Effect of hemorrhagic shock on liver and muscle glycogen content in high altitude acclimatized rats

Abstract

Experiments were undertaken with 23 high - altitude acclimatized and 27 control sea-level rats to determine the effect of hemorrhagic shock at sea level on their liver, heart and skeletal muscle glycogen content and some blood parameters and to relate these hemorrhagic responses to their hemorrhagic tolerance. The rats in each group were divided into 3 subgroups. Animals in subgroups I and II were non-hemorrhaged and sacrificed under anesthesia at 0 and 150 min, respectively, while rate in subgroup III were bled into a reservoir which maintain mABP at 35 mmHg. At 150 min of hemorrhagic hypotension, an amount of the shed blood remaining in the reservoir was reinfused (approximately 35 %MBL). Hematocrit, plasma glucose and blood lactate were measured at the initial, 40-60 min of hypotension, and at 10 min after blood reinfusion at the end of 150 min hypotension. The liver, heart and soleus (SOL) and extensor digitorum longus (EDL) muscles were immediately excised and fixed in liquid nitrogen for determination of their glycogen content. It was found that chronic exposure to high altitude caused lower liver, hearth and EDL glycogen content compared to the controls. The initial blood withdrawal (IBW), the maximum blood loss (MBL) and also the time to maximum blood loss (TMBL) were significantly greater while the blood volume reinfused to maintain the level of hypotension was less in the altitude-acclimatized rats than those of the control rats. Glycogen content was found to be depleted in liver, reduced in EDL, increased in myocardium, and not changed in SOL by hemorrhagic shock and these post-hemorrhagic glycogen levels were similar in both animal groups. In contrast, blood lactate concentration was significantly higher in the control rats than that of the altitude rats. It is concluded that the higher tolerance to hemorrhagic hypotension in the high-altitude acclimatized rats than the control rats was not attributed to the levels of hyperglycemia induced by hemorrhage or to the initial and the post-hemorrhagic levels of glycogen (indication of the carbohydrate reserves) in the liver and skeletal muscles of the two animal groups. Such the difference in hemorrhagic tolerance is associated with the blood lev