硝普钠溶液配置后不同时间段的稳定性

目的 探讨硝普钠溶液的稳定性和临床上硝普钠溶液配置后的使用时限。方法 对不同时间段避光条件下的不同浓度、酸碱度、温度的硝普钠溶液,用电位滴定法测定其硝普钠药物含量,用氰化物检查法测定其降解产物氰化物的含量。结果 0．005％～0．02％浓度的硝普钠溶液在pH5．0～7．0、温度10℃～25℃时及常规的避光条件下,配制后24小时内是稳定的,其氰化物含量及硝普钠药物含量均符合要求。结论 硝普钠溶液在一定的pH、温度及合适的避光条件下,在体外比较稳定,使用时间适当延长是可行的。     

心脏瓣膜替换患者术前准备及术后处理：附79例病例分析

对７９例心脏瓣膜替换患者术前准备及术后处理经验进行总结，提出除应用强心、利尿和极化液治疗外，可加用血管扩张剂，少数给予多巴胺药物，对改善心功能有益。其中２２例术后应用Ｓｗａｎ－Ｇａｎｚ导管，２４例利用保留左房导管的方法进行了血液动力学监测和Ｆｏｒｅｓｔｅｒ心功能分类，表明该方法对准确判断病情和合理应用药物，从而提高危重患者治愈率起到重要作用。     

The pharmacology of carvedilol

Carvedilol is a potent antihypertensive agent with a dual mechanism of action. At relatively low concentrations it is a competitive -adrenoceptor antagonist and a vasodilator, whereas at higher concentrations it is also a calcium channel antagonist. The antihypertensive activity of carvedilol is characterized by a decrease in peripheral vascular resistance, resulting from the vasodilator activity of the compound, with no reflex tachycardia, as a result of -adrenoceptor blockade. The antihypertensive activity of carvedilol is associated with an apparent renal sparing effect in that the reduction in mean arterial blood pressure does not compromise renal blood flow or urinary sodium excretion. Studies on the mechanism of action of carvedilol indicate that the compound is a potent competitive antagonist of ₁- and ₂-adrenoceptors with a dissociation constant (K_B) of 0.9 nM at both -adrenoceptor subtypes. Carvedilol is also a potent ₁-adrenoceptor antagonist (K_B = 11 nM), which accounts for most, if not all, of the vasodilating response produced by the compound. At concentrations above 1 M, carvedilol is a calcium channel antagonist. This activity can be demonstrated in vivo at doses that represent the higher end of the anti-hypertensive dose-response curve. Although the calcium-channel blocking activity of carvedilol may not contribute to the antihypertensive activity of the compound, it may play a prominent role in certain peripheral vascular beds, such as the cutaneous circulation, where marked increases in blood flow are observed. The data indicate that carvedilol is an antihypertensive agent that is both a -adrenoceptor antagonist and a vasodilator. The vasodilating activity of carvedilol results largely from ₁-adrenoceptor blockade, and its -adrenoceptor blocking activity prevents reflex tachycardia. In some regional vascular beds, such as the cutaneous circulation, the calcium-channel blocking activity of carvedilol may be responsible for increasing the blood flow.     

Impaired endothelium-dependent vasodilation of coronary resistance vessels in severely stunned porcine myocardium

The effect of stunning on endothelium-dependent responses of resistance vessels in vivo remains of interest. We utilized the coronary pressure-flow relationship during maximal vasodilation in anesthetized swine to identify subtle changes in flow reserve within stunned myocardium. Prior to and following stunning, the coronary pressure-flow relationship during maximal doses of intracoronary adenosine was compared with that of the endothelium-dependent vasodilator ATP. In 11 anesthetized swine, 30 min of partial LAD occlusion and 40 min of reperfusion reduced fractional shortening from 16±4% to 6±5% (p<0.05). This caused a rigtward shift of the coronary pressure-flow relationships during infusions of either adenosine or ATP, suggestive of increased extra vascular compressive forces. With adenosine, the slope of the linear portion of the relationship (i.e., coronary pressures >30 mmHg) was 1.31±0.54 ml/min-mmHg at baseline and 1.30±0.55 ml/min-mmHg following stunning (NS). With ATP however, the slope decreased from 1.34±0.48 ml/min-mmHg at baseline to 1.08±0.47 ml/min-mmHg following reperfusion (p<0.05), indicating an attenuation of endothelium-dependent vasodilator capacity. In five of the animals, the slope of the pressure-flow relationship during intracoronary nitroprusside was unchanged post-stunning, side was unchanged post-stunning, which is similar to the adenosine results. In conclusion, the data support the hypothesis that endo-thelium-dependent vasodilation of resistance vessels in the intact animal is altered within severely stunned myocardium. The rightward shift of the coronary pressure-flow relation ships with both classes of vasodilators suggest that extra vascular factors may also play a role in limiting coronary flow reserve.Supported by grants from the Minnesota Medical Foundation, American Heart Association-Minnesota Affiliate and VA Merit Review (E.O.M.)     

Effect of cilostazol on experimental diabetic neuropathy in the rat

Summary Two proposed mechanisms of diabetic neuropathy are microvascular ischaemia and a reduction in Na,K-ATPase activity. We evaluated the effect of cilostazol, a drug that is both a potent phosphodiesterase inhibitor that normalizes nerve Na,K-AT-Pase and a vasodilator, on nerve blood flow (NBF) to determine whether it would improve experimental diabetic neuropathy. We examined whether epineurally applied cilostazol acted as a vasodilator on the peripheral nerve of normal and diabetic rats, and whether feeding the rats a cilostazol-supplemented diet could improve diabetic neuropathy. Cilostazol increased nerve blood flow (NBF) in a dose-dependent fashion with an EC₅₀ of 10^–5.74 mol/l. Cilostazol also normalized NBF in experimental diabetic neuropathy with a 10^–4 mol/l local application on the sciatic nerve. In diabetic neuropathy, a cilostazol-supplemented diet improved both NBF and nerve conduction in a dose- and time-dependent fashion. Potential mechanisms of action of cilostazol on the nerve include its effect on NBF, Na, K-ATPase, and restoration of the thromboxane:prostacyclin ratio. Cilostazol may have potential in the treatment of diabetic neuropathy.Abbreviations EDN Experimental diabetic neuropathy - NBF nerve blood flow - STZ streptozotocin - NRC control rats receiving normal diet - NRH control rats receiving a high (0.1%) cilostazol diet - CSH STZ rats receiving high (0.1%) cilostazol diet - CSL STZ rats receiving low (0.03%) cilostazol diet - CV conduction velocity     

Haemorheologic studies in patients with reduced coronary vasodilator capacity but normal coronary angiogram (syndrome X)

The cause of syndrome X, i.e. typical angina, positive exercisetest, normal coronary angiogram, normal resting cardiac function,but reduced coronary vasodilator capacity is still unknown.The purpose of the study was to investigate blood fluidity asa possible cause of syndrome X. Haematocrit, plasma viscosity,erythrocyte aggregation, and erythrocyte deformability wereexamined in 14 patients with syndrome X (group 1), 24 patientswith typical angina, positive exercise test, but normal coronaryvasodilator capacity (group 2), and 37 patients with atypicalchest pain and normal coronary arteries (control group). Coronaryvasodilator capacity was determined by the argon method. Comparedwith normals, patients with syndrome X showed an elevated plasmaviscosity (1.31 ±0.05 mPas vs l.26±0.04 mPas,2P>001), an elevated erythrocyte photometric aggregationindex (141 ±27% vs 100 ±23%, 2?>001) and areduced erythrocyte filterability (0.51 ±0.12 vs 0.66± 0.09, 2P > 0.01). Significant differences in thehaemorheologic parameters between group 1, group 2 and the controlgroup, however, were not detected. Multiple regression analysisdid not reveal a significant relationship between coronary vasodilatorcapacity and the haemorheologic parameters tested. The datasuggest that the reduction in coronary vasodilator capacityin patients with syndrome X cannot be attributed to haemorheologicalterations.