高渗氯化钠对心钠素及同源性洋地黄样物质的影响

比较３０例硬膜外阻滞择期手术病人，输入７．５％ＨＳ和５％ＧＳ后血浆ＡＮＰ、ＥＤＬＳ及血流动力学的变化。输入ＨＳ后ＡＮＰ明显升高，ＥＤＬＳ短暂降低，６０ｍｉｎ完全恢复，主动脉顺应性快速增加。输入ＧＳ后ＡＮＰ有增加趋势，但无统计学意义。ＥＤＬＳ显著降低，６０ｍｉｎ时仅为基础值的３／５。ＴＰＲ持续增加，ＣＯ和ＳＶ短暂降低，并伴有血压明显下降。     

高渗氯化钠溶液对水钠调节激素的影响

比较３０例硬膜外阻滞择期手术患者，输入７．５％ＨＳ和５％ＧＳ后血浆ＡＤＨ、ＰＲＡ、ＡⅡ及ＡＬＤ变化。输入 ＨＳ后 １０分钟 ＡＤＨ增加 ３３％，ＡⅡ、ＡＬＤ分别下降 ３７． ４％和 １６． ５％，６０分钟时 ＡＤＨ仍维持在高水平，ＡⅡ、ＡＬＤ亦未完全恢复。输入ＧＳ后 ＡＤＨ有增加趋势，但无统计学意义，Ａ Ⅱ于 １０分钟时轻度降低，６０分钟恢复，ＡＬＤ逐渐增加，６０分钟最明显（增加 ４６． ２％）。提示 ＨＳ可刺激 ＡＤＨ释放，抑制ＲＡＡＳ活性，激素的变化对ＨＳ改善肾功能可能具有重要介导作用。     

高渗氯化钠溶液对前列环素和内皮素的影响

比较３０例硬膜外阻滞择期手大患者，输入７．５％ＨＳ和５％ＧＳ后血浆ＰＧＩ２、ＥＴ及血流动力学的变化。输入ＨＳ后ＰＧＩ２明显升高，ＥＴ显著降低，伴主动脉顺应性快速增加。输入ＧＳ后１０分钟ＰＧＩ２和ＥＴ均无明显变化，６０分钟时ＰＧＩ２轻度增加，ＥＴ亦有上升，但较离散；ＴＰＲ持续增加，ＣＯ和ＳＶ短暂降低，血压明显下降。本研究提示ＰＧＩ２和ＥＴ在ＨＳ降低外周血管阻力、改善血流动力学过程中可能起着重要的介导作用。     

高渗氯化钠对水钠调节激素的影响

本文叙述了高渗氯化钠对ＡＤＨ、ＲＡＡＳ、ＥＤＬＳ、ＡＮＰ以及ＥＴ的影响。高渗氯化钠可刺激神经垂体释放ＡＤＨ，抑制ＲＡＡＳ活性，增加ＥＤＬＳ和ＡＮＰ分泌，降低血ＥＴ浓度。上述变化和相互作用有利于降低外周血管阻力和后负荷，增加心输出量，改善微循和灌注，增加肾血流量、尿量及肌酐清除率，预防肾衰及肺、脑水肿等，特别对ＨＳ能改善血流动力学具有重要的意义。     

经气管超声多普勒测定心排血量的临床应用及评价

心脏手术和腹腔镜胆囊切除术（ＬＣ）各２０例，术中采用ＴＴＤ连续监测ＣＯ；心脏手术病人术前行彩色超声（ＥＣＨＯ）测定主动脉直径（ＡＯＤ）并与ＴＴＤ测定的ＡＯＤ进行相关分析。结果：ＴＴＤ与ＥＣＨＯ的ＡＯＤ高度相关（ｒ＝０．９３，ｎ＝２０）；心脏手术病人ＣＯ在术毕明显增加，ＳＶＲ降低，ＣＶＰ和ＨＲ无显著变化；ＬＣ病人ＣＯ在气腹后１、５ｍｉｎ明显降低，ＳＶＲ在气腹后增加，ＭＡＰ在气腹后５、１０ｍｉｎ升高，     

高浓度葡萄糖对人腹膜间皮细胞的损伤作用及对其增殖的影响

高浓度葡萄糖对人腹膜间皮细胞的损伤作用及对其增殖的影响臧燕，侯凡凡，杨铁成，杨满球ＨＩＧＨＧＬＵＣＯＳＥＩＮＤＵＣＥＳＣＥＬＬＤＡＭＡＧＥＡＮＤＩＮＨＩＢＩＴＳＣＥＬＬＰＲＯＬＩＦＥＲＡＴｌＯＮＩＮＨＵ－ＭＡＮＰＥＲＩＴＯＮＥＡＬＭＥＳＯＴＨＥＬＩＡ...     

髓过氧化酶─—过氧化氢─—卤素系统对肾小球白蛋白通透性的作用

髓过氧化酶─—过氧化氢─—卤素系统对肾小球白蛋白通透性的作用李惊予ＲａｍＳｈａｒｍａ王海燕Ｖ．Ｊ．ＳａｖｉｎＲＯＬＥＯＦＭＹＥＬＯＰＥＲＯＸＩＤＡＳＥ－ＨＹＤＲＯＧＥＮＰＥＲＯＸｌＤＥ－ＨＡＬＩＤＥＳＹＳＴＥＭＩＮＧＬＯＭＥＲＵＬＡＲＰＥＲＭＥＡＢＩ...     

ATP和SNP控制性降压对血流动力学的影响

对比研究三磷酸腺苷（ＡＴＰ）和硝普钠（ＳＮＰ）控制性降压对氯胺酮麻醉犬血流动力学的影响。选择犬１４只，随机分为ＡＴＰ组和ＳＮＰ组，由股静脉持续输入ＡＴＰ和ＳＮＰ使ＭＡＰ降低３０％￣４０％，维持３０ｍｉｎ，分别于降压前、降压后１５ｍｉｎ、３０ｍｉｎ及停止降压后１５ｍｉｎ用Ｓｗａｎ－Ｇａｎｚ漂浮导管测定血流动力学指标。结果表明，ＡＴＰ、ＳＮＰ降压期间ＳＶＲ、ＬＶＳＷ显著降低，ＣＯ、ＰＣＷＰ、ＳＶ、ＲＶ     

冬虫夏草对5／6肾切除大鼠肾脏病理改变的影响

冬虫夏草对５／６肾切除大鼠肾脏病理改变的影响程庆，于力方，师锁柱，陈香美ＥＦＦＥＣＴＯＦＣＯＲＤＹＣＥＰＳＳＩＮＥＮＳＩＳＯＮＲＥＮＡＬＨＩＳＴＯＬＯＧＩＣＡＬＣＨＡＮＧＦＳＩＮ５／６ＮＥＰＨＲＥＣＴＯＭＩＺＥＤＲＡＴ￥ＣｈｅｎｇＱｉｎｇｌｉ；ＹｕＬ...     

高渗盐水治疗犬严重失血性休克时血浆中血管紧张素Ⅱ／心钠素…

本研究采用特异性的入免法测定７．５％氯化钠／４．２％右旋糖酐４０（ＨＳＤ）和０．９％乳酸钠林格氏液（ＬＲ）治疗犬严重失血性休克前后血浆中血管紧张素Ⅱ（ＡＧＴⅡ）心钠素（ＡＮＰ）含量的变化，发现ＨＳＤ较ＬＲ能在快速提高平均动脉压（ＭＡＰ）同时迅速恢复ＡＧＴⅡ／ＡＮＰ的平衡，及早地解除微血管痉挛，缩短缺血时间，减轻缺血再灌注损伤。本实验提示：ＨＳＤ快速恢复内源性损伤和抗损伤物质的平衡，可能是其抗休克的     

不同二氧化碳气腹压力对家兔心肌细胞的影响

目的　研究不同CO2 气腹压力对家兔心肌超微结构的影响。方法　 1 8只健康家兔 ,随机分为三组。A组气腹压力 1 0mmHg ,B组 1 5mmHg ,C组 2 0mmHg。用氯胺酮和地西泮肌注麻醉。测定气腹前和气腹后 30、6 0min的MAP、CVP ,HR ,测定同一时点的内皮素 (ET)、洋地黄物质(EDLS)和心肌酶谱。实验结束 ,取左室内壁心肌组织行电镜观察。结果　 (1 )血液动力学变化 :三组的HR组内、组间比较均无差异。CVP组内比较 ,三组气腹前与气腹后 30、6 0min ,差异非常显著(P <0 0 1 ) ;组间比较 ,气腹后 30、6 0min ,A组与B组、C组差异显著 (P <0 0 5 ) ,B组与C组间无差异。MAP组内比较 ,C组气腹前与气腹后 6 0min差异显著 (P <0 0 5 ) ;组间比较 ,A组与C组、B组与C组间差异显著 (P <0 0 5 )。 (2 )EDLS :组内组间均无差异 ,但气腹后 30、6 0min时的血浆水平比气腹前增加。 (3)ET :组内组间均无差异 ,但组内比较总体呈下降趋势。 (4 )心肌酶谱 :心肌酶随气腹时间的延长和压力的升高呈上升趋势。乳酸脱氢酶 (LDH) :B组气腹前与气腹后 6 0min比较差异显著 (P <0 0 5 )。天冬氨酸转移酶 (AST) :B组气腹前与气腹后 6 0min比较差异显著 (P <0 0 5 )。 (5 )心肌超微结构的变化 :A、B、C三组动物心肌组织均有不同程度的超微结     

Hyper osmolality does not modulate natriuretic peptide concentration in patients after coronary artery surgery

Background: The heart secretes natriuretic peptides (NPs) in response to myocardial stretch. Measuring NP concentrations is a helpful tool in guiding treatment. It has been suggested that sodium ion and hyperosmolality could affect NP excretion. If this is true, peri-operative NP measurements could be inconsistent when hypertonic solutions are used. With different osmolalities but equal volumes of hydroxyethyl starch (HES) – and hypertonic saline (HS) – infusions, this double-blinded study tested the hypothesis that osmolality modulates the excretion of NPs.
Methods: Fifty coronary surgery patients were randomized to receive within 30 min 4 ml/kg either HS or HES post-operatively. Samples for analysis of atrial NP (ANP), brain NP (BNP), plasma and urine sodium and osmolality and urine oxygen tension were obtained before and 60 min after starting the infusions and on the first post-operative morning. The haemodynamic parameters were measured at the same time points.
Results: Plasma osmolality and sodium increased only in the HS group. Changes in plasma BNP and ANP levels did not differ between the groups ( P =0.212 and 0.356). There were no correlations between NP levels and osmolality or sodium at any time point. In the HS group, urine volume was higher (3295 vs. 2644 ml; P <0.05) and the need for furosemide treatment was less (0.4 vs. 3.8 mg; P <0.01) than in the HES group.
Conclusions: The absence of effects of plasma sodium content or hyperosmolality on NP release validates the value of NPs as a biomarker in peri-operative patients.     

低温暴露对失血性休克血流动力学和氧动力学的影响

目的 研究低温暴露对失血性休克猪血流动力学和氧动力学的影响.方法 巴马小型猪16头,采用随机数字表法分为2组(每组8头):常温对照组(C组)和低温实验组(H组).2组猪均在15 min内按全身血容量的40％(即按30 ml/kg计算)匀速放血制备休克模型后,分别置于20℃～22℃常温和0℃～5℃低温环境中,监测和计算放...     

Vasoactive peptides during long-term follow-up of patients after cardiac transplantation.

BACKGROUND: Vasoactive peptides are accepted indicators of the degree of heart failure and its progression or improvement following medical therapy. Normalization of cardiac hemodynamics by cardiac transplantation (HTx) may lead to normalization of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) plasma levels shortly after the procedure. METHODS: Long-term follow-up was done for 14 consecutive patients, 12 men and 2 women, 49 years of age (range 24 to 64 years). ANP and BNP were measured by radioimmunoassay (RIA) in central venous plasma samples (before breakfast, at steady state) at the following intervals after HTx: 7 to 30 (1), 31 to 60 (2), 61 to 90 (3), 120 to 180 (4) and 210 to 365 (5) days. RESULTS: During follow-up, ANP decreased significantly within 2 months after HTx and continued of this level, whereas BNP decreased continuously without reaching normal values. The mean ratio of ANP:BNP increased from 3.23 to 8.01 during follow-up. Whereas right atrial pressure (RAP), right ventricular pressure (RVP), right ventricular end-diastolic pressure (RVEDP) and pulmonary capillary wedge pressure (PCWP) did not change during follow-up, cardiac output (CO) improved slightly, but significantly from 5.21 liters/min to 5.9 liters/min (p = 0.035). CONCLUSIONS: Normalization of left ventricular function after orthotopic HTx does not induce an early diminution of ANP and BNP plasma levels to normal concentrations. Although elevated ANP concentrations showed only minimal changes within 1 year, BNP decreased significantly as early as 2 months after HTx, without reaching normal values during the year of follow-up. Also, the ratio of ANP and BNP increased significantly from 3.23 to 8.01. These results demonstrate the contribution of other factors beyond cardiac function that determine the levels of these peptides.     

一氧化碳对脑缺血脂质过氧化物及Na+-K+ATP酶的影响及其限速酶在脑缺血中的表达

目的 观察一氧化碳(CO)对局灶性脑缺血脑组织脂质过氧化物及Na+-K+ATP酶的影响以及血红素氧合酶(HO-1)在脑缺血中的表达.方法 将SD大鼠随机分为3组,使用HO诱导剂、HO抑制剂腹腔注射为实验组,对照组注入生理盐水,12 h后制备大鼠局灶性脑缺血模型.缺血后24 h检测CO浓度、丙二醛(MDA)、超氧化物歧化酶(SOD)及Na+-K+ATP酶活性.对大鼠脑缺血后早期不同时间点进行HO-1免疫组织化学及病理学研究,并应用计算机图像分析技术检测HO-1表达的强弱.结果 与对照组比较,HO诱导剂组CO浓度显著升高1.36倍(P<0.01),HO抑制剂组CO浓度显著降低26.4%(P<0.01).HO诱导剂组MDA减少11.3%(P<0.01),SOD及Na+-K+ATP酶活性分别升高6.8%和20.1%(P均<0.05),而HO抑制剂组MDA增加12.4%(P<0.05),SOD及Na+-K+ATP酶活性分别降低8.2%和18.9%(P均<0.05).免疫组织化学显示缺血后30 min神经元和胶质细胞即有HO-1阳性表达,随着时间推移,HO-1的表达逐渐增强.结论 CO可对局灶性缺血的脑组织起保护作用.脑缺血时脑内HO-1的表达可能是脑组织对自身损伤的恢复机制之一.     

Atrionatriuretic peptide improves left ventricular function after myocardial global ischemia-reperfusion in hypoxic hearts

Atrionatriuretic peptide (ANP) is reported to be useful for attenuating myocardial ischemia–reperfusion injury and improving left ventricular function after reperfusion. However, ANP may be either ineffectual or harmful in cases where the myocardium has been chronically hypoxic since birth. This can be a result of the concomitant high levels of cyclic guanosine monophosphate (cGMP) produced within the myocardium. This study aimed to verify the validity of using ANP to improve left ventricular function after myocardial ischemia–reperfusion injury. For this purpose, a cyanotic congenital disease model that was developed using isolated rat hearts was used. Hearts were obtained from Sprague‐Dawley rats that were housed from birth until 6 weeks of age either in a hypoxic environment with 13–14% FiO₂ (hypoxic group) or in ambient air (normoxic group). These hearts were subjected to 30 min of normothermic global ischemia followed by 30 min of reperfusion using the Langendorff technique. Left ventricular functional recovery in hearts administered ANP (0.1 µM) into the reperfusion solution was compared with those hearts that were not administered ANP in both hypoxic (without ANP: n = 6, with ANP: n = 6, with ANP and HS‐142‐1[an antagonist of ANP]: n = 6) and normoxic hearts (without ANP: n = 6, with ANP: n = 6). In the hypoxic hearts, ANP administration improved the percent recovery of the left ventricular developed pressure (76.3 ± 9.2% without ANP vs. 86.9 ± 6.7% with ANP), maximum first derivative of the left ventricular pressure (82.4 ± 1.1% without ANP vs. 95.8 ± 6.5% with ANP), and heart rate (85.6 ± 4.7% without ANP vs. 96.1 ± 5.2% with ANP) after reperfusion. The improvement and recovery of these cardiac functions were closely related to significantly increased levels of postischemic cGMP release after ANP administration. The effect of ANP was blocked by HS‐142‐1. The improvements observed in the hypoxic group were similar to those found in the normoxic group. ANP administration during reperfusion improved left ventricular function after myocardial acute global ischemia–reperfusion equally in both the chronically hypoxic and age‐matched normoxic groups.     

Heat shock preconditioning on mitochondria during warm ischemia in rat livers

BACKGROUND: The aim of this study was to investigate the effects of stress tolerance from heat shock preconditioning on changes in mitochondrial functions during ischemia-reperfusion injury of the liver. MATERIALS AND METHODS: Rats were divided into a heat shock group (group HS) and a control group (group C). In group HS, rats received heat shock pretreatment 48 h prior to ischemia-reperfusion. Heat shock pretreatment was performed in a water bath at 42 degrees C for 15 min under general anesthesia. In group C, the same treatment was done with the water bath at 37 degrees C instead of at 42 degrees C. A 30-min warm ischemia by cramping the hepatoduodinal ligament (Pringle's maneuver) followed by a 60-min reperfusion was administered to all rats. Changes in membrane potential of hepatic mitochondria (MPM); mitochondrial respiratory function before ischemia (n = 5), after ischemia (n = 10), and after reperfusion (n = 10); and ATP recovery after reperfusion were compared between the groups. RESULTS: After a 30-min ischemia, MPM in group C decreased significantly and did not recover even after reperfusion. On the other hand, MPM in group HS was maintained even after a 30-min ischemia and 60 min into reperfusion as well. The respiratory control ratio (RCR) of the mitochondria in group C decreased to as low as 5.06 +/- 0.72 after a 30-min ischemia, but in group HS, RCR was maintained near a normal level. The ATP level recovered significantly earlier in group HS than in group C after reperfusion. CONCLUSIONS: Heat shock preconditioning of the liver protected mitochondria from loss of membrane integrity during ischemia and contributed to their ability to produce energy-rich phosphates during reperfusion.     

高渗氯化钠高氧液对失血性休克家兔血乳酸和动脉血气的影响

目的:观察高渗氯化钠高氧液对失血性休克家兔动脉血气和血乳酸值的影响，评价其对失血性休克的早期救治效果。方法:制备高渗氯化钠溶液(HS)、生理盐水高氧液（NSO）和高渗氯化钠高氧液(HSO)。30只雄性家兔制备失血性休克模型［于10min内使平均动脉压（MAP）降至40mmHg（1mmHg＝0.133kPa），维持60min］，随机分为NSO，HS，HSO组3个治疗组。分别按6mL/kg剂量5min内静脉输入NSO,HS和HSO。记录休克前后及给药后心率（HR）、呼吸（RR）、MAP及尿滴（UD），测定休克前、休克60min，给药后30，60，120min时血乳酸（BL）和动脉血气值。最后观察尸肺，测定肺系数。结果:HS和HSO组均显著地改善MAP，HR和UD，降低BL，改善代谢性酸中毒,肺系数明显低于NSO组。HSO与NSO及HS比较，能更显著地降低血BL，提高动脉血氧饱和度（SaO2）和动脉血氧分压（PaO2）。结论:HSO较HS和NSO能更显著地降低血BL,提高SaO2和PaO2，对失血性休克的早期救治具有较高的使用价值。     

低血容量性休克大鼠缺氧诱导因子1α的表达及其在血管低反应性发生中的作用

目的观察低血容量性休克大鼠肠系膜上动脉(SMA)血管组织中缺氧诱导因子1α(HIF-1α)的表达情况及其与血管低反应性发生的关系。方法将112只SD大鼠建立低血容量性休克模型后分为休克组(56只)、给药组(56只,于建立休克模型前4 h在大鼠腹腔内注射9μg／kg寡霉素)。于伤后0.0(10-15 min)、0.5、1．0、2．0、3．0、4．0、6．0 h,采大鼠动脉血后处死大鼠取SMA,每组每时相点8只。采用离体血管环张力测定技术测定血管环对梯度浓度去甲肾上腺素(NE)的收缩力;逆转录-聚合酶链反应(RT-PCR)半定量分析法检测SMA血管组织中HIF-1α、诱导型一氧化氮合酶(iNOS)、血红素氧合酶1(HO-1)mRNA的表达水平;连二亚硫酸钠还原法和硝酸还原酶法分别测定其全血一氧化碳(CO)浓度和血浆一氧化氮(NO)含量。另取8只大鼠作为正常对照组,不作处理,留取标本检测以上指标。结果与正常对照组比较,休克组大鼠伤后早期(0．0-1．0 h)血管反应性增高,伤后0．5 h达峰值,血管环对NE的最大收缩反应(Emax)增大,NE的50％最大效应的负对数克分子浓度(pD2)减小;伤后0．5-1．0 h Emax值均高于正常对照组(P<0．01);休克中、后期,血管反应性进行性下降,Emax减小、pD,增大,伤后4．0 h Emax低于正常对照组(P<0．01)。给药组伤后早期(0．0-1．0 h)血管反应性增高部分受抑制(P<0．05),伤后0．5 h Emax值为(2．01±0．22) g／mg,明显低于休克组[(2．96±0．18)g／mg,P<0．05]。休克晚期给药组血管反应性轻度回升,与休克组伤后4．0、6．0 h比较,差异有统计学意义(P<0．05或0．01)。与正常对照组比较,休克组伤后HIF-1αmRNA的表达呈稳步增高,伤后4．0 h达峰值(P<0．01);iNOS、HO-1mRNA表达水平亦逐渐增高,分别于伤后2．0、4．0 h达峰值(P<0．01)。与正常对照组比较,休克组随着病情的发展全血CO浓度和血浆NO含量呈逐渐升高的趋势。与休克组相比,给药组全血CO浓度基本稳定在正常范围内,血浆NO含量也明显降低。结论低血容量性休克可引起血管反应性的双相变化。HIF-1α在血管低反应性的形成中发挥了重要作用。