Progression Toward Decompensated Right Ventricular Failure in the Ovine Pulmonary Hypertension Model.

Progression Toward Decompensated Right Ventricular Failure in the Ovine Pulmonary Hypertension Model.
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DOI:
10.1097/mat.0000000000001417
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发表时间:
2022-02-01
期刊:
ASAIO journal (American Society for Artificial Internal Organs : 1992)
影响因子:
--
通讯作者:
Bacchetta M
Bacchetta M
中科院分区:
其他
文献类型:
--
作者:
Ukita R;Tumen A;Stokes JW;Pinelli C;Finnie KR;Talackine J;Cardwell NL;Wu WK;Patel Y;Tsai EJ;Rosenzweig EB;Cook KE;Bacchetta M

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肺动脉高压(PH)患者的失代偿性右心室衰竭(RVF)是致命的,治疗选择有限。新型机械循环支持系统具有治疗裂谷热的潜力,但开发这些装置需要复制在人类中观察到的病理生理学的大型动物疾病模型。我们以前报道了一种有效的疾病模型的PH羊通过结扎左肺动脉(PA)和渐进闭塞的主要PA。在这里,我们提出了一个急性慢性裂谷热与此模型。逐渐PA捆扎使RV压力升高(最大RV收缩压/平均压力= 95 mmHg/56 mmHg)。临床结果和实验室血清参数表明适当的生理代偿7周。然而,混合静脉饱和度在第7周急剧下降,肌酐在第9周显著升高。到第10周,动物出现依赖性皮下水肿。随后,该动物在全身麻醉诱导期间死亡。尸检评价显示有数升胸腔积液和腹水、右心室扩张、偏心性右心室肥大和心肌纤维化。所提出的情况下,支持该模型的相关性,人类裂谷热继发于PH的病理生理学和它的价值,在新的设备,治疗和干预措施的发展。
Decompensated right ventricular failure (RVF) in patients with pulmonary hypertension (PH) is fatal, with limited treatment options. Novel mechanical circulatory support systems have therapeutic potential for RVF, but development of these devices requires a large animal disease model that replicates the pathophysiology observed in humans. We previously reported an effective disease model of PH in sheep through ligation of the left pulmonary artery (PA) and progressive occlusion of the main PA. Here, we present a case of acute on chronic RVF with this model. Gradual PA banding raised the RV pressure (maximum RV systolic/mean pressure = 95 mmHg/56 mmHg). Clinical findings and laboratory serum parameters suggested appropriate physiologic compensation for 7 weeks. However, mixed venous saturation declined precipitously on week 7, and creatinine increased markedly on week 9. By the 10th week, the animal developed dependent, subcutaneous edema. Subsequently, the animal expired during induction of general anesthesia. Post-mortem evaluation revealed several liters of pleural effusion and ascites, RV dilatation, eccentric RV hypertrophy, and myocardial fibrosis. The presented case supports this model’s relevance to human pathophysiology of RVF secondary to PH and its value in the development of novel devices, therapeutics, and interventions.