Chronic heart failure model with microembolization of canine coronary arteries

犬冠状动脉微栓塞慢性心力衰竭模型

• 批准号: 59870032
• 负责人: INOUE Michitoshi
• 金额: $ 15.36万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Developmental Scientific Research
• 财政年份: 1984
• 资助国家: 日本
• 起止时间: 1984 至 1985
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-59870032/
• 关键词: chronic heart failure; myocardial ischemia; microembolization; 交感神経活性; β受容体

To investigate whether disseminative coronary embolization with microspheres elicits the chronic heart failure, we observed serial changes in hemodynamics, coronary circulation, histology and <beta> -receptor density after the coronary embolization with microspheres of 15- m ( ) in dogs. Immediately after the coronary embolization, a marked myocardial ischemia was elicited; lactate production, a decrease in fractional shortening and patchy ischemia (succinic dehydrogenase staining) were observed with an increase in coronary blood flow. A week after embolization, however, the resting coronary blood flow recovered to the control with absense of myocardial necrosis, but coronary flow reserve was significantly decreased. Histological examination indicated a delayed recovery from myocardial ischemia. Up to 5 hours, the patchy ischemia of 100-200 um( ), severe intracellular edema and a decrease in glycogen granules were observed. After a week, microscopic view demonstrated the apparently nor … More mal myocardium except a few myocytolytic lesions. Glycogen granules were markedly increased and mitochondriosis and rough endoplasmic reticulum were also observed, indicating compensatory metabolic hyperfunction. Hemodynamic studies 24 hours after microsphere embolization revealed a marked cardiac dysfunction; mean aortic pressure and dP/dt were markedly decreased, whereas the time constant of isovolumic left ventricular pressure decay (T) was increased. These hemodynamic changes were almost recovered after a week except for the diastolic function. Cardiac response to isoproterenol were preserved in both acute and chronic phases. Myocardial norepinephrine content was preserved 24 hours but it was significantly decreased a week after the microsphere embolization. In contrast, <beta> -adrenergic density was increased in the chronic phase. Therefore, the apparently normal systolic function despite the depletion of myocardial norepinephrine may be compensated by an increase in <beta> -adrenoceptor density. These results indicate that the prolonged myocardial ischemia elicits the prestage of chronic heart failure; q depletion of myocardial norepinephrine and impairement of diastlic function. Less

为探讨弥散性微球栓塞冠状动脉是否诱发慢性心力衰竭，我们观察了犬冠状动脉微球栓塞后血流动力学、冠状动脉循环、组织学和受体密度的变化<beta>。冠状动脉栓塞后立即引起明显的心肌缺血;随着冠状动脉血流量增加，观察到乳酸产生、缩短分数减少和斑片状缺血（琥珀酸脱氢酶染色）。栓塞后1周，冠脉血流恢复正常，无心肌坏死，但冠脉血流储备明显下降。组织学检查表明心肌缺血恢复延迟。在5小时内，观察到100-200 μ m（）的斑片状缺血、严重的细胞内水肿和糖原颗粒减少。一周后，显微镜观察显示， ...更多信息 除少数肌细胞溶解性病变外，心肌正常。糖原颗粒明显增加，并观察到肥大和粗面内质网，表明代偿性代谢功能亢进。微球栓塞后24小时的血流动力学研究显示明显的心功能不全;平均主动脉压和dP/dt显著降低，而等容左心室压力衰减的时间常数（T）增加。除舒张功能外，上述血流动力学变化在一周后基本恢复。异丙肾上腺素的心脏反应在急性期和慢性期均保持不变。心肌去甲肾上腺素含量在24小时内保持不变，但在微球栓塞后一周显著下降。相反，<beta>肾上腺素能密度增加，在慢性期。因此，尽管心肌去甲肾上腺素耗竭，但明显正常的收缩功能可通过肾上腺素能受体密度的增加而得到补偿<beta>。结果表明，心肌缺血时间延长，可诱发慢性心力衰竭前期，心肌去甲肾上腺素耗竭，心肌功能损害。少

项目成果

日本バイオレオロジー学会論文集. 8. (1985)

日本生物流变学会会刊8。（1985）

Circulation. 70-4. (1984)

循环。

Japanese Circulation Journal. 49-3. (1985)

日本流通杂志。

American Journal Physiology. (1986)

美国生理学杂志。

American Journal of Physiology. (1986)

美国生理学杂志。