Lang C H
Department of Surgery, State University of New York, Stony Brook 11794-8191, USA.
Shock. 1994 Jan;1(1):36-42. doi: 10.1097/00024382-199401000-00007.
The purpose of the present study was to determine whether the intracerebroventricular (ICV) injection of carbachol enhances whole body glucose utilization and, if so, how this cholinergic agonist influences in vivo regional glucose uptake. An ICV cannula and vascular catheters were placed in rats prior to the experiment. Whole body glucose flux was assessed in overnight-fasted conscious unrestrained rats using [3-3H]glucose. Hyperglycemia was elicited 30 min after carbachol (50 nmol), and resulted from an increased rate of hepatic glucose production (135%) that exceeded an elevated rate of peripheral glucose uptake (105%). The glucose metabolic clearance rate was not altered by carbachol. Despite the hyperglycemia, no compensatory increase in plasma insulin levels were observed. Carbachol, however, did increase glucagon (64-164%), catecholamines (3.5- to 15-fold), and corticosterone (62-160%). Complete alpha- and beta-adrenergic blockade prevented the carbachol-induced changes in glucose flux. In vivo glucose uptake (Rg) by individual tissues was determined at the peak of the carbachol-induced hyperglycemia, using [2-14C]deoxyglucose. In addition, a separate group of control rats received an intravenous hormone infusion that increased plasma glucose, glucagon, and catecholamine levels to the same extent seen in carbachol-treated rats. The Rg in liver, spleen, and lung was elevated to a similar extent in carbachol-treated (60, 47, and 48%, respectively) and hormone-infused (60, 53, and 70%, respectively) rats. In contrast, whereas the hormone infusion increased Rg by ileum, skin, and kidney (80, 67, and 110%, respectively), no change was observed in these tissues from rats injected with carbachol.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是确定脑室内注射卡巴胆碱是否能增强全身葡萄糖利用，若能增强，这种胆碱能激动剂如何影响体内局部葡萄糖摄取。实验前在大鼠体内植入脑室内插管和血管导管。使用[3-³H]葡萄糖评估过夜禁食、清醒且不受束缚的大鼠的全身葡萄糖通量。注射卡巴胆碱（50 nmol）30分钟后引发高血糖，这是由于肝脏葡萄糖生成速率增加（135%），超过了外周葡萄糖摄取升高的速率（105%）。卡巴胆碱未改变葡萄糖代谢清除率。尽管出现高血糖，但未观察到血浆胰岛素水平有代偿性升高。然而，卡巴胆碱确实增加了胰高血糖素（64%-164%）、儿茶酚胺（3.5至15倍）和皮质酮（62%-160%）。完全的α和β肾上腺素能阻断可防止卡巴胆碱诱导的葡萄糖通量变化。在卡巴胆碱诱导的高血糖峰值时，使用[2-¹⁴C]脱氧葡萄糖测定各个组织的体内葡萄糖摄取（Rg）。此外，另一组对照大鼠接受静脉激素输注，使血浆葡萄糖、胰高血糖素和儿茶酚胺水平升高至与卡巴胆碱处理大鼠相同的程度。在卡巴胆碱处理的大鼠（分别为60%、47%和48%）和激素输注的大鼠（分别为60%、53%和70%）中，肝脏、脾脏和肺的Rg升高程度相似。相比之下，虽然激素输注使回肠、皮肤和肾脏的Rg增加（分别为80%、67%和110%），但注射卡巴胆碱的大鼠这些组织未观察到变化。（摘要截断于250字）
