Post-ischemic release of nucleosides and oxypurines in isolated rat hearts. Possible involvement of ventricular fibrillation

Summary In isolated perfused rat hearts global ischemia for 2, 5, and 15 min was produced. Depending on the duration of the ischemia, postischemic reperfusion led to the release of adenosine and its catabolites, and to more or less severe ventricular tachyarrhythmias. When ventricular fibrillation occurred, a highly significant increase in the purine release was observed compared with non-fibrillating hearts. Prevention of fibrillation by antiarrhythmic drugs decreased the purine release in a highly significant way. After only 2 min of ischemia, reperfusion did not lead to ventricular fibrillation. Electrical induction of fibrillation during the reperfusion in these hearts provoked the release of very high amounts of the purine compounds. A similar effect of electrically-induced fibrillation was also obtained in hearts without a previous ischemic period. The findings suggest that ventricular fibrillation is able to induce the release of purine derivatives from the heart.     

艾司洛尔控制开颅手术苏醒期脑过度灌注的效果

目的 通过监测脑血流速度、颈静脉球部血氧饱和度(SjvO2)、血压、心率(HR)和不良反应发生率等,综合评价艾司洛尔用于控制开颅手术苏醒期患者脑过度灌注的效果.方法 选择择期在全身麻醉下行开颅肿瘤切除术的患者,随机分为艾司洛尔组(E组,20例)和对照组(C组,20例).E组患者从拔管即刻起给予艾司洛尔0.6 mg·kg1·h-1静脉持续滴注15 min C组患者从拔管即刻起给予0.9%氯化钠溶液静脉持续滴注.分别监测两组患者术前、术后拔管即刻及拔管后15、30、45、60 min时的大脑中动脉平均血流速度(MCAVm)、SivO2平均动脉压(MAP)及HR,并记录不良反应发生例数.结果 E组术后15和30 min的MCA Vm、sjvO2及HR均显著低于C组(P值均<0.01),术后15 Min的MAP显著低于C组(P<0.05).无一例患者发生与艾司洛尔相关的药物不良反应.结论 艾司洛尔是控制术后脑过度灌注的理想药物.     

Effects of exercise on vasodilatory capacity in endurance- and resistance-trained men

To determine vasodilatory responsiveness we measured forearm blood flow (FBF) following reactive hyperemia (RH), prior to and following a bout of maximal aerobic exercise in endurance- (n=14) and resistance-trained men (n=10). Both groups were similar in height, body mass, and percentage body fat. Using strain-gauge plethysmography, resting FBF was higher in the resistance-trained group [4.82 (0.84) vs 3.33 (1.17) ml min⁻¹ 100 ml⁻¹ of tissue; P<0.05]. However, the resistance-trained group had a 17%–29% lower pre-exercise FBF response to RH for the first 45 s (P<0.05). Following the maximal exercise bout there were no group differences in FBF. Post-exercise FBF was higher compared to pre-exercise values in both the endurance- (P<0.001) and resistance- (P<0.01) trained groups. Endurance-trained men appear to have a greater peak vasodilatory capacity compared to resistance-trained men, and acute maximal exercise increased the vasodilatory capacity in both groups. Acute exercise also equalized the peak vasodilatory response between the endurance- and resistance-trained groups, suggesting the potential for flow-mediated vasodilatation was similar for both groups. Electronic Publication     

Regional cerebral blood flow after occlusion of the middle cerebral artery

Occlusions of the middle cerebral artery (MCA) are mostly of embolic origin (appr. 80%) and give rise to about one third of all ischemic strokes, most of these being major strokes. MCA occlusions lasting for less than 1/2 h are tolerated without occurrence of permanent tissue damage. Occlusions lasting between 1/2 h to 4-8 h lead to permanent tissue damage and neurological deficits that are proportional to the duration of occlusion. Maximal tissue damage is obtained after 4-8 h occlusion. A cerebral blood flow of 8-23 ml/100 gr/min is sufficient for cellular viability but insufficient for normal tissue function ("ischemic penumbra"). Cellular function is completely abolished in the interval 8-16 ml/100 gr/min and flow at that level is tolerated only for 1-3 h before neuronal death ensues. In the interval 18-23 ml/100 gr/min there is some functional activity although it is reduced. Experimental and clinical evidence suggests that flow in this interval may be tolerated for several days, months or even longer ("chronic ischemic penumbra"). After MCA occlusion the blood flow falls below 8 ml/100 gr/min in most cases and permanent MCA occlusion always leads to relatively large areas of frank infarction. The ischemic infarcts may be surrounded by collaterally perfused areas where the blood flow is pressure-dependent (impaired autoregulation) and quite commonly insufficient for normal neuronal function (below 23 ml/100 gr/min). Such collaterally perfused areas may include a "chronic ischemic penumbra". Emboli causing MCA occlusions commonly disintegrate and/or migrate more peripherally within the first few weeks post stroke. This leads to reperfusion and changes of ischemic infarcts into hyperemic infarcts where flow is severely increased. The vascular reactivity is completely abolished in hyperemic infarcts and the hyperemic state lasts for about two weeks. Probably, anemic infarcts are equivalent to ischemic infarcts while the hemorrhagic variety is equivalent to hyperemic infarcts. The "partial infarct" with selective neuronal necrosis occurs in experimental animals after MCA occlusions of less than four h but not after permanent MCA occlusion. The significance of partial infarction in human stroke is not clarified. The extent of irreversible tissue damage can be reduced only if therapy sets in within 4-8 h after the occlusion. If a "chronic penumbra" exists the extension of reversible tissue damage can be reduced if therapy aimed at increasing the blood flow in the penumbra sets in within weeks or even months after the stroke.(ABSTRACT TRUNCATED AT 400 WORDS)     

Rectal Mucosa Damage in Rabbits After Subchronical Application of Suppository Bases

The effect of suppository bases on rabbit rectal mucosa was investigated using six triglyceride bases, polyethylene glycol, and a triglyceride base combined with monoglycerides or fatty acids and methyl esters of those acids. Rectal irritation was evaluated and scored according to defined pathological features. Pure triglycerides and a triglyceride to which a nonionic surfactant was added caused severe mucosal damage with ulceration and inflammation. Hyperemia was characteristic for irritation by polyethylene glycol suppositories. Mucosal damage by a pure triglyceride combined with monoglycerides or fatty acids and methyl esters of those acids was similar but statistically less pronounced than with all other bases.     

Dysregulation of oxygen hemodynamic responses to synaptic train stimulation in a rat hippocampal model of subarachnoid hemorrhage

We investigated microvascular reactivity to synaptic train stimulation after induction of subarachnoid hemorrhage in adult rats, analyzing tissue oxygen levels [pO₂] in intact hippocampus. In control rats, hippocampal pO₂ averaged 11.4 mm Hg whereas hemodynamic responses averaged 13.1 mm Hg (to a 25 s train). After subarachnoid hemorrhage (at 2 days), we recorded a dramatic elevation in baseline pO₂ in the hippocampus (to 68.4 mm Hg) accompanied by inverted pO₂ responses to synaptic train stimulation (−9.46 mm Hg). These significant changes in baseline hippocampal pO₂ and inverted pO₂ responses after subarachnoid hemorrhage indicate severe alterations of neurovascular coupling and neuronal viability.     

20-MHz Ultrasound for Measurements of Flow-Mediated Dilation and Shear Rate in the Radial Artery

A high-frequency scanning system consisting of a 20-MHz linear array transducer combined with a 20-MHz pulsed Doppler probe was introduced to evaluate the degree of radial artery flow-mediated dilation (FMD [%]) in two groups of patients after 5?min of controlled forearm ischemia followed by reactive hyperemia. In group I, comprising 27 healthy volunteers, FMD (mean?±?standard deviation) was 15.26?±?4.90% (95% confidence interval [CI]: 13.32%–17.20%); in group II, comprising 17 patients with chronic coronary artery disease, FMD was significantly less at 4.53?±?4.11% (95% CI: 2.42%–6.64%). Specifically, the ratio FMD/SR (mean?±?standard deviation), was equal to 5.36?×?10^?4?±?4.64?×?10^?4 (95% CI: 3.54?×?10^?4 to 7.18?×?10^?4) in group I and 1.38?×?10^?4?±?0.89?×?10^?4 (95% CI: 0.70?×?10^?4 to 2.06?×?10^?4) in group II. Statistically significant differences between the two groups were confirmed by a Wilcoxon–Mann–Whitney test for both FMD and FMD/SR (p?<0.01). Areas under receiver operating characteristic curves for FMD and FMD/SR were greater than 0.9. The results confirm the usefulness of the proposed measurements of radial artery FMD and SR in differentiation of normal patients from those with chronic coronary artery disease.     

Application of non-invasive detection of peripheral vascular dysfunction in ovarian hyperstimulation syndrome (OHSS): A pilot study of clinical relevance

ObjectiveThe current study tested the hypothesis that vascular endothelial function, as reflected by the reactive hyperemia index (RHI), and biochemical factors, including VEGF, TNFα, CRP, inhibin A, and inhibin B, were involved in the pathogenesis of ovarian hyperstimulation syndrome (OHSS).Materials and methodsThis study was conducted between June 2010 and June 2012, enrolling 15 patients with OHSS and 6 healthy control subjects <45 years of age. Detailed clinical parameters were reviewed, including serum VEGF, TNFα, CRP, inhibin A, inhibin B, and hematocrit. RHI assessed by novel automatic peripheral arterial tonography was used to evaluate the vascular endothelial function.ResultsTwenty-one subjects were evaluated. There was no significant difference between patients with OHSS and control subjects with respect to VEGF, TNFα, CRP, inhibin A and inhibin B. The RHI was not significantly different between patients with OHSS and control subjects (mean, 1.8 ± 0.4 vs. 1.7 ± 0.2). The hematocrit was significantly different between patients with OHSS and control subjects.ConclusionsOur preliminary data did not reveal direct evidence of vascular endothelial dysfunction in patients with OHSS. To identify whether RHI could reflect vascular endothelial dysfunction in patients with OHSS, more cases with different severities of OHSS should be recruited in the future study.