干扰素2-2b致功血2例

干扰素a－2b是国内首先引进的抗病毒药物，至今、为提高疗效国内外学者仍在努力探索剂量和疗程、同时随量的增大付作用也逐步增多、早期付作用可在用药中克服而中晚期付作用除增加病人的痛苦也会发生不可逆的后果被迫停药。现有二例丙型肝炎因用干扰素a－Zb出现月经周期紊乱、功血报告如下：例1，女、38a．于1994年6月患急性丙型肝炎（丙），无输血和手术史。经二月住院治疗症状稳定、阳性体征消失，肝功能恢复正常，但抗-HCV阳性、HCyRNA阳性。8月始采用IFNα-2b、300万u、肌注、隔日一次，用药周余中有流感样综合征和肌肉酸痛、坚持…     

2型糖尿病合并胆结石2例

1临床资料例1 :男,74岁,以头晕,行走不稳2天入院。有10年的2型糖尿病病史。门诊行头颅CT检查示:腔隙性脑梗死,查体:神志清,精神差,双肺呼吸音清晰,心音A2>P2 ,心率92次/分,心律齐,各瓣膜区未闻及杂音。腹平软,无压痛,莫菲氏征阴性,按腔隙性脑梗死治疗。住院后第6日出现高热,体温达39℃,寒颤,无恶心、呕吐,仍无腹痛及腹部压痛,无黄染,寻找高热原因,做腹部B超,发现胆结石、胆囊化脓。例2 :男性,81岁,以纳差10天入院,有15年2型糖尿病病史。门诊头颅CT报多发性腔隙性脑梗死,入院查体:神志清,精神差,双肺呼吸音粗,心率89次/分,A2>P2 ,心律齐,…     

HIVl+2高值假阴性2例

艾滋病在中国的流行己进入快速增长时期,随着艾滋病病毒感染者的不断增加,以机会性感染而进入综合性医院就医的患者日益增多.     

藻酸双酯钠治疗儿童原发性肾病综合征31例

应用藻酸双酯钠(PSS)治疗31例原发性肾病综合征(PNS)患儿(男19例,女12例;年龄6.3±S2.0a),剂量1-2mg/(kg·d)。另10例患儿用泼尼松2mg/(kg·d)治疗作为对照。治疗3mo临床均有效。PSS组出现血液流变学指标改善及胆固醇、甘油三酯和载脂蛋白B_(100)水平显著下降。提示PSS治疗儿童PNS有效。     

Pharmacological studies on the TXA2 synthetase inhibitor (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoic acid (OKY-046)

The effects of (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoic acid (OKY-046) on thromboxane A2 (TXA2) synthetase in vitro and on experimental animal models of sudden death and cerebral infarction were studied. IC50 values of OKY-046 for the TXA2 synthetase of human, rabbit, dog and guinea pig washed platelets were 0.004, 0.004, 0.26 and 2.4 microM, respectively. OKY-046 at concentrations up to 1 mM, however, did not inhibit prostacyclin (PGI2) synthetase from bovine aorta microsomes or cyclooxygenase and PGE2 isomerase from sheep seminal vesicle microsomes. Similarly, platelet 12-lipoxygenase was not affected by OKY-046. Evidence for a re-direction of arachidonate metabolism from thromboxane synthesis toward PGI2 synthesis was obtained using rat peritoneal cells. Namely, OKY-046 increased PGI2 production accompanied by an inhibition of TXA2 production at a concentration of more than 1 microM. OKY-046 at a dose of 0.1 mg/kg (i.v.) in dogs inhibited the aortic and mesenteric arterial contraction of rabbit induced by the addition of arachidonate to extracorporated blood of the dogs. OKY-046 at a dose of 0.3 mg/kg (i.v.) prevented the arachidonate-induced sudden death and also decreased the incidence of cerebral infarction induced by injection of arachidonate into the internal carotid artery in rabbits. Aspirin also decreased the incidence of cerebral infarction at a dose of 30 mg/kg (i.v.). These results suggest that OKY-046 may be valuable for the treatment of cerebrovascular and cardiovascular diseases associated with vasoconstriction and thrombosis due to TXA2.     

维吾尔族肾病综合征患儿他克莫司全血谷浓度监测分析

目的监测维吾尔族原发性肾病综合征(PNS)患儿他克莫司全血谷浓度并分析相关临床数据,以期为维吾尔族PNS患儿个体化应用他克莫司提供依据。方法对接受他克莫司治疗的70例维吾尔族PNS患儿的血药浓度、生化检验指标及合并用药进行回顾性调查分析,探讨他克莫司全血谷浓度与临床疗效的相关性,根据临床疗效分为完全缓解组(CR组)、部分缓解组(PR组)、未缓解组(NR组)。结果CR组剂量标准化谷浓度为(2.95±1.17)ng/mL/[mg/(kg·d)]、PR组剂量标准化谷浓度为(4.22±2.92)ng/mL/[mg/(kg·d)]、NR组剂量标准化谷浓度为(1.72±1.43)ng/mL/[mg/(kg·d)],三组比较差异有统计学意义(P<0.05),但三组给药剂量差异无统计学意义(P>0.05)。他克莫司治疗维吾尔族PNS患儿的缓解率为75.71%。结论他克莫司全血谷浓度与药物剂量及相关药物代谢基因相关,在全血谷浓度达5~10 ng/mL时,可达到满意的治疗效果。     

Effects of cadmium on platelet thromboxane and vascular prostacyclin production

The interaction between cadmium and arachidonic acid metabolism in platelets and vascular tissue was evaluated, in ex vivo experiments, by determining the thromboxane levels in serum and the prostacyclin production by the aortic walls in cadmium-treated rabbits. Cadmium given parenterally for 4 days in doses of 0.25, 0.5, and 1 mg/kg/day produced a dose-dependent increase of serum thromboxane B₂ levels. The effect of cadmium on prostacyclin release was biphasic. The metal, in doses of 0.25 and 0.5 mg/kg/day, inhibited prostacyclin production in an inverse ratio with administered doses. At the higher dose (1 mg/kg/day) cadmium caused an increase in prostacyclin formation. The present results suggest that the vascular action of cadmium is due, in part at least, to the involvement of the vascular-wall and platelet prostaglandin systems.     

Effect of COX-1/COX-2 inhibition versus selective COX-2 inhibition on coronary vasodilator responses to arachidonic acid and acetylcholine

The effect of a nonselective COX-1/COX-2 inhibitor, naproxen, was compared with a COX-2-selective inhibitor (SC-58236) on coronary vasodilatory responses in the anesthetized dog. Coronary vasodilation was induced by direct intracoronary injection of acetylcholine (ACH) and arachidonic acid (AA) in control animals and in those treated with either naproxen (1, 3, or 10 mg/kg p.o. 24 h prior to the experiment) or SC-58236 (1, 5, or 15 mg/kg p.o. 24 h prior to the experiment). Naproxen, at 10 mg/kg, significantly attenuated the AA-induced vasodilation (prostacyclin dependent) with no effect on ACH-induced vasodilation (nitric oxide dependent). SC-58236 failed to attenuate either AA- or ACH-induced vasodilation. Ex vivo assays were utilized to establish inhibition of COX-2 (lipopolysaccharide-stimulated prostaglandin E2 formation) and COX-1 (serum thromboxane B2) in blood taken from dogs administered 1, 3, or 10 mg/kg naproxen or 15 mg/kg SC-58236. Naproxen (3 and 10 mg/kg) and SC-58236 (15 mg/kg) markedly reduced the lipopolysaccharide-induced prostaglandin E2 formation, whereas SC- 58236 (15 mg/kg) had no effect on serum thromboxane B2. Naproxen significantly reduced thromboxane B2 at all three doses studied. Furthermore, naproxen (10 mg/kg p.o.) significantly inhibited the AA-induced platelet aggregation (thromboxane B2 dependent), whereas SC-58236 had no effect. Collectively, these results demonstrate that SC-58236 is selective for COX-2, while naproxen is a nonselective inhibitor. These data also suggest that vasodilatory responses to AA in the dog are primarily COX-1 dependent. Selective COX-2 inhibition does not affect either prostacyclin or nitric oxide mediated vasodilation in the canine coronary circulation.     

三七总皂甙对大鼠颈内动脉、肠系膜前动脉血流动力学的作用比较

三七总皂甙(PNS)30～150mg·kg~(-1)iv使麻醉SD大鼠的MBP.ICAR.MAR下降11％～19％.14％～27％,23％～39％;使MBF增加16％～51％;PMS100.150mg·kg~(-1)使ICBF先增加25％后减少8％～17％.维拉帕米(Ver)150μg·kg~(-1)iv除不使ICBF减小外,也表现出类似效应。表明PNS,Ver对颈内动脉的扩张作用弱于对肠系膜前动脉的扩张作用。具有明显的作用选择性。     

Nifedipine reduces arrhythmias but does not alter prostanoid release during coronary artery occlusion and reperfusion in anaesthetised greyhounds

We examined the effects of nifedipine, a calcium slow-channel blocking drug, on haemodynamics, blood gases, cardiac arrhythmias, and prostanoid release in anaesthetised greyhounds before, during, and after a 40-min occlusion of the left anterior descending coronary artery. Fifteen minutes after commencing treatment with nifedipine (5 micrograms/kg + 0.67 micrograms kg-1 min-1), there were significant reductions in arterial blood pressure, left ventricular end-diastolic pressure, and vascular resistance, with increases in cardiac output and stroke volume. Although coronary artery blood flow was unchanged, oxygen extraction was decreased, indicating that nifedipine reduced oxygen consumption. Nifedipine prevented the haemodynamic changes that occur in control dogs during acute myocardial ischaemia and markedly reduced the number of arrhythmias during coronary artery occlusion. The incidence of ventricular fibrillation induced by release of the occlusion was significantly reduced from 88% in the control group to 22% in the group receiving nifedipine. The release of thromboxane B2 and 6-keto PGF1 alpha (stable breakdown products of thromboxane A2 and prostacyclin, respectively) from the acutely ischaemic myocardium was not altered by nifedipine. It is concluded that this low dose of nifedipine had marked antiarrhythmic activity during both coronary artery occlusion and reperfusion. The relationship to dosage and possible mechanisms for this effect are discussed.     

Roles of endogenous prostacyclin and thromboxane A2 in the ischemic canine heart

The ability of the ischemic heart to release prostacyclin (PGI2) and thromboxane A2 (TXA2) was studied, together with the effects of these substances on the ischemic myocardium in open-chest dogs. We measured the plasma levels of 6-keto-PGF1 alpha and TXB2--which are stable metabolites of PGI2 and TXA2, respectively--as well as lactate and coronary venous blood flow. The dogs were divided into three groups of eight animals which received indomethacin (5 mg/kg), (E)-3-[4-l-imidazolylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate (OKY-046) (1 mg/kg), or the vehicle. A transient increase in 6-keto-PGF1 alpha was observed in the great cardiac vein 5 min after the ligation of the left anterior descending coronary artery (LAD). TXB2 and lactate increased 30 and 15 min, respectively, after the ligation. Indomethacin prevented significant increases in 6-keto-PGF1 alpha and TXB2, but accelerated the lactate release. OKY-046 prevented significant increases in TXB2 and lactate release, but did not counteract the increase in 6-keto-PGF1 alpha. Although coronary venous flow decreased significantly 5 min after the ligation in every group, the flow returned to the preligation level 15 min after the ligation in the OKY-046 and the vehicle groups. Thus, we have demonstrated the release of PGI2 and TXA2 from the ischemic heart and suggest beneficial effects of PGI2 and of a selective inhibitor of thromboxane synthetase on the ischemic myocardium.     

Effects of phospholipases A2 from Vipera russelli snake venom on blood pressure, plasma prostacyclin level and renin activity in rats

Vipera russelli venom contains several isoenzymes of phospholipase A2 (PLA2) which were isolated by column chromatography. The effects of PLA2 fractions on blood pressure, plasma prostacyclin level and renin activity were studied in normotensive and renal hypertensive rats. PLA2 fractions II-5, II-7, III-3 and III-6 (0.1 mg/kg) injected i.v. into rats decreased the arterial blood pressure. The hypotensive action of PLA2 fractions was not affected by heat treatment (70-80 degrees C, 30 min, pH 6.8). After indomethacin (30 mg/kg, i.v.), the hypotensive response to PLA2 was markedly reduced. Plasma prostacyclin (PGI2) and thromboxane A2 (TXA2) levels were measured by radioimmunoassays of their degradation products, 6-keto-PGF1 alpha and TXB2, respectively. PLA2 fractions (0.1 mg/kg) induced an increase in plasma PGI2 and TXA2 levels. There was a positive linear correlation between the PLA2-induced hypotensive effect and the ratio of increased 6-keto-PGF1 alpha to TXB2 (r = 0.83) in normotensive rats. In renal hypertensive rats, the increase in PGI2 level was larger than in normotensive rats. Plasma renin activity was also measured by the radioimmunoassay. Plasma renin activity was reduced by PLA2 fractions in renal hypertensive rats, but not in normotensive rats. These results suggest that the hypotensive effect of PLA2 fractions in normotensive rats may be partly due to the increase in plasma prostacyclin and thromboxane A2 levels. In addition to the larger increase in plasma PGI2 level, the reduction in plasma renin activity may also contribute to the greater hypotensive effect of PLA2 fractions in renal hypertensive rats.     

Total saponins of Panax notoginseng protected rabbit iliac artery against balloon endothelial denudation injury

AIM: To investigate whether total Panax notoginseng saponins (PNS) could protect endothelium of rabbit iliac artery against balloon endothelial denudation (BED) injury. METHODS: The morphology changes of the endothelium were observed with scanning electron microscope (SEM) and hematoxylin and eosin stain after BED of rabbit iliac artery at 0,4,6, and 8 week respectively. Vascular endothelial growth factor (VEGF) and matrix