Cambiasso M J, Chiaraviglio E
Instituto de Investigación Médica, Mercedes y Martin Ferreyra, Cordoba, Argentina.
Behav Neural Biol. 1992 Nov;58(3):190-5. doi: 10.1016/0163-1047(92)90454-c.
Acute reversible lesion in the medial preoptic area (MPOA) by unilateral injection of the local anesthetic lidocaine chlorhydrate (1 microliter, 20 ng/microliters) causes a transient increase in water intake induced by water deprivation in rats. Since lidocaine suppresses the nervous activity, leaving intact fibers of passage and blood vessels, the results suggest an intrinsic inhibitory action of the MPOA on the regulation of water intake. Drinking elicited a return to volumes similar to those of control rats, 3-4 h after lidocaine administration. Lidocaine released into the lateral preoptic area (LPO) slightly decreased or did not change water intake, as compared with controls. The urinary excretion in the MPO group was higher than that of the controls and the LPO, while this last group excreted significantly less urine. The ablation of the POA with lidocaine suggests that the medial aspect of the POA has an intrinsic inhibitory factor influencing drinking, while the lateral aspect did not show a relevant effect.
通过单侧注射局部麻醉剂盐酸利多卡因(1微升,20纳克/微升)造成内侧视前区(MPOA)的急性可逆性损伤,会使大鼠因缺水引起的饮水量短暂增加。由于利多卡因抑制神经活动,而使传导纤维和血管保持完好,结果表明MPOA对水摄入调节具有内在抑制作用。利多卡因给药后3 - 4小时,饮水量恢复到与对照大鼠相似的水平。与对照组相比,注入外侧视前区(LPO)的利多卡因使饮水量略有减少或无变化。MPO组的尿排泄量高于对照组和LPO组,而LPO组的尿量排泄明显较少。用利多卡因消融视前区表明,视前区内侧具有影响饮水的内在抑制因子,而外侧未显示出相关作用。