Vitagliano S, Berrino L, D'Amico M, Maione S, De Novellis V, Rossi F
Institute of Pharmacology and Toxicology, Faculty of Medicine and Surgery, 2nd University of Naples, Italy.
Neuropharmacology. 1996 May;35(5):625-31. doi: 10.1016/0028-3908(96)84633-8.
The aim of this study was to investigate whether nitric oxide (NO) is involved in cardiorespiratory regulation in the nucleus tractus solitarii (NTS). Unilateral microinjections (50 nl) of the NO-donor, sodium nitroprusside (SNP, 40-100-200 mM), into the NTS of anaesthetized rats elicited dose-dependent apnea (7.3 +/- 2.3 sec; 28.6 +/- 5.7 sec; 35.6 +/- 6.4 sec, respectively; n = 6) and a decrease in arterial blood pressure (8.4 +/- 3.1 mmHg; 18.2 +/- 5.8 mmHg; 25.8 +/- 6.7 mmHg, respectively; n = 6). Similarly, unilateral micro-injections (50 nl) of another NO-donor, 3-morpholinosydnonimine (SIN-1, 20-40-100 mM), also induced apnea (5.1 +/- 2.4 sec; 8.7 +/- 4.3 sec; 26.3 +/- 6.4 sec, respectively; n = 6) and a decrease in arterial blood pressure (6.2 +/- 2.3 mmHg; 11.1 +/- 3.3 mmHg; 18.3 +/- 6.1 mmHg, respectively; n = 6). The SNP- and SIN-1-induced apnea and arterial blood pressure decrease were significantly (p < 0.01) blocked by a 3 min pretreatment with two calcium-channel blockers, diltiazem (0.1 mM) and cobalt (10 mM), while lower doses (diltiazem 0.01 and cobalt 1) were ineffective. Microinjections of diltiazem (0.01 mM) and cobalt (1 mM) alone did not induce any change in basal cardiorespiratory values like diltiazem (0.1 mM) and cobalt (10 mM). These data suggest that NO may be involved in NTS cardiorespiratory regulation via calcium-channel activation.
本研究的目的是调查一氧化氮（NO）是否参与孤束核（NTS）中的心肺调节。将NO供体硝普钠（SNP，40 - 100 - 200 mM）单侧微量注射（50 nl）到麻醉大鼠的NTS中，引发了剂量依赖性呼吸暂停（分别为7.3±2.3秒；28.6±5.7秒；35.6±6.4秒；n = 6）以及动脉血压下降（分别为8.4±3.1 mmHg；18.2±5.8 mmHg；25.8±6.7 mmHg；n = 6）。同样，将另一种NO供体3 - 吗啉代辛二酰亚胺（SIN - 1，20 - 40 - 100 mM）单侧微量注射（50 nl），也诱导了呼吸暂停（分别为5.1±2.4秒；8.7±4.3秒；26.3±6.4秒；n = 6）以及动脉血压下降（分别为6.2±2.3 mmHg；11.1±3.3 mmHg；18.3±6.1 mmHg；n = 6）。用两种钙通道阻滞剂地尔硫䓬（0.1 mM）和钴（10 mM）进行3分钟预处理，可显著（p < 0.01）阻断SNP和SIN - 1诱导的呼吸暂停和动脉血压下降，而较低剂量（地尔硫䓬0.01和钴1）则无效。单独注射地尔硫䓬（0.01 mM）和钴（1 mM）不会像地尔硫䓬（0.1 mM）和钴（10 mM）那样引起基础心肺值的任何变化。这些数据表明，NO可能通过钙通道激活参与NTS心肺调节。
