Kuschinsky W, Wahl M
Pflugers Arch. 1979 Oct;382(1):81-5. doi: 10.1007/BF00585908.
The aim of the present study was to correlate locally at the same pial artery the vascular reaction with the perivascular pH during the initial phase of functional hyperemia. As a model of functional hyperemia, bicuculline (3 mg/kg i.v.) induced seizure was taken. Normally, a strong increase of blood pressure occurs together with the start of seizure. Since a discrimination between metabolically induced and pressure dependent vascular reactions is not possible under such conditions, the cats (anesthetized with 40--50 mg/kg chloralose) received in addition 3 mg/kg phentolamine and 10 mg/kg pentobarbital. Under these conditions a significant increase of blood pressure started only 50 s after the onset of seizure. Perivascular pH was recorded using spear type pH microelectrodes in the subarachnoid space surrounding a pial artery. The diameter of the respective artery was measured continuously. After onset of seizure an immediate, increasing perivascular acidosis developed which was accompanied by an increase in pial arterial diameter. The maximal decrease of pH was 0.29 units and occurred 30 s after the start of seizure. These data show that a decrease in perivascular pH can be one factor mediating functional hyperemia in the brain.
本研究的目的是在功能充血的初始阶段,在同一软脑膜动脉局部将血管反应与血管周围pH值相关联。以荷包牡丹碱(3mg/kg静脉注射)诱发的癫痫发作作为功能充血的模型。正常情况下,癫痫发作开始时血压会大幅升高。由于在这种情况下无法区分代谢诱导的血管反应和压力依赖性血管反应,因此给猫(用40 - 50mg/kg氯醛糖麻醉)额外注射3mg/kg酚妥拉明和10mg/kg戊巴比妥。在这些条件下,癫痫发作开始后仅50秒血压才开始显著升高。使用矛型pH微电极记录软脑膜动脉周围蛛网膜下腔的血管周围pH值。连续测量相应动脉的直径。癫痫发作开始后,立即出现进行性血管周围酸中毒,并伴有软脑膜动脉直径增加。pH值的最大下降为0.29个单位,发生在癫痫发作开始后30秒。这些数据表明,血管周围pH值降低可能是介导脑功能充血的一个因素。