Lohinai Z, Balla I, Marczis J, Vass Z, Kovách A G
Experimental Research Department-2nd Institute of Physiology, Semmelweis University Medical School, Budapest, Hungary.
Arch Oral Biol. 1996 Jul;41(7):699-704. doi: 10.1016/s0003-9969(96)00030-1.
The aim was to examine whether (1) blood flow and vascular resistance are altered in response to exogenous nitric oxide and (2) whether endogenous synthesis of nitric oxide participates in the haemodynamic regulation of the submandibular, parotid and pancreatic glands. Experiments were performed on anaesthetized, artificially ventilated cats. Mean arterial blood pressure, heart rate, blood gases, cardiac output and tissue blood flow were determined before and 15 min after intravenous administration of either the nitric oxide donor SIN-1 (3-morpholinosydnonimine, 1 mg/kg, n = 10) or the competitive nitric oxide synthase inhibitor NOLA (NG-nitro-L-arginine, 30 mg/kg, n = 9) blood flow was measured by a radioactive-labelled microsphere method. In the SIN-1 group, in spite of a serious decrease in mean arterial blood pressure (p < 0.001), the blood flow in the glands remained unchanged. The vascular resistance decreased after SIN-1 in the submandibular and pancreatic glands (p < 0.001 and p < 0.05, respectively), and was slightly reduced in the parotid. The NOLA increased mean arterial blood pressure (p < 0.01) and reduced the blood flow in the submandibular and pancreatic glands (p < 0.01 and p < 0.001, respectively), but the decrease in the parotid was not significant. Vascular resistance increased after NOLA in all three glands (p < 0.05, p < 0.001 and p < 0.05). These findings suggest that basal nitric oxide production in these exocrine glands is sufficient to modulate vascular resistance. Moreover, the release of endogenous NO from the nerves and/or endothelium is probably involved in the regulation of vascular tone. The nitric oxide-dependent component of blood-flow regulation, however, seems to be less pronounced in the parotid gland.
（1）外源性一氧化氮是否会引起血流和血管阻力的改变；（2）内源性一氧化氮的合成是否参与下颌下腺、腮腺和胰腺的血流动力学调节。实验在麻醉、人工通气的猫身上进行。在静脉注射一氧化氮供体SIN-1（3-吗啉代辛二亚胺，1mg/kg，n = 10）或竞争性一氧化氮合酶抑制剂NOLA（NG-硝基-L-精氨酸，30mg/kg，n = 9）之前及之后15分钟，测定平均动脉血压、心率、血气、心输出量和组织血流量。血流量通过放射性标记微球法测量。在SIN-1组中，尽管平均动脉血压显著下降（p < 0.001），但腺体的血流量保持不变。SIN-1注射后，下颌下腺和胰腺的血管阻力降低（分别为p < 0.001和p < 0.05），腮腺的血管阻力略有降低。NOLA使平均动脉血压升高（p < 0.01），并降低了下颌下腺和胰腺的血流量（分别为p < 0.01和p < 0.001），但腮腺血流量的减少不显著。NOLA注射后，所有三个腺体的血管阻力均增加（p < 0.05、p < 0.001和p < 0.05）。这些结果表明，这些外分泌腺中基础一氧化氮的产生足以调节血管阻力。此外，神经和/或内皮释放内源性一氧化氮可能参与血管张力的调节。然而，一氧化氮依赖性的血流调节成分在腮腺中似乎不太明显。
