The effect of experimental frost-bite on the responses of the rabbit ear-artery to adrenergic and electrical stimulation

The aim of the present investigation was to study the effect of sub-zero temperatures on the adrenergic activated, smooth muscle-contraction of a peripheral blood-vessel. The central ear-artery of the rabbit was used for this purpose. The artery was stimulated to contract in vitro by activation of phentolamine sensitive, post-junctional, a-adrenoceptors by use of noradrenaline, or by noradrenaline released from noradrenergic nerves in the blood-vessel following electrical field stimulation. The effect of freezing the tissue in vivo for 15 min at sub-zero temperatures (–4, - 6 and – 9 ^oC) was studied in vitro. Exposure to – 4 and – 6 ^oC did not alter the apparent affinity (ED₆₀) of noradrenaline significantly, when measured immediately, or 2 or 6 days after exposure. The maximal response to noradrenaline was reduced by approximately 54, 74 and 100% following exposure to – 4 , – 6 and – 9 ^oC, respectively. The response was completely restored after 2 and 6 days of regeneration in vivo following exposure to – 6 ^oC, whereas the response after exposure to – 9 ^oC was restored by only about 8 and 30% after 2 and 6 days regeneration, respectively. The maximal response to electrical field stimulation, which was completely inhibited by tetrodotoxin and phentolamine, was reduced by approximately 92% after exposure for 15 min to –4 and – 6 ^oC, while it was completely inhibited after exposure to – 9 ^oC. The response was restored by only 15–20% following 2 and 6 days in vivo after exposure to – 6 ^oC. No regeneration of the contraction induced by the electrical stimulation was observed after 2 or 6 days following exposure to –9 ^oC. The results of the present study suggest that noradrenergic nerves in the central ear-artery of the rabbit are more sensitive to subzero temperatures than are the post-junctional, noradrenergic α-receptors and the smooth muscle of the blood-vessel. The damage induced by freezing appeared to be both time and temperature dependent and there was only limited restoration of the nervous function 6 days after severe freezing.     

Dual action of angiotensin II on coronary resistance in the isolated perfused rabbit heart

Summary We studied the functional role of angiotensin II (AII) receptor subtypes and vasodilatory endothelial autacoid release in response to AII in isolated perfused rabbit hearts. AII infusion induced biphasic changes in coronary perfusion pressure (CPP): an initial increase was followed by a decrease until a plateau was reached. At higher concentrations of AII (10 nmol/l) this plateau phase was lower than the initial CPP level. AII infusion elicited inverse changes in peak left ventricular pressure (LVP): coronary constriction was associated with a transient decline, and during the plateau phase LVP was clearly increased. AII also moderately augmented prostacyclin (PGI₂) release from the coronary vascular bed. The AII-induced changes in CPP, LVP, and PGI₂ release were effectively inhibited by the AT₁ receptor subtype antagonist ICI D8731 (30 nmol/l), but not by the AT₂ receptor antagonist CGP 42112 (30 nmol/l). The adenosine A₁ receptor antagonist 8-phenyltheophylline (0.1 mol/l) attenuated the decline in CPP following the constriction phase without affecting the changes in LVP during AII infusion. The cyclooxygenase inhibitor diclofenac (1 mmol/l) had no effect on the AII-induced changes in CPP, whereas the nitric oxide-synthase inhibitor N^G-nitro-L-arginine (30 mol/l) markedly potentiated the vasoconstriction but was without effect on the plateau phase of the response. In contrast to AII, the thromboxane analogue U46619 elicited sustained increases in CPP which were associated with slight decreases in LVP.In conclusion, AII induced a biphasic pressor response in the rabbit coronary vascular bed consisting of a transient vasoconstriction followed by a dilatation especially at higher concentrations of AII, an effect which was independent of the endothelial autacoids nitric oxide and PGI₂. The AII-induced dilatation probably reflected rapid desensitization of the coronary arterial smooth muscle to the constrictor effect, and the concomitant accumulation of vasodilatory metabolites such as adenosine, generated during the positive inotropic action of AII. All the effects of AII in the rabbit heart appeared to be mediated via the AT, receptor subtype localized on coronary endothelial and smooth muscle cells, as well as on cardiomyocytes.On leave from the Department of Biomedical Sciences, University of Tampere, P.O. Box 607, FIN-33101 Tampere, FinlandCorrespondence to: I. Pörsti     

家兔肝缺血再灌注损伤脂质过氧化的动态变化及川芎嗪干预的机制

目的：观察肝缺血再灌注损伤时脂质过氧化的动态变化和川芎嗪的干预作用,并探讨其机制。方法：复制健康家兔肝缺血再灌注损伤模型,随机分为对照组（n=10）和川芎嗪组（n=10）。连续观察缺血前、缺血25min、再灌注25min、60min及120min时血浆中丙二醛（MDA）含量、超氧化物歧化酶（SOD）、黄嘌呤氧化酶（XO）及谷丙转氨酶（ALT）活性的动态变化,并观察川芎嗪对不同时限上述指标的影响。结果：随缺备再灌注时间的延长,对照组的MDA、XO和ALT呈阶梯式的明显升高,SOD呈逐渐显降低的变化;川芎嗪组的上述指标在再灌注的各时限与对照组比较差异均有显或非常显性意义（P＜0.05或P＜0.01）。结论：肝缺血再灌注损伤时脂质过氧化反应呈进行加重的变化;川芎嗪能抑制氧自由基的生成,增强对氧自由基的清除,从而起着良好的抗脂质过氧化作用。     

葛根素对兔脊髓缺血再灌注损伤的保护作用

目的：研究葛根素对兔脊髓缺血再灌注损伤的作用。方法：20只雄性新西兰大白兔随机分成缺血组（A组,n=10）及葛根素组（B组,n=10),夹闭腹主动脉肾下段20min,建立兔脊髓腰尾段血模型,B组于夹闭前10min静脉注射葛根素30mg.kg^-1,A组则静脉注射生理盐水,测定夹闭前、后及再灌注后血浆中丙二醛（MDA）浓度及超氧化物歧化酶（SOD)活性,再灌注4,8,12,24及48h分别对动物后肢运动功能评分;再灌注48h后,处死动物,制作切片,观察其组织病理变化。结果缺血及再灌注后B组MDA值明显低于A组（P＜0．05）,而OD活性明显高于A组（P＜0．05）;再灌注后4,8,12,24及48h时的神经功能评分B组明显高于A组（P＜0．05）;光镜下,与A组相比,B组脊髓组织损伤显著减轻,形态基本正常的前角细胞较多。结论葛根素对兔脊髓缺血再灌注损伤有显著的保护作用。     

肾炎灵冲剂对家兔慢性肾小球肾炎的作用

目的 :观察肾炎灵冲剂对家兔慢性肾小球肾炎的作用。方法 :用大鼠肾小球基底膜和弗氏佐剂 ,给家兔注射 ,复制出慢性肾小球肾炎模型。给肾炎灵冲剂 ,观察尿蛋白、血清尿素氮、肌酐、血清白蛋白、球蛋白及肾组织的病理学改变。结果 :肾炎灵冲剂可剂量依赖性地降低尿蛋白(P<0 .0 5)、血清尿素氮 (P<0 .0 5)、肌酐 (P<0 .0 5)的水平 ,提高血清白蛋白的水平 (P<0 .0 5) ,减轻肾小球病变。结论 :肾炎灵冲剂对家兔慢性肾小球肾炎具有保护作用     

胎兔骨髓基质前成骨细胞的培养及鉴定

为了证实体外培养的胎兔骨髓基质骨祖细胞具有成骨细胞系特征。采用胎兔长管骨骨髓细胞 ,加入 DMEM培养 ,传代四代后 ,用活体相差显微镜、透射电镜、组织化学染色、免疫组化等方法进行观测。结果显示体外培养的基质细胞具有成骨细胞系特征。提示胎兔骨髓基质骨祖细胞 ,可以作为修复骨缺损的种子细胞。     

低温盐水局部灌注对脊髓缺血损伤的保护作用

目的 探讨低温生理盐水脊髓灌注对兔主动脉阻断致脊髓缺血的保护作用。方法 ２０只健康成年新西兰白兔,阻断肾动脉水平腹主动脉６０ｍｉｎ建立兔脊髓缺血损伤模型,随机分２组（ｎ＝１０）,Ａ组：缺血对照;Ｂ组：缺血＋脊髓低温盐水灌注。结果 （１）各组血压心率无明显差别;（２）Ｂ组兔下肢功能恢复良好,而Ａ组瘫痪;（３）脊髓形态学显示Ａ组中央灰质聚集性坏死,巨噬细胞浸润,尼氏体消失,核仁模糊,Ｂ组未见Ａ组的形态     

五种生长因子mRNA在兔角膜中的表达

目的 了解ＥＧＦ、ＴＧＦ－α、ｂＦＧＦ、ＴＧＦ－β１和ＰＤＧＦ在兔角膜上皮和基质中的表达情况,探讨其在角膜伤口愈合中的作用。方法 应用原位核酸分子杂交方法检测兔角膜上皮和基质中ＥＧＦ、ＴＧＦ－α、ｂＦＧＦ、ＴＧＦ－β１和ＰＤＧＦ ｍＲＮＡＲ的表达。结果 ＥＧＦ、ＴＧＦ－α和ＰＤＧＦ ｍＲＮＡ仅在正常角膜上此细胞层表达,基质中未见表达;ｂＦＧＦ和ＴＧＦ－β１ ｍＲＮＡ在正常角膜伤口和基质中均有表达。     

兔体外循环对胃泌素及其受体的影响

目的　研究体外循环 (CPB)过程中胃泌素及胃泌素受体的释放对胃液 p H值的影响 .方法　采用兔 CPB模型 ,分别测定 CPB过程中胃液的 p H值 ,胃液及血清中胃泌素质量浓度 ,并通过原位杂交的方法检测胃泌素受体 m RNA在胃肠道粘膜中的表达 .结果　 CPB过程中胃液的 p H值 (2 .2 1±0 .2 2 )与血液的 p H值 (7.40± 0 .15 )呈明显相关性 (P<0 .0 1) ,而且胃液的 p H值随 CPB时间增加 ,CPB组 (2 .2 1±0 .2 2 )较对照组明显降低 (5 .30± 0 .17,P<0 .0 1) .胃液及血清中胃泌素质量浓度随体外循环时间延长较对照组明显增高 .胃泌素受体 m RNA的表达量 (0 .43± 0 .0 4) %随 CPB时间增加较对照组明显增加 (0 .2 7± 0 .0 8) % ,(P<0 .0 1) .结论　 CPB过程中随时间延长 ,胃液及血清中胃泌素浓度增高 ,胃液 p H值降低及胃泌素受体 m RNA的表达量增高使胃粘膜处于高酸环境中 ,是 CPB术后发生胃肠道并发症的潜在的危险因素     

同浓度不同用量的乙醇对家兔左心室内压的影响

采用静脉内注射 5 0 %乙醇的方法 ,观察同浓度不同用量乙醇对家兔左心室内压的影响。结果显示给予乙醇后 ,大多数左心室内压降低 ,个别左心室内压不变。随着乙醇量的增加 ,左心室内压下降愈明显 (P <0 .0 5 )。提示高浓度乙醇可降低左心室内压 ,由于个体差异 ,乙醇对左心室内压的效应也略有不同