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Acute respiratory acidosis decreases left ventricular contractility but increases cardiac output in dogs.
急性呼吸性酸中毒降低了狗的左心室收缩力,但增加了心输出量。

摘要

To understand the cardiovascular response to respiratory acidosis, we measured hemodynamics, left ventricular pressure, and left ventricular volume (three ultrasonic crystal pairs) during eucapnia and respiratory acidosis in 10 fentanyl-anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope (Emax) and intercept (V0) of the left ventricular end-systolic pressure-volume relation determined by combining end-systolic points from a vena caval occlusion and from brief aortic cross-clamping. Respiratory acidosis (pH 7.09, Pco2 92 mm Hg) reduced contractility by a decrease in Emax (11.4 to 9.2 mm Hg/ml, p less than 0.01) with no change in V0. Despite this, cardiac output increased (1.7 to 2.1 l/min, p less than 0.01), and heart rate increased (96 to 121 beats/min, p less than 0.05), with no change in blood pressure. Systemic vascular resistance fell by 26% (p less than 0.01). During eucapnia, propranolol reduced Emax (11.4 to 4.6 mm Hg/ml, p less than 0.01) with no change in V0. After propranolol treatment, respiratory acidosis further reduced Emax (4.6 to 3.6 mm Hg/ml, p less than 0.05) and increased end-systolic volume more than before propranolol (p less than 0.001). Now cardiac output did not increase even though heart rate increased (81 to 106 beats/min, p less than 0.001) and systemic vascular resistance fell by 20% (p less than 0.01). We conclude that the effect of respiratory acidosis on the circulation is to increase venous return (equals cardiac output) in the face of decreased left ventricular contractility. The beta-adrenergic response to respiratory acidosis substantially ameliorated the increase in end-systolic volume and supported the increase in venous return but did not alter the associated tachycardia or vasodilation. Respiratory acidosis, like propranolol treatment, decreases contractility by decreasing Emax.

译文

为了了解心血管对呼吸性酸中毒的反应,我们测量了血流动力学、左心室压力和左心室容积 (三个超声晶体对) 10 只芬太尼麻醉开胸犬的桉树症和呼吸性酸中毒期间。左心室收缩力主要通过测量斜率 (Emax) 和截距 (V0) 来评估通过结合来自腔静脉闭塞的收缩末期点和来自短暂的主动脉交叉钳夹的收缩末期点确定的左心室收缩末期压力-容量关系。呼吸性酸中毒 (pH 7.09,Pco2 92毫米 Hg) 通过 Emax (11.4-9.2毫米 Hg/ml,p 小于 0.01) 的减少减少收缩力,而 v0 没有变化。尽管如此,心输出量增加了 (1.7 到 2.1 升/分钟,p 小于 0.01),心率增加了 (96 到 121 次/分钟,p 小于 0.05), 血压没有变化。全身血管阻力下降了 26% (p 小于 0.01)。在桉树中,普萘洛尔降低了 Emax (11.4 到 4.6毫米 Hg/ml,p 小于 0.01),而 v0 没有变化。心得安治疗后,呼吸性酸中毒进一步降低了 Emax (4.6-3.6毫米 Hg/ml,p 小于 0.05),比心得安治疗前增加了收缩末期容积 (p 小于 0.001)。现在,即使心率增加 (81 到 106 次/分钟,p 小于 0.001),全身血管阻力下降 20% (p 小于 0.01),心输出量也没有增加。我们得出结论,面对左心室收缩力下降,呼吸性酸中毒对循环的影响是增加静脉回流 (等于心输出量)。对呼吸性酸中毒的 β-肾上腺素能反应显著改善了收缩末期容量的增加,支持了静脉回流的增加,但没有改变相关的心动过速或血管舒张。呼吸性酸中毒,如普萘洛尔治疗,通过降低 Emax 降低收缩力。

Respiratory acidosis

内分泌 代谢性疾病 疾病
概述  :  

呼吸性酸中毒是一种医疗急症,其中通气量的减少(通气不足)会增加血液中二氧化碳的浓度,并降低血液的pH值(通常称为酸中毒)。作为人体细胞的呼吸作用二氧化碳连续地生产,如果肺不能通过肺泡通气充分排出,这种CO2会迅速累积。因此,肺泡通气不足会导致PaCO2升高(称为高碳酸血症)。增加的 CO2反过来降低了HCO3- / PaCO2比值,并且降低pH值。原因急性:当突然通气失败时,就会发生急性呼吸性酸中毒。这种通气衰竭可能是由于脑部疾病或药物引起的中央呼吸中枢抑制,神经肌肉疾病(如重症肌

respiratory   英 /rɪˈspɪrət(ə)ri/   美 /ˈrɛspərəˌtɔri/

释    义   adj. 呼吸的

释    义   respiration n. 呼吸;呼吸作用

               respire vi. 呼吸

               respire vt. 呼吸

例    句   Our ventilatory capacity—the ability to move oxygen in and out of our lungs — increases as we develop our respiratory muscles. 我们的呼吸能力---我们肺部输入和输出氧气的能力---随着我们呼吸肌肉的发达而提高。

 

acidosis   英 /,æsɪ'dəʊsɪs/   美 /,æsɪ'dosɪs/

释    义   n. [内科] 酸中毒,酸毒症;酸液过多症

释    义   acidotic adj. 酸中毒的;[分化] 定酸量的

               cidity n. 酸度;酸性;酸过多;胃酸过多

例    句   Acidosis can occur irrespective of the amount of oxygen in the air being breathed . 不管吸入的空气中的氧气量有多少酸中毒都可发生。

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