粉防己碱对大鼠心肌缺血再灌注时心肌ATP酶活性的影响

实验旨在观察在体大鼠短暂缺血后心肌膜ＡＴＰ酶活性的变化及粉防己碱（Ｔｅｔ）的作用。分离缺血１５ｍｉｎ、再灌注２ｈ后及在缺血再灌注前给Ｔｅｔ的大鼠心肌粗制质膜和内质网,测定质膜Ｎａ＋－Ｋ＋－ＡＴＰ酶和内质网Ｃａ２＋－ＡＴＰ酶活性。结果表明,心肌缺血１５ｍｉｎ后二酶活性均明显降低,分别为假结扎组的６３．６％和７２．６％（Ｐ＜０．０１）,再灌注后Ｎａ＋－Ｋ＋－ＡＴＰ酶活性有所恢复,再灌注３０ｍｉｎ时为假结扎组的７２．１％（Ｐ＜０．０１）,而Ｃａ２＋－ＡＴＰ酶活性则进一步下降,再灌注３０ｍｉｎ时为假结扎组的５０．４％（Ｐ＜０．０１）,再灌注后２ｈ二酶活性分别升高至假结扎组的８０．９％和６５．３％（Ｐ＜０．０１）。在缺血前２０ｍｉｎ分别给予Ｔｅｔ６４．２和９６．３μｍｏｌ／ｋｇ及硝苯啶（０．２３μｍｏｌ／ｋｇ）,能明显减少内质网Ｃａ２＋－ＡＴＰ酶活性的降低。结果提示心肌膜ＡＴＰ酶活性的降低可能参与了短暂心肌缺血所致再灌注损伤的发生机制,Ｔｅｔ可减少缺血和／或再灌注时内质网Ｃａ２＋－ＡＴＰ酶活性降低。     

心肌缺血时腺苷对绵羊浦肯野纤维If电流的影响

目的和方法：用双微电极电压钳技术,观察腺苷（ａｄｅｎｏｓｉｎｅ,Ａｄ）对绵羊心室浦肯野纤维起搏离子流Ｉｆ的影响。结果：在正常台氏液中加入１０＾－５ｍｏｌ／Ｌ Ａｄ灌流１５ｍｉｎ和３０ｍｉｎ后,在－７０￣－１２０ｍＶ所有膜电位,Ｉｆ离子流幅值均降低（ｎ＝１２,Ｐ〈０．０５￣０．０１）,引起激活曲线向超极化方向移位,但Ｉｆ稳态激活时间无明显改变。“缺血”１５ｍｉｎ和３０ｍｉｎ后,在－７０￣－１２０ｍＶ     

福尔马林致痛后大鼠中脑导水管周围灰质甲啡肽及脊髓背角P物质含量的变化

本文用免疫组化方法结合计算机图像处理技术观察大鼠后脚掌皮下注射福尔马林后脊髓背角Ｐ物质免疫阳性反应（ＳＰＬＩ）变化的节段性分布及中脑导水管周围灰质（ＰＡＧ）内甲啡肽样免疫阳性反应（ＭＥＬＩ）的变化。结果显示,注射福尔马林后,脊髓腰段（Ｌ１－２,Ｌ４－５）背角ＳＰＬＩ显著增强（Ｐ＜．０５）,３０ｍｉｎ组与６０ｍｉｎ组相比较无显著变化（Ｐ＞０．０５）;胸脊髓（Ｔ８）无显著变化（Ｐ＞０．０５）;颈脊髓背角ＳＰＬＩ有增强趋势（０．０５＜Ｐ＜０．１）;ＰＡＧ中ＭＥＬＩ减弱,腹外侧部３０ｍｉｎ组比６０ｍｉｎ组变化更大（Ｐ＜０．０５）。ＰＡＧ中ＭＥＬＩ与脊髓背角ＳＰＬＩ变化的时相关系提示福尔马林致痛引起的脊髓背角Ｐ物质的增多可能与ＰＡＧ中甲啡肽及阿片受体活动有关。     

急性低氧诱导大鼠皮层和海马区自由基增殖

实验模型采用麻醉大鼠人工吸入１０．５％－１１．０％氮氧混合气体（相当于５０００ｍ海拔高度），于低氧前５ｍｉｎ由股静脉注入α－苯基－Ｎ－叔丁基甲亚胺－Ｎ－氧化物（ＰＢＮ，α－ｐｈｅｎｙｌ－ｔｅｒ－ｂｕｔｙｌｎｉ－ｔｒｏｎｅ）。结果发现低氧１５ｍｉｎ后，皮层和海马ＰＢＮ－自旋加合物电子自旋共振（ＥＳＲ，ｅｌｅｃｔｒｏｎ ｓｐｉｎ ｒｅｓｏｎａｎｃｅ）信号强度显著大于常氧对照组（ｎ＝５，Ｐ〈０．０１）。     

肿瘤坏死因子介导病理性氧供应依赖性的实验研究

本研究采用抗肿瘤坏死因子单克隆抗体预先保护实验动物,用ＥＬＩＳＡ法测定血浆中肿瘤坏死因子（ＴＮＦ）浓度,藉以考察ＴＮＦ在内毒素诱导病理性氧供应依赖性（ＰＯＳＤ）模型中是否起介导作用。结果表明,（１）ＴＮＦ浓度内毒素组显著高于对照组,抗体保护组显著低于无关抗体组（Ｐ＜０．０１）。（２）在Ｖｏ＿２－Ｄｏ＿２关系中,抗体保护组可清楚地分为依赖段和非依赖段两部分,其临界氧运输量和合并氧提取率分别为１０．８０±３２１ｍｌ·ｍｉｎ￣（－１）·ｋｇ￣（－１）和０．６９０,而无关抗体组则只有依赖段,合并氧提取率为０．４０８,显著低于抗体保护组。从而证明,ＴＮＦ在内毒素所致的ＰＯＳＤ现象中起介导作用。     

α受体激动对绵羊心肌瞬时性内向离子流的影响

用乙酰毒毛旋花子甙元（ＡＳ）０．０５μｍｏｌ／Ｌ诱发绵羊心浦肯野纤维产生稳定的瞬时性内向离子流（Ｉｔｉ）,用普萘洛尔０．５μｍｏｌ／Ｌ阻断β受体,观察α受体激动剂苯肾上腺素（ＰＥ）０．３,１．０μｍｏｌ／Ｌ对Ｉｔｉ幅值与时程的影响。ＰＥ１．０μｍｏｌ／Ｌ灌流２０,５０ｍｉｎ时Ｉｔｉ幅值分别由对照值１２．８±１．９ｎＡ减小至１０．７±１．２ｎＡ（ｎ＝５,Ｐ＜０．０５）与９．６±１．９ｎＡ（ｎ＝５,Ｐ＜０．０１）;ＩｔｉＤ５０时程分别由对照值１４５±２４．４ｍｓ延长至１８３．３±２８．１ｍｓ（ｎ＝５,Ｐ＜０．０５）与２０７．５±３４．２ｍｓ（ｎ＝５,Ｐ＜０．０１）,ＰＥ对Ｉｔｉ的抑制作用呈剂量依赖性与时间依赖性。Ｉｔｉ到达峰值的时间和回复到基线的时间都延长,提示ＰＥ作用下Ｉｔｉ通道动力学发生了变化。如果在β受体激动剂异丙肾上腺素（ＩＳＯ）１．０μｍｏｌ／Ｌ增强Ｉｔｉ的基础上,ＰＥ１．０μｍｏｌ／Ｌ灌流１０ｍｉｎ,对Ｉｔｉ幅值的抑制及时程的延长作用更显著,Ｉｔｉ幅值由对照值１５．６±３．２ｎＡ减小到１０．３±２．２ｎＡ;ＩｔｉＤ５０由９２．５±１４．３ｍｓ延长到１３２．５±３６．０ｍｓ（ｎ＝５,Ｐ＜０．０１）。     

急性低氧对大鼠血粘度,红细胞变形能力和左心室功能的影响

健康ＳＤ雄性大鼠,体重２５０—３００ｇ,麻醉、气管插管,用人工呼吸机经气袋供气,自发吸入氧浓度为９％的氧氮混合气,用ＳＭＵＰ－ＰＣ生物信号处理系统处理左心室功能。结果：（１）急性低氧经动脉血气分析可见ＰａＯ２下降（Ｐ＜０．０１）,ｐＨ值升高（Ｐ＜０．０５）,ＰａＣＯ２稍下降（Ｐ＞０．０５）,左心室功能各指标如ＬＶＰ,ＨＲ,Ｖｍｐ,±ｄｐ／ｄｔｍａｘ,Ｖｃｅ４０,Ｖｍａｘ,Ｌ０、等均下降;血液流变学指标如全血粘度（高、低切值及其还原值）升高,红细胞滤过指数（ＩＦ）升高;复氧后上述各指标恢复正常。（２）静脉注射心得安（０．５ｍｇ／Ｋｇ）后,使急性低氧诱发的左心室功能各指标更加明显下降,而血液流变学各值不再明显上升;静脉注射酚妥拉明（３ｍｇ／Ｋｇ）后,使急性低氧诱发的血液流变学各值上升不明显。（３）石炭酸破坏双侧颈动脉窦区后也可致低氧诱发的左心室功能各指标进一步下降,而血液流变学指标也不再明显上升。结果提示：急性低氧可引起左心室功能下降和全血粘度升高,红细胞变形能力降低,复氧后可恢复;交感神经活动及颈动脉窦区化学感受性反射可能对抗低氧诱发的左心室功能的下降,促进血粘度的升高。     

白斑狗鱼血液生理、生化指标值和血液流变学常值的研究

作者于１９９５年１１月在新疆额尔其斯河水系进行了调查，首次测试了白斑狗鱼血液生理，生化常值和血液流为学常值，结果发现，白斑狗鱼的全血粘度和血浆粘度均比茯它鱼类高，影响白斑狗鱼全血粘度的主要因子有红细胞压积（ＨＣＴ），血红蛋白（Ｈｂ），红细胞聚集性Ａ１，Ａ２，血浆粘度（η）而影响其血浆粘度的主要因子为血清胆固醇（ＣＨＯ），白斑狗鱼血清白蛋白（ＡＰ）与血清球蛋白（ＧＰ）之比为０．５７。     

高原红细胞增多症患者红细胞二磷酸甘油酸和氧亲和力变化的探讨

在海拔４３００ｍ地区,对１８名移居汉族、２４名世居藏族和２１名高原红细胞增多症（ＨＡＰＣ）患者测定了２,３—二磷酸甘油酸（２,３—ＤＰＧ）和肺通气功能,并进行了血气分析。结果显示：ＨＡＰＣ患者的全血和红细胞内２,３—ＤＰ６浓度均显著高于健康组,但世居、移居健康组之间无明显差异。ＨＡＰＣ组的红细胞２,３—ＤＰＧ和Ｐｄｏ＿２呈显著负相关（ｒ＝—０．７７１,Ｐ＜０．０１）,而在健康组无显著相关（ｒ＝—０．２６,Ｐ＞０．０５）。ＨＡＰＣ组与健康组相比,ｐＨ、Ｐａｏ＿２和Ｓａｏ＿２降低,Ｐａｃｏ＿２和肺泡动脉氧分压差增高。ＨＡＰＣ病人Ｐ＿（５０）为３．７５±０．６６ｋＰａ,健康组为３．４０±０．１２ｋＰａ（Ｐ＜０．０５）,Ｐ＿（５０）与２,３－ＤＰＧ呈正相关（ｒ＝０．５９２,Ｐ＜０．０５）。ＨＡＰＣ组最大呼气中段流量和５０％肺活量最大呼气量明显低于健康组（Ｐ＜０．０１）。本研究提示：①ＨＡＰＣ患者的低氧血症可能与血中２,３－ＤＰＧ浓度过高有关;②轻度肺功能异常亦可促使红细胞进一步增多。     

缺氧—再给氧刺激培养的脑微血管内皮细胞表达细胞间粘附分子—1

在缺氧－再给氧条件下,观察了体外分离培养的大鼠脑微血管内皮细胞表面粘附分子ＩＣＡＭ－１的表达及中性粒细胞与内皮细胞粘附作用的改变。结果表明,单纯缺氧１０ｈ不引起内皮细胞ＩＣＡＭ－１的上调,再给氧６ｈＩ－ＣＡＭ－１的表达升高（Ｐ＜０．０１）,再给氧１２ｈ表达量增加了１００％（Ｐ＜０．０１）,此时中性粒细胞与内皮细胞的粘附作用也明显增强（Ｐ＜０．０１）。缺氧前用盐酸川芎嗪（２ｍｇ／ｍｌ）预处理内皮细胞可阻断ＩＣＡＭ－１的表达（Ｐ＜０．０１）,同时也可降低ＰＭＮ与内皮细胞的粘附（Ｐ＜０．０５）。结果提示,脑微血管内皮细胞在缺氧－再给氧刺激下可自身调节Ｉ－ＣＡＭ－１的表达,为中性粒细胞与内皮细胞的粘附提供特异的结合位点。     

Absence of adrenergic red cell pH and oxygen content regulation in American eel (Anguilla rostrata) during hypercapnic acidosis in vivo and in vitro

Summary American eels (Anguilla rostrata) were exposed to acute (30 min) external hypercapnia (1% CO₂ or 5% CO₂ in air) in order to assess the involvement of circulating catecholamines in regulating red blood cell (RBC) pH and oxygen content during whole blood acidosis. Plasma adrenaline levels increased approximately 5-fold during severe hypercapnia yet absolute levels remained below 1.0 nM; plasma noradrenaline levels were unchanged. Both RBC pH and oxygen bound to haemoglobin ([O₂]/[Hb]) conformed to in vitro relationships with whole blood pH (pHe) indicating absence of regulation during hypercapnia in vivo. Pre-treatment of eels with - or -adrenoceptor antagonists, phentolamine or propranolol was without effect on RBC pH or [O₂]/[Hb] during hypercapnia. Further, intra-arterial injection of adrenaline (final plasma concentration=134 nM) or noradrenaline (final plasma concentration = 34 nM) into hypercapnic eels 5 min prior to blood sampling did not modify any measured blood variable RBC nucleoside triphosphate (NTP) levels, RBC pH and [O₂]/[Hb]. In vitro, the application of adrenaline or noradrenaline to eel RBC's during graded normoxic hypercapnia or hypoxic hypercapnia (noradrenaline only) did not affect RBC pH significantly. RBC NTP levels were depressed by noradrenaline in vitro but only during hypoxic hypercapnia.The results demonstrate adrenergic insensitivity of eel RBC's in vivo even under conditions (acidosis, hypoxemia) known to enhance catecholamine-mediated RBC responses in other species. We conclude that the American eel has no capacity to regulate RBC pH during hypercapnia and consequently [O₂]/[Hb] is reduced in accordance with the in vitro Root effect.     

Thrombocyte aggregation in the plasma and whole blood and ATP secretion during hypoxia in cats

Platelet aggregation in platelet rich plasma and whole blood, as well as ATP secretion were studied during hypoxia in cats. A significant inhibition of collagen-induced aggregation in plasma and whole blood and ADP-induced aggregation in plasma alone with a parallel decrease of platelet ATP secretion were demonstrated. The data obtained are indicative of an important modulatory role of eicosanoids in the vascular wall interaction during hypoxia with a possible involvement of thromboxane A2.     

急、慢性缺氧对大鼠凝血机能的影响

本文讨论了实验性缺氧对大鼠凝血机能产生的影响。实验结果表明,大鼠在模拟8000米高度两小时后,血小板凝聚性、血小板因子3活性明显增加,纤溶活性下降,同时,纤维蛋白原含量和因子X也明显下降。大鼠在模拟7000米经36天间歇性慢性缺氧,血小板计数、血小板凝聚性,血小板因子3活性、纤维蛋白原含量、因子X活性均显著增加,部分凝血活酶时间缩短、纤溶活性下降,明显地出现凝血增强的趋势。本文还讨论了抗缺氧药物复方党参、异叶青兰对人鼠急性缺氧时凝血机能的影响。     

Adrenaline in various organs of the rat: its origin, location and diurnal fluctuation

In order to examine the origin and location of adrenaline in peripheral organs of mammals, adrenaline and noradrenaline were measured in several organs of the rat after adrenalectomy, guanethidine treatment and imipramine injection. One week after bilateral adrenalectomy, adrenaline disappeared almost completely from the heart, spleen and submaxillary gland. Chronic administration of guanethidine caused decreases in both noradrenaline and adrenaline in the peripheral organs. Injection of imipramine induced a reduction of adrenaline concentration in the spleen and submaxillary gland. It is considered that adrenaline in the peripheral organs of mammals is mostly derived from the adrenal gland and that circulating adrenaline is taken up by sympathetic nerve endings in the organs. The adrenaline content of the peripheral organs increased after electric foot-shock and changed according to the time of day. The peak of the circadian rhythm appeared about 6 hours after the peak of the urinary adrenaline rhythm. These findings suggest that adrenaline in body organs plays some role in the responses of the sympathetic nervous system to stressful conditions or even to daily activities.     

Thrombocyte aggregation in plasma and whole blood during hyperventilation (hypocapnia) in cats

Platelet aggregation in platelet rich plasma (PRP) and whole blood was simultaneously studied in acute experiments on cats in hypocapnic conditions. ADP-induced aggregation increase was determined in PRP and whole blood. Contradictory results were obtained during platelet aggregation induced by collagen and arachidonic acid: increased aggregation in PRP and decreased aggregation in whole blood. The data obtained suggest that ADP is a risk factor for the onset of intravascular thrombosis.     

Platelet inhibition by nitrite is dependent on erythrocytes and deoxygenation

BACKGROUND: Nitrite is a nitric oxide (NO) metabolite in tissues and blood, which can be converted to NO under hypoxia to facilitate tissue perfusion. Although nitrite is known to cause vasodilation following its reduction to NO, the effect of nitrite on platelet activity remains unclear. In this study, the effect of nitrite and nitrite+erythrocytes, with and without deoxygenation, on platelet activity was investigated. METHODOLOGY/FINDING: Platelet aggregation was studied in platelet-rich plasma (PRP) and PRP+erythrocytes by turbidimetric and impedance aggregometry, respectively. In PRP, DEANONOate inhibited platelet aggregation induced by ADP while nitrite had no effect on platelets. In PRP+erythrocytes, the inhibitory effect of DEANONOate on platelets decreased whereas nitrite at physiologic concentration (0.1 μM) inhibited platelet aggregation and ATP release. The effect of nitrite+erythrocytes on platelets was abrogated by C-PTIO (a membrane-impermeable NO scavenger), suggesting an NO-mediated action. Furthermore, deoxygenation enhanced the effect of nitrite as observed from a decrease of P-selectin expression and increase of the cGMP levels in platelets. The ADP-induced platelet aggregation in whole blood showed inverse correlations with the nitrite levels in whole blood and erythrocytes. CONCLUSION: Nitrite alone at physiological levels has no effect on platelets in plasma. Nitrite in the presence of erythrocytes inhibits platelets through its reduction to NO, which is promoted by deoxygenation. Nitrite may have role in modulating platelet activity in the circulation, especially during hypoxia.     

Effect of a fall of blood pressure on the release of catecholamines in the hypothalamus

The posterior hypothalamus of anaesthetized cats was superfused through a push-pull cannula and the release of endogenous catecholamines was determined in the superfusate which was continuously collected in 15 min periods. Fall in blood pressure elicited by nitroprusside or bleeding led to an increased rate of release of noradrenaline, adrenaline and dopamine in the hypothalamus. Transection of the brain causal to hypothalamus greatly reduced the rate of resting release of the catecholamines and abolished the enhancing effects of bleeding and nitroprusside. Determination of the catecholamines in samples which were collected in 90 s periods suggested a different pattern of release of the three catecholamines. Further shortening of the collection period (10 s) showed that the fall in blood pressure immediately increased the release of dopamine, while the rates of release of noradrenaline and adrenaline were increased gradually. Hypotension did not influence the rates of release of the catecholamines in the anterior hypothalamus. It is concluded that dopamine, adrenaline and noradrenaline systems of the hypothalamus are involved in the regulation of the arterial blood pressure. The different patterns of release might indicate that dopamine exerts a different function from those of noradrenaline and adrenaline in the normalization of the blood pressure after acute hypotension.     

Release of histamine and adrenaline in vivo following intravenous administration of neurotensin

Plasma histamine levels of rats anesthetized with pentobarbital sodium were significantly increased by intravenous administration of neurotensin (NT, 1 nmole/kg) with the maximum effect at 3 min, and a return to the initial levels in 20 min. Treatment of animals with compound 48/80 or disodium cromoglycate completely inhibited the elevation of histamine level by NT, however, treatment with reserpine or diphenhydramine and adrenalectomy did not affect the elevation. Plasma adrenaline levels increased transiently 1 min after NT injection, and adrenalectomy and treatment with compound 48/80 or diphenhydramine markedly reduced the elevation of adrenaline levels after NT injection. Plasma levels of noradrenaline were unchanged upon NT injection. These results provide direct evidence of the release of endogenous histamine and adrenaline following NT administration, and suggest the contribution of these amines to the NT-induced triphasic blood pressure responses (the first depressor, second pressor and third depressor responses) reported previously.     

游泳训练对高血压大鼠血压及血栓前状态分子的影响*

目的: 观察10周游泳训练对自发性高血压大鼠(SHR)血压及血栓前状态分子血管性血友病因子(vWF)、组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制物(PAI-1)的影响。方法: 选取10周龄雄性SHR(18只),随机分为对照组(8只)和训练组(10只),SHR训练组进行5次/周,每次60 min,共持续10周的无负重游泳训练,期间每2周测定大鼠血压。10周训练后,分别测定两组SHR血小板聚集率、血浆vWF、t-PA和PAI-1。结果: 与对照组相比,训练组SHR经4周游泳训练后,血压显著下降(P＜0.05),经10周游泳训练后,血压、血小板聚集率、血浆vWF水平、PAI-1活性显著降低(P＜0.01),血浆t-PA活性显著提高(P＜0.01)。结论: 适宜游泳训练能有效平抑(或改善)SHR的血压,坚持4周训练即可产生显著的作用,还可明显改善SHR血栓前状态,预防高血压血栓性并发症。     

Circulating catecholamines in acute asthma.

Plasma catecholamine concentrations were measured in 15 patients (six male) aged 14-63 years attending the casualty department with acute severe asthma (peak expiratory flow 27% (SEM 3%) of predicted). Nine patients were admitted and six were not. The plasma noradrenaline concentration, reflecting sympathetic nervous discharge, was two to three times normal in all patients and was significantly higher in those who required admission compared with those discharged home (mean 7.7 (SEM 0.6) v 4.7 (0.5) nmol/l (1.3 (SEM 0.1) v 0.8 (0.08) ng/ml); p less than 0.001). Plasma adrenaline concentration, however, was not increased in any patient. This surprising failure of the plasma adrenaline concentration to increase during the stress of an acute attack of asthma was unexplained and contrasts with the pronounced rise in plasma adrenaline and noradrenaline concentrations in acute myocardial infarction, heart failure, and septicaemia. The failure of plasma adrenaline concentration to increase in acute asthma is unlikely to be explained by adrenal exhaustion, but it may be another example of impaired adrenaline secretion in asthma.