Lin Pao-Yen, Lin Bo-Wen, Lai Tong-Sian, Yang Yan-Hsiang, Jiang Meei Jyh
Department of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Division of Cardiovascular Surgery, Department of Surgery, National Cheng Kung University Hospital, Tainan, Taiwan.
PLoS One. 2025 Jan 13;20(1):e0316607. doi: 10.1371/journal.pone.0316607. eCollection 2025.
Clarifying the inceptive pathophysiology of hypertensive heart disease helps to impede the disease progression. Through coarctation of the infrarenal abdominal aorta (AA), we induced hypertension in minipigs and evaluated physiological reactions and morpho-functional changes of the heart. Moderate aortic coarctation was achieved with approximately 30 mmHg systolic pressure gradient in minipigs. Hypertension was assessed by pressure increment of the carotid artery. Perioperative heart rate (HR) was recorded. We measured aortic flow rate and pressure proximal to coarctation to calculate hydraulic power, an indicator for cardiac workload, and resistance. The hearts harvested at sacrifice were examined for myocardial hypertrophy, fibrosis, and dysfunction. The parameters capable of indicating high-workload heart and their prediction effectiveness were determined by cluster and receiver operating characteristic (ROC) analyses. Prolonged AA coarctation for 8-12 weeks induced hypertension in a portion of minipigs. The cluster of minipigs exhibiting increased aortic hydraulic power displayed hypertension and mean HR elevation without changing arterial resistance. Notably, the blood pressure and HR were measured under full anesthesia, equivalent to resting status. Myocardial hypertrophy was not detected at the tissue, cellular or molecular levels. Expression of biomarkers for cellular stress and heart failure didn't increase except for heat shock protein 40. ROC analysis showed that aortic hydraulic power, resting HR, and mean blood pressure, but not arterial resistance, can serve as the indicators for high-workload hearts. These results suggested that resting HR increase in hypertensive pigs indicates hearts with high workload. Heart failure may develop without appropriate treatment.
阐明高血压性心脏病的初始病理生理学有助于阻止疾病进展。通过缩窄肾下腹主动脉(AA),我们在小型猪中诱导高血压,并评估心脏的生理反应和形态功能变化。在小型猪中实现了约30 mmHg的收缩压梯度的中度主动脉缩窄。通过颈动脉压力升高评估高血压。记录围手术期心率(HR)。我们测量主动脉缩窄近端的血流速率和压力,以计算水力功率(心脏工作负荷的指标)和阻力。对处死后收获的心脏进行心肌肥大、纤维化和功能障碍检查。通过聚类和受试者工作特征(ROC)分析确定能够指示高工作负荷心脏的参数及其预测有效性。延长AA缩窄8 - 12周在一部分小型猪中诱导高血压。表现出主动脉水力功率增加的小型猪群显示出高血压和平均HR升高,而动脉阻力没有变化。值得注意的是,血压和HR是在完全麻醉下测量的,相当于静息状态。在组织、细胞或分子水平未检测到心肌肥大。除热休克蛋白40外,细胞应激和心力衰竭生物标志物的表达没有增加。ROC分析表明,主动脉水力功率、静息HR和平均血压,而不是动脉阻力,可作为高工作负荷心脏的指标。这些结果表明,高血压猪静息HR升高表明心脏工作负荷高。未经适当治疗可能会发生心力衰竭。