Buchweitz-Milton E, Weiss H R
Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854-5635.
Neurol Res. 1990 Sep;12(3):169-75. doi: 10.1080/01616412.1990.11739938.
This study quantitatively determined the effect of salbutamol (1 microgram kg-1), a beta 2-adrenoceptor agonist, on the perfusion of the brain microvasculature, cerebral O2 consumption, O2 extraction and cerebral blood flow (CBF) in conscious rat. Indices of arteriolar and capillary structure and the percentage of the total cerebral microvascular volume/mm3 (% Vv) and number/mm2 (% Na) perfused were determined. These parameters were obtained from the perfused microvessels, identified by the presence of fluorescein isothiocyanate (FITC) - dextran, and compared with the entire microvascular bed, identified by alkaline phosphatase stain. Cerebral O2 extraction was determined microspectrophotometrically and CBF was determined using 14[C]iodoantipyrine in another group of salbutamol-treated rats. The acute administration of salbutamol did not alter systemic arterial blood pressure. Significant tachycardia was noted in the salbutamol-treated rats. Salbutamol resulted in a significant increase in the percentage of arterioles perfused. Average percentage perfused capillary Na increased significantly from 46 +/- 2 to 88 +/- 1%; %Vv increased significantly and similarly in the arteriolar and capillary beds in all brain regions examined. Average cerebral O2 consumption increased significantly from 3.0 +/- 0.2 to 7.4 +/- 0.7 ml O2 min-1 100 g-1 with salbutamol, while cerebral O2 extraction was unchanged. Average CBF increased from 50 +/- 2 to 142 +/- 9 ml min-1 100 g-1 with salbutamol. Salbutamol may increase the perfusion of the regional microvasculature by increasing cerebral O2 consumption (metabolic vasodilation) and CBF and microvascular perfusion secondarily, although a direct effect of salbutamol on cerebral microvessels cannot be ruled out.
本研究定量测定了β2肾上腺素能受体激动剂沙丁胺醇（1微克/千克）对清醒大鼠脑微血管灌注、脑氧消耗、氧摄取及脑血流量（CBF）的影响。测定了小动脉和毛细血管结构指标以及每立方毫米灌注的全脑微血管体积百分比（%Vv）和每平方毫米数量百分比（%Na）。这些参数取自灌注微血管（通过异硫氰酸荧光素（FITC）-葡聚糖的存在来识别），并与通过碱性磷酸酶染色识别的整个微血管床进行比较。在另一组用沙丁胺醇治疗的大鼠中，用显微分光光度法测定脑氧摄取，用14[C]碘安替比林测定CBF。急性给予沙丁胺醇未改变体循环动脉血压。在用沙丁胺醇治疗的大鼠中观察到显著的心动过速。沙丁胺醇导致灌注小动脉的百分比显著增加。灌注毛细血管Na的平均百分比从46±2显著增加到88±1%；在所有检查的脑区，小动脉和毛细血管床中的%Vv均显著且类似地增加。使用沙丁胺醇时，平均脑氧消耗从3.0±0.2显著增加到7.4±0.7毫升氧/分钟·100克-1，而脑氧摄取未改变。使用沙丁胺醇时，平均CBF从50±2增加到142±9毫升/分钟·100克-1。沙丁胺醇可能通过增加脑氧消耗（代谢性血管舒张）和CBF以及继发的微血管灌注来增加局部微血管灌注，尽管不能排除沙丁胺醇对脑微血管的直接作用。
