Lee J C, Downing S E
Proc Soc Exp Biol Med. 1983 Dec;174(3):401-6. doi: 10.3181/00379727-174-41754.
The effects of acute hypercapnia on cardiac contractility and their dependence on adrenergic pathways were studied in 27 piglets anesthetized with pentobarbital (30 mg/kg, ip). Aortic pressures and flow, and heart rate were held constant; atropine was used to produce parasympathetic blockade. Hypercapnia was achieved by addition of CO2 to the respirator. In the control group (N = 7) the first derivative of left ventricular (LV) pressure (dP/dtmax) increased significantly following induction of severe hypercapnia (PaCO2 greater than 80 mm Hg; pH less than 7.00). There were no significant changes in LV end diastolic pressure. The magnitude of the positive inotropic responses was unaltered by ganglionic blockade with tetraethylammonium chloride (100 mg) (N = 5). In contrast, no change in LV dP/dtmax was observed during hypercapnia in piglets (N = 15) subjected to beta-adrenoreceptor blockade with practolol (4 mg/kg). Our findings indicate that the increased cardiac contractility during acute severe hypercapnia is not dependent upon the integrity of the neural reflex system. Rather, it is due to adrenal release of catecholamines into the circulation. These animals are highly resistant to the intrinsic cardiac depressant action of hypercapnic acidosis.
在27只用戊巴比妥（30毫克/千克，腹腔注射）麻醉的仔猪中，研究了急性高碳酸血症对心脏收缩力的影响及其对肾上腺素能途径的依赖性。主动脉压力、流量和心率保持恒定；使用阿托品产生副交感神经阻滞。通过向呼吸机中添加二氧化碳来实现高碳酸血症。在对照组（N = 7）中，诱导严重高碳酸血症（动脉血二氧化碳分压大于80毫米汞柱；pH小于7.00）后，左心室（LV）压力的一阶导数（dP/dtmax）显著增加。左心室舒张末期压力无显著变化。用氯化四乙铵（100毫克）进行神经节阻滞（N = 5）后，正性肌力反应的幅度未改变。相比之下，在用心得宁（4毫克/千克）进行β-肾上腺素能受体阻滞的仔猪（N = 15）中，高碳酸血症期间未观察到左心室dP/dtmax的变化。我们的研究结果表明，急性严重高碳酸血症期间心脏收缩力的增加不依赖于神经反射系统的完整性。相反，它是由于肾上腺将儿茶酚胺释放到循环中。这些动物对高碳酸血症性酸中毒的内在心脏抑制作用具有高度抗性。
