Kasuda H, Shimizu R, Yoshizawa Y, Akazawa S, Nemoto K, Inoue S, Nozawa K
Masui. 1989 Mar;38(3):300-11.
In pentobarbital-pancuronium anesthetized open chest dogs, left ventricular pressure (LVP), first derivative of LVP (dp/dt) and left ventricular end-diastolic pressure (LVEDP) were measured by a micromanometer tipped catheter, stroke volume and cardiac output (CO) by an electromagnetic flow meter and coronary sinus blood flow (CSBF), by a thermal dilution catheter, respectively. Mean arterial pressure (mAP), mean pulmonary arterial pressure (mPAP), lead II of ECG and esophageal temperature were monitored. Blood gas, catecholamines and lactate of arterial blood and coronary sinus blood were measured and myocardial lactate extraction ratio (MCL) was calculated. As an index of contraction, maximum positive dp/dt (+dp/dt max), and as an index of relaxation, the time constant (T) of isovolumic left ventricular pressure fall were employed, respectively. Acute hypoxia was induced by the inhalation of a 5% O2-95% N2 gas mixture and arterial blood oxygen pressure was maintained between 15 and 20 mmHg. Along with the advancement of hypoxia, +dp/dt max, CO and mAP gradually increased and peaked in 5 minutes. Thereafter, these parameters began to decrease and CO fell to zero in 20 minutes. mPAP and HR slowly increased and peaked in 9 and in 12 minutes, respectively. T was progressively prolonged throughout the hypoxia. CSBF/CO ratio was increased and stayed at a high level even after CO began to decrease. MCL decreased and changed from positive values to negative ones in 5 minutes. Epinephrine and norephinephrine concentrations slowly increased and peaked in 16 minutes. A gradual decrease in the R wave, shortening of the R-R interval and lengthening of the QTc interval were observed in ECG. This study indicated that the left ventricular relaxing function was impaired earlier than contracting function by acute hypoxia and that conversion of the augmented left ventricular contractile state to the depressed one coincided with conversion of myocardial lactate extraction to its production.
在戊巴比妥-潘库溴铵麻醉的开胸犬中，用微测压导管测量左心室压力（LVP）、左心室压力的一阶导数（dp/dt）和左心室舒张末期压力（LVEDP），用电磁流量计测量每搏输出量和心输出量（CO），用热稀释导管测量冠状窦血流量（CSBF）。监测平均动脉压（mAP）、平均肺动脉压（mPAP）、心电图Ⅱ导联和食管温度。测定动脉血和冠状窦血的血气、儿茶酚胺和乳酸，并计算心肌乳酸摄取率（MCL）。分别采用最大正向dp/dt（+dp/dt max）作为收缩指标，等容左心室压力下降的时间常数（T）作为舒张指标。通过吸入5%O₂-95%N₂混合气体诱导急性缺氧，使动脉血氧分压维持在15至20mmHg之间。随着缺氧的进展，+dp/dt max、CO和mAP逐渐升高，并在5分钟时达到峰值。此后，这些参数开始下降，CO在20分钟时降至零。mPAP和心率缓慢升高，分别在9分钟和12分钟时达到峰值。在整个缺氧过程中T逐渐延长。CSBF/CO比值升高，即使在CO开始下降后仍保持在高水平。MCL下降，并在5分钟内从正值变为负值。肾上腺素和去甲肾上腺素浓度缓慢升高，在16分钟时达到峰值。心电图显示R波逐渐降低、R-R间期缩短和QTc间期延长。本研究表明，急性缺氧时左心室舒张功能比收缩功能更早受损，左心室收缩状态从增强转为抑制与心肌乳酸摄取转为产生相吻合。
