPV). Sustained HPV may result in chronic pulmonary hypertension, even chronic pulmonary heart disease, contributing to the pathogenesis of chronic pulmonary heart disease. 展开更多
关键词 potassium channel chronic pulmonary heart disease hypoxia pulmonary vasoconstriction
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Amniotic fluid embolism:literature review and an integrated concept of pathomechanism 被引量:1
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作者 Mieczyslaw Uszyński 《Open Journal of Obstetrics and Gynecology》 2011年第4期178-183,共6页
Literature concerning procoagulant activity of the amniotic fluid and pathomechanism of amniotic fluid embolism (AFE) was surveyed and a new concept of its pathogenesis, called the integrated concept of AFE, was prese... Literature concerning procoagulant activity of the amniotic fluid and pathomechanism of amniotic fluid embolism (AFE) was surveyed and a new concept of its pathogenesis, called the integrated concept of AFE, was presented. According to this concept, two components of the amniotic fluid are involved: (i) apoptosis-affected amniotic cells showing a special role in the initiation of disseminated intravascular coagulation (DIC) and (ii) leukotrienes (formerly called slow-reacting substances), inducing bronchial and pulmonary vascular smooth muscle contraction. Although each of these components initiates a different pathogenic pathway, they both lead to the formation of a mechanical barrier on blood flow through the lungs (amniotic debris + microemboli) and/or functional barrier (pulmonary vasoconstriction). An old dilemma, concerning indications for heparin therapy in AFE was recalled in the light of the new concept. 展开更多
关键词 Amniotic Fluid Embolism Amniotic Cells Tissue Factor Leukotriens Disseminated Intravascular Coagulation pulmonary vasoconstriction
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