Talwar A, Hussain M E, Gupta C K, Fahim M
Department of Physiology, Vallabhbhai Patel Chest Institute, University of Delhi.
Indian J Physiol Pharmacol. 1995 Apr;39(2):106-10.
Experiments were performed on anaesthetized artificially ventilated cats to study the effects of phenylephrine (PE) on cardiovascular responsiveness, before and after induction of experimental anaemia. Acute anaemia was induced by replacement of blood by dextran in three steps of 20% each of total estimated blood volume. The effect of PE (20 micrograms/kg) was investigated at four stages: control and after 1st, 2nd and 3rd exchanges of blood. Induction of anaemia produced a significant increase in heart rate (HR) and cardiac output (CO) and a decrease in right atrial pressure (RAP). No significant change in mean arterial pressure (MAP), LV dP/dt max and blood gas tension was observed. Administration of bolus dose of PE produced a rapid rise in MAP, LVdP/dt max, and a decrease in HR without a change in the RAP. The pattern of response to PE was similar after induction of acute anaemia, however the magnitude of the response was significantly reduced. The attenuation in the response to PE was related to the fall in the haematocrit (HCT) level. This shows that induction of experimental anaemia, produced an increase in CO due to an increase in HR and SV and the effect of PE on cardiovascular responsiveness was significantly attenuated. The reduced sensitivity to PE during acute anaemia could be due to many factors such as inadequate O2 supply, effect of local vasodilating agents or some other cardiotonic agents which are known to contribute to vascular responsiveness.
在人工通气的麻醉猫身上进行实验,以研究去氧肾上腺素(PE)在实验性贫血诱导前后对心血管反应性的影响。通过用右旋糖酐分三步替换血液来诱导急性贫血,每次替换量为估计总血容量的20%。在四个阶段研究了PE(20微克/千克)的作用:对照阶段以及第一次、第二次和第三次血液交换后。贫血诱导导致心率(HR)和心输出量(CO)显著增加,右心房压力(RAP)降低。未观察到平均动脉压(MAP)、左心室dp/dt最大值和血气张力有显著变化。静脉推注PE导致MAP、左心室dp/dt最大值迅速升高,HR降低,而RAP无变化。急性贫血诱导后对PE的反应模式相似,但反应幅度显著降低。对PE反应的减弱与血细胞比容(HCT)水平的下降有关。这表明实验性贫血的诱导由于HR和每搏输出量(SV)的增加导致CO增加,并且PE对心血管反应性的作用显著减弱。急性贫血期间对PE敏感性降低可能是由于许多因素,如氧气供应不足、局部血管扩张剂的作用或其他一些已知有助于血管反应性的强心剂的作用。