Wang Lu, Luo Hui, Qin Gang, Cao Yanan, Gao Xiaowei, Zhang Zhong, Ye Zhi, Zhang Junjie, Guo Qulian, Wang E
Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.
Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.
J Cardiothorac Vasc Anesth. 2017 Dec;31(6):2027-2034. doi: 10.1053/j.jvca.2017.02.049. Epub 2017 Feb 13.
The relationship between left ventricular function and afterload has not been investigated as much as the right ventricular function under chronic pulmonary hypertension (PH) during anesthesia. This study was designed to investigate effects of sevoflurane on the intrinsic coupling relationship between the left ventricle and systemic vasculature in the presence of PH.
A randomized, controlled study.
University hospital.
Sprague-Dawley rats.
Monocrotaline (MCT) was injected intraperitoneally to induce a PH model.
Four weeks later, rats with MCT injection demonstrated significantly increased pulmonary arterial pressure and right/left ventricular systolic ratio of ventricular pressure (p < 0.001). Rats were treated with 1.5% sevoflurane inhalation. The PV catheters were inserted and left ventricular pressure-volume loops were measured at baseline, 30, 60, and 90 minutes during sevoflurane treatment. Preload recruitable stroke work and end-systolic elastance were decreased markedly in rats with MCT injection (p < 0.05). However, arterial elastance decreased similarly in both groups. Sarcoplasmic reticulum Ca-ATPase (SERCA2a) level was decreased and the expression of phospholamban (PLB) was increased in the PH group and after sevoflurane treatment. PH rats suffered further SERCA2/PLB ratio decrease from their already low baseline. The left ventricular contractility and ventricular-vascular coupling were decreased in rats with PH after sevoflurane inhalation.
Sevoflurane reduced SERCA2a expression and increased PLB expression in PH rats. This partially could explain why the LV contractility and ventricular-to-vasculature coupling of PH rats were attenuated after sevoflurane treatment.
在麻醉期间慢性肺动脉高压（PH）状态下，左心室功能与后负荷之间的关系尚未像右心室功能那样得到充分研究。本研究旨在探讨七氟醚对存在PH时左心室与体循环血管系统之间内在耦合关系的影响。
一项随机对照研究。
大学医院。
Sprague-Dawley大鼠。
腹腔注射野百合碱（MCT）以诱导PH模型。
四周后，注射MCT的大鼠肺动脉压及右/左心室收缩压比值显著升高（p<0.001）。大鼠接受1.5%七氟醚吸入治疗。插入PV导管，并在七氟醚治疗期间的基线、30、60和90分钟测量左心室压力-容积环。注射MCT的大鼠预负荷可招募搏功和收缩末期弹性明显降低（p<0.05）。然而，两组动脉弹性下降程度相似。PH组及七氟醚治疗后肌浆网Ca-ATP酶（SERCA2a）水平降低，受磷蛋白（PLB）表达增加。PH大鼠在其本已较低的基线水平上，SERCA2/PLB比值进一步降低。吸入七氟醚后，PH大鼠的左心室收缩力和心室-血管耦合降低。
七氟醚降低了PH大鼠SERCA2a表达并增加了PLB表达。这部分可以解释为什么七氟醚治疗后PH大鼠的左心室收缩力和心室-血管耦合减弱。
