| 摘要: | 中文摘要 在失血性休克，感壓反射敏感度減弱目前被認為可能跟交感神經活性受抑制有關，目前已知一氧化氮可能會抑制交感神經活性和心臟血管功能。因此，嚴重失血時，一氧化氮的增加可能是造成感壓反射敏感度減弱的原因。本實驗採用56隻雄性Spargue Dawley大白鼠，體重介於250~280g，以腹腔注射sodium pentobarbital(50 mg/kg,ip)麻醉。分別於左右股動靜脈插管，從導管施打藥物、失血處理及血壓心跳的測量。中樞給藥則是從側腦室插管施打藥物。L-NAME(N-omega-nitro-L-arginine methyl ester；30mg/kg)，及7-NI(7-Nitroindazole；50mg/kg)，L-arginine(87mg/kg)分別是非選擇性一氧化氮抑制劑、神經性一氧化氮抑制劑及一氧化氮的前驅物質。靜脈處理是注射L-NAME、L-arginine、7-NI，腦室內處理是注射L-NAME、L-arginine。失血處理是從動脈導管將血液抽出，直到血壓降到40~50mmHg為準。感壓反射敏感度是以線性迴歸方法評估。結果：靜脈注射L-NAME抑制一氧化氮，可以使血壓上升及反射性心跳抑制(p<0.05)，L-arginine組的血壓及心跳均無顯著改變。感壓反射方面，正常對照組及L-NAME、L-arginine組的失血前感壓反射敏感度分別是-2.4±0.4, -2.9±0.4, -2.8±0.3 bpm/mmHg，失血後正常組及L-NAME、L-arginine組感壓反射敏感度均顯著受到抑制(-0.4±0.1;-0.8±0.3;0.1±0.1 bpm/mmHg ; p<0.05)。7-NI組，抑制中樞一氧化氮的血壓明顯上升但心跳沒有顯著改變，L-NAME-icv(5mg/15ul/rat)組，血壓及心跳都顯著上升(p<0.05)，在L-arginine-icv(8.7mg/kg)組，血壓及心跳都沒有顯著改變。感壓反射方面，7-NI、L-NAME-icv、L-arginine-icv組的失血前感壓反射敏感度分別是-2.3±0.2, -2.3±0.1, -2.2±0.2 bpm/mmHg，失血後7-NI及L-NAME-icv組的感壓反射敏感度保持不變，L-arginine-icv組則顯著受抑制(0.1±0.1 bpm/mmHg;p<0.05)。從這些結果得知，失血性休克時感壓反射確實受到抑制，而感壓反射的抑制可能跟中樞的一氧化氮增加有關。; VII. 英 文 摘 要 It has been suggested that this BRS attenuation may be related to the inhibition of sympathetic nerve activity in hemorrhagic shock. NO may inhibit sympathetic activity and cardiovascular function. Thus, over production of NO in severe hemorrhage may be responsible for BRS (arterial baroreflex sensitivity) depression. In the present study, 56 male Sprague Dawley rats, weighing 250~280 g, were anesthetized with sodium pentobarbital ( 50 mg/kg, ip ). Both left and right femoral veins and arteries were catheterized for drug administration, beeding, and blood pressure measurements.The intracerebroventricular catheter was used for administration of L-NAME-icv(5mg/kg/rat), L-arginine-icv(8.7mg/kg). N-nitro-L-arginine methyl ester (L-NAME, 30mg/kg, iv) 、7-nitroindazole (7-NI, 50mg/kg, iv) and L-arginine(87mg/kg, iv) were used for inhibition and increase of peripheral or central NO prodution. Hemorrhage was induced by bleeding from the arteral line and completed when blood pressure fell below 40~50 mmHg . BRS was assessed by linear regression method. Intravenous bolus injections of 30 mg/kg of L-NAME increased baseline mean arterial pressure (MAP) and decrease heart rate (HR) ( p< 0.05). L-Arginine (87 mg/kg i.v.)did not significant change mean arterial pressure (MAP) and heart rate (HR). The BRS before hemorrhage were -2.4±0.4, -2.9± 0.4, and -2.8± 0.3( bpm/mmHg) for the N/S, the L-NAME, and the L-arginine groups, respectivety. After hemorrhage, the BRS of the N/S、L-NAME and L-arginine groups were all attenuated significantly (-0.4± 0.1、-0.8±0.3 and 0.1±0.1 (bpm/mmHg; p<0.05 ). Intra-lateral cerebroventricular(icv) administration of L-NAME(5mg/kg/rat) elicited significant increases in arterial blood pressure and heart rate. Intravenous administration of 7-NI elicited significant increases in arterial blood pressure but not change heart rate. Icv administration of L-NAME(5mg/kg/rat) not elicited significant increases in arterial blood pressure and heart rate. On the other hand, L-arginine-icv(8.7mg/kg),did not elicited significant change in arterial blood pressure and heart rate. The BRS before hemorrhage were -2.3±0.2, -2.3±0.1, and -2.2±0.2 for the 7-NI, L-NAME-icv, and L-arginine-icv groups, respectivety. The BRS of the 7-NI, L-NAME-icv group remained unchanged (-2.2±0.7 and -2.3±0.2). The BRS of the L-arginine-icv group were aattenuated significantly(0.1±0.1). It is concluded that the BRS is attenuated in hemorrhagic shock.This attenuation of BRS may be related to the central production of NO. |
