普鲁卡因-安氟醚静吸复合全麻下硝酸甘油控制性降压对动脉血气的影响

以９例ＡＳＡⅠ～Ⅱ级、在普鲁卡因－安氟醚静吸复合全麻下择期手术的成人患者为对象，观察了硝酸甘油（ＮＴＧ）控制性降压（ＭＡＰ下降３０％）对动脉血气的影响。结果：与对照组相比，降压期间ＰａＯ２、ＢＥ明显下降，ＰａＣＯ２、Ｐａ－ｅｔＣＯ２明显升高。说明ＮＴＧ控制性降压可给血气带来不良影响。     

不同血管保存液对人桡动脉血管移植物的抗痉挛作用

目的 研究不同的血管保存液对人离体桡动脉痉挛的缓解与预防能力。方法 非体外循环冠状动脉旁路手术(OPCAB)19例患者,应用“无接触(No Touch)”外科技术获取自体桡动脉,保留未处理的远段0.8～1.5cm。应用血管环灌流技术(Organ Bath)比较不同保存液的抗痉挛作用和预防痉挛作用。结果 血管环灌流实验显示,在对痉挛状态桡动脉的舒张能力方面,PS、VG、DG、NG溶液均可以在10min内100％舒张血管,舒张曲线显示舒张能力依次为VG、DG、NG、PS,但差异无显著性(P>0.05),在预先浸泡处理桡动脉45～60min后,除对照组(Ringer's Solution)外,所有血管保存液均可以有效地预防离体桡动脉的痉挛,各组间差异无显著性(P>0.05)。结论 罂粟碱溶液、VG、DG、NG溶液均有较好的抗血管痉挛作用,单从抗血管痉挛角度考虑可以用作CABG手术中桡动脉的准备液。     

硝酸甘油加多巴酚丁胺治疗难治性心力衰竭体会

目的 :探讨用硝酸甘油加多巴酚丁胺治疗难治性心力衰竭。方法 :以阳泉钢铁集团有限公司医院 30例顽固性心力衰竭患者为研究对象 ,其中男性 18例 ,女性 12例 ,年龄 37岁～ 81岁 ,平均 5 6岁 ,心功能均为 级～ 级 ,在综合治疗同时 ,加用小剂量硝酸甘油加多巴酚丁胺开始 ,以后据病情逐渐增加剂量 ,把血压维持在正常水平 ,结果 :30例患者中 ,显效 2 0例 ,有效 9例 ,无效 1例 ,总有效率 96 .6 %。结论 :在强心、利尿等基础治疗的前提下 ,用硝酸甘油加多巴酚丁胺治疗难治性心力衰竭 ,既能通过多巴胺直接增强心肌收缩力作用 ,增加心排血量 ,提高血压 ,抵消硝酸甘油不良反应 ,可能发挥硝酸甘油扩张动、静脉 ,减轻心脏前后负荷 ,改善全身及肾血流灌注 ,在临床上值得进一步研究探讨     

颅脑手术中应用硝酸甘油或复合艾司洛尔调控血压效果的比较

目的：比较艾司洛尔复合硝酸甘油（NTG）降压与单纯硝酸甘油降压效果。方法：36例ASA Ⅰ-Ⅱ级颅外择期手术病人分为两组：艾司洛尔复合NTG组18例,单纯NTG组18例,观察并比较两组控制性降压时血气,血液动力学的变化。结果：艾司洛尔能明显加快NTG起效速率,NTG用量减少55．7％,并能抑制单纯NTG控制性降压时反射性心率增快;停止降压后血压平衡上升,RPP值下降;PaO2,BE仅轻度下降,与单纯NTG组比较有显著差异。结论：艾司洛尔复合NTG控制性降压有明显的协同作用。无反跳现象,对动脉血气影响小。     

直立倾斜试验加硝酸甘油含化诊断血管迷走性晕厥的临床研究

目的评价硝酸甘油(NTG)含化加异丙肾上腺素倾斜试验(ITTT)诊断血管迷走性晕厥(VS)的价值.方法将72例VS患者和36例正常对照组随机均分成ITTT和ITTT+NTG组.结果ITTT+NTG组敏感性高于ITTT(93.1%和76%,P＜0.05)有显著性差异.结论ITTT+NTG含化是一种安全、耐受性好、敏感性高,特异性强的诊断VS的方法.     

尼卡地平和硝酸甘油在体外循环中血压控制的比较

目的比较尼卡地平和硝酸甘油在体外循环中控制高血压的效果及对血流动力学的影响。方法40例冠状动脉旁路术(CABG)病人在体外循环(CPB)中平均动脉压升至10.7kPa时给予尼卡地平或硝酸甘油。将病人随机分为尼卡地平和硝酸甘油组,每组20例。观察两药起效时间,维持平均动脉压(MAP)在665～9.31kPa时所需剂量,开放升主动脉后心脏自动复跳情况以及停机后血流动力学的变化。结果将MAP从10.7kPa降至6.65～9.31kPa时,应用尼卡地平0.5mg,所需时间为(3.8±1.3)min,维持MAP在6.65～9.31kPa时所需剂量为(1.2±0.4)μg·kg     

合心爽,硝酸甘油治疗不稳定型心绞痛对比研究

目的 比较用硝酸甘油和合心爽治疗９８例不稳定型心绞痛的疗效。方法 随机分组,分别静滴合心爽和硝酸甘油,以难治性心绞痛、心肌梗塞或缺血性猝死为治疗终点。结果 发展为难治性心绞痛或心肌梗塞病例在合心爽组为５人,硝酸甘油组为１１人,发生心肌梗塞者合心爽组３人,硝酸甘油８人,缺血性猝死者合合爽组无,硝酸甘油组１人。结论 静脉用合心爽治疗不稳定型心绞痛疗效优于硝酸甘油（Ｐ〈０．００１）。     

超氧阴离子与硝酸甘油耐药关系的实验研究

目的 :采用持续经皮贴硝酸甘油 ( 0 .4mg/h) 72小时建立大白兔耐药模型 ,用鲁米诺化学发光技术测量血管壁超氧阴离子 (·O-2 )水平 ,探讨·O-2 水平与硝酸酯耐药性的关系。方法 :动物随机分为硝酸甘油组和对照组 ,贴膜 72小时后获取胸主动脉 ,观察血管环对不同浓度硝酸甘油的舒张反应和测量血管组织·O-2 、丙二醛 (MDA)水平和超氧化物歧化酶 (SOD)活性。结果 :硝酸甘油组血管环对硝酸甘油舒张反应明显减弱 (最大舒张反应 58.76±1 2 .96%vs94.68± 3.2 3% ,P <0 .0 5) ,硝酸甘油组血管组织·O-2 水平较对照组显著增加 ( 2 31 7.38± 889.0 3vs50 8±1 70 .94cps/g .ml,P <0 .0 5) ,而SOD活性和MDA水平无显著改变 (P >0 .0 5)。结论 :持续经皮贴硝酸甘油 72小时血管环产生了明显耐药 ,耐药的产生可能与血管壁超氧阴离子增加有关     

Nitroglycerin-inhibited whole blood aggregation is partially mediated by calcitonin gene-related peptide–a neurogenic mechanism

1. The role of the vasculature and calcitonin gene-related peptide (CGRP) in nitroglycerin (NTG)-mediated platelet inhibition was studied.
2. In vitro incubations of CGRP in whole blood induced a dose-dependent inhibition of platelet aggregation with an IC₅₀ of 62.1 nM.
3. The platelet inhibition induced by CGRP was blocked by co-incubation of 0.53 μM CGRP_8-37, as well as 30 μM N^G-nitro-monomethyl-L-arginine (L-NMMA).
4. In a separate group of experiments, 100 nM NTG in rat whole blood (WB) induced platelet inhibition of 6.0±1.3% (mean±s.d.), which was enhanced to 77.6±3.5% by the addition of rat aortic tissue (AT) (P<0.001). The inclusion of CGRP_8-37 with NTG and AT in WB reduced platelet inhibition to 31.6±6.8% (P<0.01). Incubation of WB and AT with 30 μM L-NMMA reduced NTG-induced inhibition of platelet aggregation to 26.4±4.2% (P<0.001).
5. It is concluded that vascular tissue contributes to the antiplatelet mechanism of action of NTG. Furthermore, NTG apparently evokes the release of CGRP from vascular tissue and this neuropeptide contributes to the antiplatelet actions of NTG.
6. The antiplatelet activity of CGRP in whole blood is mediated primarily through the activation of nitric oxide synthase.

     

Effects of intravenous nitroglycerin combined with dopamine on intracranial pressure and cerebral arteriovenous oxygen difference in patients with acute subarachnoid haemorrhage

Summary The effects of intravenous nitroglycerin (NTG) combined with dopamine on intracranial pressure (ICP) and cerebral arteriovenous oxygen difference (AVDO₂) were studied in 11 patients with acute subarachnoid haemorrhage (SAH). The study was performed on Days 1 to 3 of SAH after aneurysmal clipping. Treatment consisted of an intravenous drip infusion of NTG in increasing incremental doses of 0.5, 1.0, 1.5, 2.0, and 2.5 g/kg/min at one-hour intervals. Dopamine (5 to 10 g/kg/min) was also given concurrently to maintain systemic blood pressure. ICP values before NTG administration ranged from 7 to 24 mmHg (mean, 11.91±5.30 mmHg). ICP began to increase immediately after the adminisration of NTG 0.5 g/kg/min and peaked at 14.64±5.93 mmHg 10 minutes after onset of infusion. Thereafter, ICP gradually returned to pretreatment levels. Increasing the dose of NTG failed to induce further significant rises in ICP. Mean AVDO₂ before NTG administration was 4.69±0.62 ml/dl. This parameter showed no significant change during NTG infusion, although cerebral perfusion pressure decreased to between 75% to 94% of the control value after NTG administration. These results indicate that continuous NTG infusion combined with dopamine does not have adverse effects on ICP (the ICP increase is minimal and transient) and may even have beneficial effects on CBF in patients with acute SAH.