Takeda K, Shimizu T, Nakamura Y, Masuda T, Kono K, Takahashi M, Oyama M, Yagi S
Department of Medicine, Dokkyo University School of Medicine, Tochigi, Japan.
Jpn Circ J. 1992 Sep;56(9):929-35. doi: 10.1253/jcj.56.929.
We used the left ventricular (LV) end-systolic force-diameter (Fes-Des) relation to evaluate the effect of an alpha1-adrenoceptor antagonist (bunazosin hydrochloride) on the contractility of the beta-blocked left ventricle. Nine adult mongrel dogs were instrumented with ultrasonic crystals to measure LV diameter and a micromanometer to measure LV pressure. Beta-adrenergic and vagal blockade was induced with intravenous propranolol (2 mg/kg) and atropine (0.2 mg/kg), respectively, and preload was decreased by inferior vena caval occlusion. The slope (Ec) and extrapolated diameter intercept (Do) of the LV Fes-Des relation were derived from end-systolic data obtained in the control state (after beta-blockade) and after bunazosin infusion (1 mg/kg). Ec was used as a new index of LV contractility. After bunazosin infusion, the heart rate and Ec were decreased by 7 and 22%, respectively, in comparison with the control state, whereas Do did not change. These results indicate that alpha1-adrenoceptor blockade significantly reduces myocardial contractility in the beta-blocked canine heart, perhaps by decreasing the intracellular calcium concentration and/or myosin ATPase activity.
我们使用左心室(LV)收缩末期力-直径(Fes-Des)关系来评估α1-肾上腺素能受体拮抗剂(盐酸布那唑嗪)对β受体阻滞剂作用下左心室收缩性的影响。对9只成年杂种犬植入超声晶体以测量左心室直径,并植入微测压计以测量左心室压力。分别通过静脉注射普萘洛尔(2mg/kg)和阿托品(0.2mg/kg)诱导β肾上腺素能和迷走神经阻滞,并通过下腔静脉闭塞降低前负荷。左心室Fes-Des关系的斜率(Ec)和外推直径截距(Do)来自于对照状态(β受体阻滞剂后)和布那唑嗪输注(1mg/kg)后获得的收缩末期数据。Ec被用作左心室收缩性的新指标。与对照状态相比,布那唑嗪输注后心率和Ec分别降低了7%和22%,而Do没有变化。这些结果表明,α1-肾上腺素能受体阻滞可能通过降低细胞内钙浓度和/或肌球蛋白ATP酶活性,显著降低β受体阻滞剂作用下犬心脏的心肌收缩性。