灯盏生脉胶囊抗大鼠局灶性脑缺血-再灌注损伤作用研究

目的 研究灯盏生脉胶囊抗大鼠局灶性脑缺血 再灌注损伤的作用。方法将58只雄性SD大鼠随机分为4组，即假手术组10只，0.9%氯化钠溶液组和灯盏生脉胶囊高、低剂量组各16只。假手术组行假手术，其他3组制作大脑中动脉缺血 再灌注模型。假手术组和0.9%氯化钠溶液组于术前72，48，24，0.5 h及术后22 h灌胃给予0.9%氯化钠溶液，灯盏生脉胶囊低、高剂量组在相同时点分别按0.36和0.72 g·kg 1剂量灌胃给予灯盏生脉胶囊内容物悬浊液4 mL；各组大鼠均在最后一次给药后2 h处死，于脑缺血2 h和再灌注2和22 h分别进行神经行为学评分，再灌注22 h后测定大鼠血清乳酸脱氢酶活性及脑梗死体积百分比，观察脑组织病理学改变。结果再灌注2 h后，灯盏生脉胶囊高剂量组神经行为学评分［(1.75±0.68)分］较0.9%氯化钠溶液组［(2.31±0.79)分］明显降低（P＜0.05）；再灌注22 h后，灯盏生脉胶囊高剂量组神经行为学评分［(1.63±0.89) 分］明显低于0.9%氯化钠溶液组［(2.38±1.09)分］（P＜0.05）。再灌注22 h后，灯盏生脉胶囊高剂量组血清乳酸脱氢酶活性［(1 331.89±366.85) U·L 1］明显低于0.9%氯化钠溶液组［(1 799.56±325.92) U·L-1］（P＜0.05），灯盏生脉胶囊高剂量组脑梗死体积百分比［(9.73±5.66)%］亦明显低于0.9%氯化钠溶液组［(18.31±6.96)%］（P＜0.05）。灯盏生脉胶囊低、高剂量组鼠脑组织缺血周围区细胞周围水肿、神经元变性和间质破坏较其他各组轻。结论灯盏生脉胶囊有一定的抗大鼠局灶性脑缺血 再灌注损伤作用，作用机制可能在于抑制缺血半暗带恶化。高剂量作用更明显。     

仙人掌多糖对大鼠局灶性脑缺血的神经保护作用

摘要目的观察仙人掌多糖对大脑中动脉栓塞（MCAO）诱导的大鼠缺血 再灌注损伤的神经保护作用。方法雄性SD大鼠随机分为假手术组、缺血组、0.9%氯化钠溶液组、仙人掌多糖治疗组（200 mg·kg－1·d －1,ip）。采用MCAO法制作大鼠缺血 再灌注损伤模型。分别于大鼠缺血2 h再灌注3,6,8 h后进行神经行为学评分;8 h后2,3,5 三苯基氯化四氮唑（TTC）染色测定脑梗死体积;缺血2 h再灌注22 h后脑组织切片苏木精 伊红（HE）染色显微镜下形态学观察。结果与0.9%氯化钠溶液组相比,再灌注8 h后仙人掌多糖治疗组神经行为学评分平均下降（2.35±0.47）分（P＜0.05）,梗死灶体积减少（P＜0.05）;大鼠皮质及海马组织神经细胞丢失、神经胶质增生、核固缩、核深染等形态学均有明显改善（P＜0.05）。结论仙人掌多糖可以缓解大鼠大脑中动脉栓塞症状,具有一定的神经保护作用。     

前列腺素E1对缺血再灌注脑损伤的干预作用

目的探讨前列腺素E1(PGE1)对缺血再灌注脑损伤的干预作用.方法采用线栓法,经颈内动脉(ICA)插入颅内深度18～20mm阻断左侧大脑中动脉,复制大鼠局灶性脑缺血再灌注模型.缺血60min,再灌注24h对每只动物进行神经症状评分后,断头取脑,并进行脑梗死体积,脑含水量测定及病理学捡查.结果①缺血再灌注模型组出现典型神经缺损症状,而PGE1三剂量组均能改善大鼠神经功能障碍,其行为评分与模型组相比有显著性差异(P＜0.05).②缺血再灌注模型组脑梗死体积百分比高达(28.40±1.8269)%,而PGE1中、高剂量组脑梗死体积百分比明显缩小[(10.25±2.772)%,(12.90±2.5772)%],与模型组相比有显著性差异(P＜0.05).③缺血再灌注模型组栓塞侧脑含水量明显增加(83.03±0.6110%),而PGE13个剂量组脑含水量均低于模型组[(79.93±0.6950)%;(79.67±1.1244)%;(80.26±1.6325)%],两者相比有显著性差异(P＜0.05).④缺血再灌注模型组脑组织病理形态学捡查可见:大量神经细胞固缩坏死,重度脑水肿,部分可见软化灶形成,而PGE13个剂量组脑水肿及神经细胞坏死程度均明显减轻,两者相比有明显差异.结论PGE1能减轻脑缺血再灌注所致的组织损伤,发挥保护作用.     

奥扎格雷钠对脑缺血再灌注后神经细胞的保护作用

目的探讨奥扎格雷钠对大鼠脑缺血再灌注损伤的脑保护作用。方法采用Longas法制备大鼠脑缺血再灌注模型,分别用奥扎格雷钠(治疗组)和0.9%氯化钠注射液(对照组)腹腔注射。观察大鼠脑梗死体积、神经功能评分、细胞凋亡数和细胞凋亡率。结果治疗组比对照组大鼠脑梗死体积明显减小,神经凋亡数较对照组显著减少(P<0.01)。对照组神经功能评分为(2.83±0.75)分,治疗组为(1.83±0.75)分,两组比较差异有统计学意义(P<0.05)。3组细胞凋亡率比较,差异有统计学意义(P<0.01)。结论奥扎格雷钠能明显减小脑缺血的梗死体积,减轻脑缺血再灌注后的神经损害,具有明显的脑保护作用。     

丙泊酚对大鼠脑缺血再灌注损伤后的保护作用及机制研究

目的 研究丙泊酚对脑缺血再灌注损伤后的保护作用机制.方法 30只大鼠随机分为假手术组、缺血再灌注组、丙泊酚治疗组,采用线栓法制做大脑中动脉缺血2h再灌注模型,再灌注24h后断头取脑,测定各组大鼠脑梗死体积和脑组织含水量,并检测各组大鼠脑组织超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO).结果 丙泊酚治疗组脑梗死体积、脑含水量均低于缺血再灌注组,差异有统计学意义(P＜0.05).丙泊酚治疗组能提高脑组织SOD活性,降低MDA活力、NO含量,同缺血再灌注组比较差异有统计学意义(P＜0.05).结论 丙泊酚能减小脑梗死体积,减轻脑水肿,抗自由基损伤,对大鼠脑缺血再灌注损伤有一定保护作用.     

丙泊酚对大鼠脑缺血再灌注损伤后的保护作用及机制研究

目的研究丙泊酚对脑缺血再灌注损伤后的保护作用机制。方法 30只大鼠随机分为假手术组、缺血再灌注组、丙泊酚治疗组,采用线栓法制做大脑中动脉缺血2h再灌注模型,再灌注24h后断头取脑,测定各组大鼠脑梗死体积和脑组织含水量,并检测各组大鼠脑组织超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)。结果丙泊酚治疗组脑梗死体积、脑含水量均低于缺血再灌注组,差异有统计学意义(P<0.05)。丙泊酚治疗组能提高脑组织SOD活性,降低MDA活力、NO含量,同缺血再灌注组比较差异有统计学意义(P<0.05)。结论丙泊酚能减小脑梗死体积,减轻脑水肿,抗自由基损伤,对大鼠脑缺血再灌注损伤有一定保护作用。     

脑缺血再灌注损伤后BMSCs 不同示踪方式的比较

目的比较脑缺血再灌注损伤后,不同示踪方式观察骨髓间充质干细胞（BMSCs）移植后的效果。方法 BMSCs 复苏培养后,分别采用5-溴脱氧尿嘧啶核苷（BrdU）、PKH26 进行标记,并且与绿色荧光蛋白（GFP）转染细胞,分别对脑缺血再灌注模型大鼠脑组织进行移植。将75 只SPF 级雄性SD 大鼠随机均分为假手术组,模型组,BrdU、 PKH26、GFP 示踪组。采用线栓改良法制备大鼠左侧大脑中动脉局灶性脑缺血再灌注损伤模型。脑缺血再灌注24 h 后,假手术组、模型组分别采用脑立体定位仪经脑实质植入10 μL 生理盐水;BrdU、PKH26、GFP 示踪组分别植入 10 μL 的BMSCs/BrdU、BMSCs/PKH26、BMSCs/GFP。采用神经行为学评分、TTC 染色、脑组织含水量法进行模型鉴定及疗效判定,采用焦油紫染色进行神经元计数,并在荧光显微镜下计数标记细胞阳性率。结果移植前细胞BrdU、 PKH26、GFP 标记率无明显差异。移植4 周后3 示踪组大鼠神经行为学评分、脑梗死体积、脑组织含水量均显著低于模型组,神经元计数显著高于模型组;神经行为学评分、脑梗死体积高于假手术组,脑组织含水量、神经元计数与假手术组差异无统计学意义;3 示踪组间上述指标差异均无统计学意义。GFP 示踪组的荧光标记细胞阳性率高于 BrdU、PKH26 示踪组。结论脑缺血再灌注损伤中,GFP 示踪方式效果更为持久,优于BrdU 和PKH26。     

尼莫地平对大鼠脑缺血再灌注损伤疗效分析

目的探讨尼莫地平对大鼠缺血再灌注损伤的保护作用。方法采用结扎颈总动脉的方法制备缺血再灌注模型,对缺血前、再灌注48h后对大鼠进行神经功能评分和脑梗死体积,对正常组、缺血前注射尼莫地平组、未注射尼莫地平组及再灌注后注射尼莫地平组4组大鼠神经功能评分和脑梗死体积。结果与模型组组相比,缺血前及灌注后静脉滴注尼莫地平大鼠神经功能缺损明显减少,脑梗死体积明显减少(P<0.05)。结论尼莫地平治疗脑缺血再灌注损伤有疗效,对脑缺血大鼠有神经保护作用,而且在缺血前给药能减少大脑梗死的面积。     

前列腺素E1对缺血再灌注脑损伤的干预作用

目的　探讨前列腺素E1 (PGE1 )对缺血再灌注脑损伤的干预作用。方法　采用线栓法,经颈内动脉(ICA)插入颅内深度18～20mm阻断左侧大脑中动脉,复制大鼠局灶性脑缺血再灌注模型。缺血60min ,再灌注24h对每只动物进行神经症状评分后,断头取脑,并进行脑梗死体积,脑含水量测定及病理学捡查。结果　①缺血再灌注模型组出现典型神经缺损症状,而PGE1 三剂量组均能改善大鼠神经功能障碍,其行为评分与模型组相比有显著性差异(P<0.05)。②缺血再灌注模型组脑梗死体积百分比高达(28.40±1.8269)%,而PGE1 中、高剂量组脑梗死体积百分比明显缩小[(10.25±2.772) %,(12.90±2.5772)%],与模型组相比有显著性差异(P<0.05)。③缺血再灌注模型组栓塞侧脑含水量明显增加(83.03±0.6110%) ,而PGE1 3个剂量组脑含水量均低于模型组[(79.93±0.6950)%;(79.67±1.1244)%;(80.26±1.6325)%],两者相比有显著性差异(P<0.05)。④缺血再灌注模型组脑组织病理形态学捡查可见:大量神经细胞固缩坏死,重度脑水肿,部分可见软化灶形成,而PGE1 3个剂量组脑水肿及神经细胞坏死程度均明显减轻,两者相比有明显差异。结论　PGE1 能减轻脑缺血再灌注所致的组织损伤,发挥保护作用。     

脑室注射纳洛酮对大鼠脑缺血再灌注损伤的保护作用

目的　探讨脑室直接灌注盐酸纳洛酮注射液 (纳洛酮 ) ,对大鼠脑缺血再灌注损伤的保护作用。方法　采用线栓法制备大鼠大脑中动脉缺血再灌注模型 ,在再灌注后的不同时间点 ( 3、6、2 4h) ;通过脑室直接灌注、腹腔注射和脑室灌注 腹腔注射的方式使用纳洛酮 ,观察用药后大鼠神经功能和组织病理学改变 ,计算脑梗死体积比 ,脑水肿体积和脑含水量。结果　与对照组相比 ,纳洛酮组的脑梗死体积比 ,脑水肿体积和脑含水量均明显减轻 ,随着缺血时间的延长这种保护作用逐渐降低 ,脑室灌注和腹腔注射联合使用的保护效果明显优于单纯脑室灌注或腹腔注射给药。结论　脑缺血再灌注后使用纳洛酮具有明显的神经功能保护作用 ,脑室灌注和腹腔注射给药的保护作用相似 ,但在损伤后的早期 ( <6h)、超早期 ( <3h)采用脑室灌注和腹腔注射联合给药的方式效果最佳     

Heightened blood pressure responsiveness to intracarotid infusion of angiotensins in the spontaneously hypertensive rat

The purpose of this study was to test the hypothesis that intracarotid infusion of angiotensin via a brachial arterial catheter results in a heightened pressor response in the alert spontaneously hypertensive rat (SHR) as previously observed for intracerebroventricular (ICV) injection of angiotensin. We infused angiotensin II and III since these ligands are equivalently potent with respect to peak pressor effect when delivered ICV. We measured somewhat greater pressor responsiveness to AII than to AIII in the Wistar-Kyoto (WKY) normotensive control strain from a baselevel of 133.1 +/- 5.8 (mean +/- SEM) to 151.3 +/- 6.2 mmHg (+13.7%) at the 100 pmol/kg/min dose of AII, and from 132.5 +/- 5.8 to 146.0 +/- 6.1 mmHg (+10.2%) for AIII. The SHR revealed a heightened pressor sensitivity to AII, from a baselevel of 170.0 +/- 3.8 to 200.6 +/- 5.9 mmHg (+18%) while the response to AIII was less dramatic, from 171.3 +/- 2.1 to 189.8 +/- 2.4 mmHg (+10.8%). These findings suggest that a similar heightened pressor responsiveness occurs to peripheral infusion of angiotensin II in the SHR as previously observed to ICV injection.     

小剂量高渗盐液在烧伤休克中的应用研究

目的探讨小剂量(3~5m l/kg)高渗盐液在烧伤休克早期应用的效果。方法随机将48例烧伤面积超过45%的患者分为两组进行复苏,一组在液体复苏前先输注3~5m l/kg的7.5%N aC l液,另一组复苏不采用高渗盐液,余复苏同第一组。结果使用高渗盐液抗休克后,治疗组与对照组比较在血压、尿量、输液量及乳酸值方面有显著性差异(P<0.05)。结论小剂量高渗盐液在大面积烧伤休克早期救治中具有明显的抗休克作用,减少复苏液体总量,在临床上有一定的应用价值。     

Impaired renal response to portal infusion of hypertonic saline in adriamycin-treated rats

1. The hepatorenal reflex plays an important role in water and salt homeostasis by matching renal excretion to gastrointestinal absorption. This homeostatic mechanism is impaired in nephrotic rats. The present study tested the hypothesis that, in nephrotic rats, the renal sodium excretion response to hypertonic saline infusion is impaired due to decreased sensitivity of the hepatoportal sodium-sensing mechanism. 2. The present study was performed in control and adriamycin (ADR)-induced nephrotic syndrome rats. After baseline data collection, urinary sodium (U(Na)V) and potassium (U(K)V) excretion responses were tested following continuous infusion of hypertonic NaCl solution (20 μL/min for 30 min) into either the femoral or mesenteric vein. A second series of experiments tested hepatic and renal nerve responses to continuous mesenteric vein infusion of hypertonic NaCl (10 μL/s for 30 s). 3. Compared with control rats, nephrotic rats displayed significantly lower baseline U(Na)V and U(K)V excretion. In control rats, mesenteric compared with femoral vein infusion of hypertonic NaCl produced a more rapid and greater increase in U(Na)V. In contrast, in nephrotic rats, femoral and mesenteric vein infusion caused similar increases in U(Na)V and the maximum increases in U(Na)V to either route of infusion were much lower in nephrotic than control rats. Furthermore, portal hypertonic saline infusion caused greater increases in hepatic nerve activity and greater decreases in renal nerve activity in control compared with nephrotic rats. 4. These data suggest that, in rats, adriamycin treatment decreases hepatoportal sodium-sensing sensitivity, leading to marked impairment of hepatorenal reflex responses, potentially contributing to salt and water retention.     

Reliable and effective oxygen-ozone therapy at a crossroads with ozonated saline infusion and ozone rectal insufflation

Objectives This review aims to highlight the advantages and safety of oxygen‐ozone therapy (OOT) and to suggest ways to enhance its acceptance. Key findings The treatment of a herniated disk by injecting a gaseous oxygen‐ozone mixture inside the nucleus pulposus is a great clinical success. However, the use of OOT lags for a number of reasons, including lack of standardization, the need for numerous treatments, lack of knowledge and even denial. Anecdotally, several million treatments by OOT have been performed worldwide indicating its usefulness, mainly in peripheral arterial diseases and age‐related macular degeneration. The scepticism that accompanies the systemic use of ozone can only be overcome by demonstrating the validity of OOT in controlled and randomized clinical trials. Cheaper and quicker methods, such as ozonating physiological saline with successive infusion as well as ozone rectal insufflations, are becoming popular, however, such alternative procedures are erratic, unstable and liable to be toxic, with deleterious consequences, and are likely to discredit the beneficial use of ozone. Summary The approval of ozone in terms of both therapeutic efficacy and safety will depend on the results achieved by authoritative clinical trials.     

A comparison of the effects of intravenous propranolol and nadolol on the renal response to hypertonic saline infusion.

Intravenous loading with 500 ml of 2.7% saline increased the clearance of PAH and inulin and urine sodium excretion in 14 healthy subjects. Intravenous propranolol (0.075 and 0.15 mg/kg) did not alter PAH or inulin clearance at rest but abolished the increase expected during saline infusion. There was no consistent effect on urinary sodium excretion. Intravenous nadolol (0.05 and 0.75 mg/kg) reduced resting PAH and inulin clearances by up to 25%. Both clearances fell significantly during saline infusion but natriuresis was not significantly reduced in spite of the changes in renal function. There was no evidence from these studies in normal volunteers that nadolol confers any advantages over propranolol in its effects on renal function.     

Taurolithocholate-induced increase in the intrabiliary pressure generated during retrograde intrabiliary infusion of saline in rats: Antagonism by taurocholate and glycocholate

Taurolithocholate (TLC) is known to produce cholestasis and certain bile acids antagonize this effect. This antagonistic relationship was studied by measuring intrabiliary pressure (IBP) and bile flow changes in pentobarbital-anesthetized male Sprague-Dawley rats weighing 329 ± 7 (SE) g. The IBP reflects the peak pressure generated during the retrograde intrabiliary infusion of saline at 2.3 μl/sec. When TLC was infused into the femoral vein at 0.46 μmol/min over a 35-min period, the IBP rose and the bile flow decreased. Upon stopping the infusion, IBP returned to control values in 30 min but the cholestasis persisted. Simultaneous infusion of taurocholate or glycocholate at 0.61 μmol/min with the TLC prevented the TLC-induced rise in IBP and the cholestasis. Infusion of 0.61 μmol dehydrocholate/min with the TLC did not antagonize the rise in IBP or the cholestasis. Because dehydrocholate was a more potent choleretic agent than taurocholate or glycocholate and it had no antagonistic effect on TLC-induced effects, it was evident that the antagonistic action of taurocholate and glycocholate was not due to their choleretic effect. In another experiment, an iv bolus injection of 100 μmol/kg, taurocholate and glycocholate alone produced a fall in IBP which lasted about 1 hr. Even though this latter kind of fall in IBP might have been consistent with an increase in biliary tree permeability, such an effect did not appear to play a role in the antagonistic effect of these bile salts against the taurolithocholate-induced change. The changes in IBP were likely the result rather than the cause of more fundamental alterations.     

Renal kallikrein-kinin system, but not renal dopamine system, mediates the natriuretic response to intravenous saline infusion in healthy Chinese subjects

1. To assess the role of renal dopamine (DA), sympathetic nervous system (SNS) activity and the renal kallikrein-kinin system in sodium excretion in Chinese subjects, we studied the effects of intravenous saline infusion on the urinary excretions of sodium, free DA, free noradrenaline (NA) and kallikrein in eight healthy males aged 23-25 years. 2. After a baseline period of 1 h (hour 0), these subjects received 11 of 0.9% saline over 2 h (hours 1 and 2), followed by a 4-h recovery period (hours 3-6). From hours 0-4, subjects remained in the supine position, except to void urine. Distilled water was given orally throughout the study to ensure an adequate diuresis. 3. A 31-39% increase in sodium excretion (P < 0.05) was seen during hours 2 and 3. Urinary DA did not change throughout the study period. Urinary free NA showed no changes while the subjects remained supine, but an increase of 91-105% (P < 0.02) was seen after the subjects became ambulatory. However, there was a 103-140% increase in urinary kallikrein excretion (P < 0.05) during the saline infusion. Urinary kallikrein was still much higher (by 74%) than the basal level 1 h after the completion of the saline infusion. 4. There is no evidence from the present study that renal DA or SNS play any role in the natriuretic response to saline infusion in Chinese subjects. The brisk urinary kallikrein response, despite a relatively small salt load, suggests that the renal kallikrein-kinin system may play an important role in extracellular fluid volume and sodium homeostasis in Chinese subjects.     

Renal kallikrein‐kinin system,but not renal dopamine system,mediates the natriuretic response to intravenous saline infusion in healthy Chinese subjects

1 To assess the role of renal dopamine (DA), sympathetic nervous system (SNS) activity and the renal kallikrein‐kinin system in sodium excretion in Chinese subjects, we studied the effects of intravenous saline infusion on the urinary excretions of sodium, free DA, free noradrenaline (NA) and kallikrein in eight healthy males aged 23–25 years.
2 After a baseline period of 1 h (hour 0), these subjects received 1 l of 0.9% saline over 2 h (hours 1 and 2), followed by a 4‐h recovery period (hours 3–6). From hours 0–4, subjects remained in the supine position, except to void urine. Distilled water was given orally throughout the study to ensure an adequate diuresis.
3 A 31–39% increase in sodium excretion (P<0.05) was seen during hours 2 and 3. Urinary DA did not change throughout the study period. Urinary free NA showed no changes while the subjects remained supine, but an increase of 91–105% (P<0.02) was seen after the subjects became ambulatory. However, there was a 103–140% increase in urinary kallikrein excretion (P<0.05) during the saline infusion. Urinary kallikrein was still much higher (by 74%) than the basal level 1 h after the completion of the saline infusion.
4 There is no evidence from the present study that renal DA or SNS play any role in the natriuretic response to saline infusion in Chinese subjects. The brisk urinary kallikrein response, despite a relatively small salt load, suggests that the renal kallikrein‐kinin system may play an important role in extracellular fluid volume and sodium homeostasis in Chinese subjects.     

精密输液器减少输液反应的疗效观察

目的探讨精密输液器减少输液反应的效果和使用安全性。方法实验组120例患儿使用精密滤过输液器,对照组120例患儿使用普通输液器。结果观察组发生不良反应4例,占3.1%,对照组发生不良反应23例,占21.7%,经x2检验,差异有统计学意义(P<0.05)。结论精密输液器能减少不良反应的发生,比普通输液器使用更加安全。