Inhibition of nitric oxide synthase by NG-nitro-L-arginine causes a preferential decrease in pancreatic islet blood flow in normal rats and spontaneously diabetic GK rats.
Inhibition of nitric oxide synthase by NG-nitro-L-arginine causes a preferential decrease in pancreatic islet blood flow in normal rats and spontaneously diabetic GK rats.
复制标题
NG-硝基-L-精氨酸抑制一氧化氮合酶会导致正常大鼠和自发性糖尿病 GK 大鼠的胰岛血流量优先减少。
作者：
A. M. Svensson;Claes;Stellan Sandler;Suad Efendić;L. Jansson
为了阐明一氧化氮（NO）对胰岛血流量的影响，在用非放射性微球技术测量胰腺血流量之前10分钟，对大鼠iv给予NO合酶抑制剂NG-硝基-L-精氨酸（N-arg; 25 mg/kg BW）。在雄性Sprague-Dawley大鼠中，N-arg引起胰岛血流量显著减少（16 +/- 4 vs. 44 +/- 8 μ l/min.g胰腺; P < 0.001），全胰腺血流量减少不太明显（0.27 +/- 0.04 vs. 0.43 +/- 0.06 ml/min.g; P < 0.05），导致胰岛血流分数显著降低（5.5 +/- 0.9% vs. 10.3 +/- 1.3%; P < 0.02）。在第二个实验中，在雄性Sprague-Dawley大鼠中注射D-葡萄糖（300 mg/kg BW，iv）诱导胰岛血流量的选择性增加（P < 0.05）。这种增加以前已被证明是由迷走神经胆碱能机制介导的。给这些大鼠注射N-arg导致胰腺（P < 0.05）、胰岛（P < 0.001）和部分（P < 0.001）胰岛血流量减少，这与血糖正常的大鼠注射N-arg后观察到的结果没有差异。此外，我们研究了前面描述的胰岛血液灌注增加，迷走神经介导的，在GK（后藤Kakizaki）大鼠，自发的非胰岛素依赖型糖尿病动物模型的F1杂交的机制。对雌性GK大鼠给予N-arg导致胰岛（P < 0.001）、胰腺（P < 0.01）和部分胰岛血流量（P < 0.001）降低至平行给药的雌性Wistar大鼠中观察到的水平。这些数据与NO是胰岛血流的重要生理调节剂的可能性是一致的。此外，GK大鼠中证实的迷走神经依赖性高水平胰岛血流量似乎是由涉及NO的机制介导的。
To elucidate the effect of nitric oxide (NO) on the blood flow of the pancreatic islets, the NO synthase inhibitor NG-nitro-L-arginine (N-arg; 25 mg/kg BW) was administered iv to rats 10 min before pancreatic blood flow was measured with a nonradioactive microsphere technique. In male Sprague-Dawley rats, N-arg induced a marked decrease in islet blood flow (16 +/- 4 vs. 44 +/- 8 microliters/min.g pancreas; P < 0.001) and a less pronounced decrease in whole pancreatic blood flow (0.27 +/- 0.04 vs. 0.43 +/- 0.06 ml/min.g; P < 0.05), leading to a markedly decreased fractional islet blood flow (5.5 +/- 0.9% vs. 10.3 +/- 1.3%; P < 0.02). In a second experiment, injection of D-glucose (300 mg/kg BW, iv) in male Sprague-Dawley rats induced a selective increase in islet blood flow (P < 0.05). Such an increase has previously been shown to be mediated by a vagal cholinergic mechanism. Administration of N-arg to these rats resulted in decreased pancreatic (P < 0.05), islet (P < 0.001), and fractional (P < 0.001) islet blood flow, which did not differ from those observed in normoglycemic rats after treatment with N-arg. Furthermore, we studied the mechanism behind the previously described increase in islet blood perfusion, mediated by the vagus nerve, in F1-hybrids of the GK (Goto-Kakizaki) rat, a spontaneous animal model of noninsulin-dependent diabetes mellitus. Administration of N-arg to female GK rats resulted in decreases in islet (P < 0.001), pancreatic (P < 0.01), and fractional islet blood flow (P < 0.001) to the levels observed in female Wistar rats treated in parallel. These data are consistent with the possibility that NO is an important physiological regulator of islet blood flow. Furthermore, the vagally dependent high levels of islet blood flow demonstrated in the GK rat appear to be mediated by a mechanism involving NO.
影响因子：
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作者：
RUBANYI, GM;VANHOUTTE, PM
通讯作者：
VANHOUTTE, PM