Efficacy and tolerance of recombinant tissue-type plasminogen activator in patients with thrombotic or embolic occlusions of leg-arteries

Summary The efficacy and safety of recombinant tissue-type plasminogen activator (rt-PA) was evaluated in 46 patients with thrombembolic arterial occlusions in leg arteries. rt-PA was given over 1–4 h with a maximum dose of 18 mg. The effect of rt-PA treatment was determined as patency of the occluded arteries in 44 different patients 14 days after treatment. In 41 patients at least one artery was recanalized (93%) by rt-PA, and in almost half of these patients (48%) no residual stenosis were detected after the lytic treatment. A slight residual stenosis was detected in 29% of the patients and a severe residual stenosis in 21%. An additional treatment with percutaneous transluminal angioplasty was performed in 23 of the 44 patients and successful in 21 (91%). In 8 patients an addition catheter-embolectomy was performed. No difference in patency rate was detected between patients with thrombotic and those with embolic occlusions. The age of the occlusion influenced the patency rate; occlusions under the age of 5 weeks showed a patency rate of 96% compared to 82% in older occlusions. The length of the occlusion did not have any influence on the outcome of the rt-PA treatment. From the results of this open study we conclude that a dose of up to 18 mg of rt-PA is both safe and effective in the treatment of thromboembolic occlusions in leg arteries.Abbreviations rt-PA recombinant tissue-type plasminogen activator - GGT gamma-glutamyltransferase - SGOT aspartate aminotransferase - SGPT alanine aminotransferase - LDH lactate dehydrogenase - PTA percutaneous transluminal angioplasty Dedicated to Prof. Dr. N. Zöllner on the occasion of his 70th birthday     

Rapid activation of glycogen synthase and protein phosphatase in human skeletal muscle after isometric contraction requires an intact circulation

The effects of isometric contraction (66% of maximal force) and recovery on glycogen synthase fractional activity (GSF) in human skeletal muscle have been studied. Biopsies were taken from the quadriceps femoris muscle at rest, at fatigue and 5 min postexercise on two occasions: after one of the contractions, the circulation to the thigh was occluded during the 5 min recovery (OCC), and after the other contraction, the circulation was intact (control, CON). During CON, GSF decreased from (mean ± SE) 0.34±0.05 at rest to 0.24±0.02 at fatigue and then increased to 0.74±0.04 at 5 min postexercise; corresponding values for OCC were 0.37±0.04, 0.25±0.04 and 0.48±0.05 (P<0.001 vs. CON for 5 min postexercise only). Compared with the value at fatigue, protein phosphatase activity (PP) increased by 79±16% during CON recovery (P<0.01), whereas no change was observed during OCC recovery. Uridine diphosphate glucose increased by approximately 2.5-fold at fatigue, remained elevated during OCC recovery, but reverted to the preexercise level during CON recovery (P<0.001 vs. OCC recovery). Glucose 6-P increased approximately 5-fold at fatigue and was higher at 5 min postexercise in OCC vs. CON recovery (8.6±1.5 vs. 4.1±0.9 mmol/kg dry wt; P<0.01). It is concluded that the rapid increase in GSF after intense exercise with an intact circulation may be at least partly attributed to an increase in the specific activity of PP. The increase in GSF during recovery in OCC may be at least partly attributed to the high glucose 6-P content in vivo, which enhances the substrate suitability of GS for PP. Thus, separate mechanisms exist for the activation of PP and GS during recovery from intense short term exercise.     

阿魏酸钠治疗视网膜静脉栓塞疗效观察

目的探讨阿魏酸钠注射液治疗视网膜静脉栓塞的临床效果。方法100例（100只眼）视网膜静脉栓塞患者，随机分成治疗组和对照组各50例。对照组给予常规治疗，治疗组给予阿魏酸钠注射液300mg／d静脉滴注，14d为一疗程。测定治疗前后视力、视网膜中央静脉血流速度、视网膜中央动脉平均收缩期峰值血流速度。结果应用阿魏酸钠治疗后，视力明显改善，视网膜中央静脉血流速度和收缩期峰值血流速度显著提高，与对照组治疗后相比均有显著性差异，疗效优于对照组。结论阿魏酸钠治疗视网膜静脉栓塞疗效显著。     

Blood pressure response to low level static contractions

Summary The present study re-examines the 15% MVC concept, i.e. the existence of a circulatory steady-state in low intensity static contractions below 15% of maximal voluntary contraction (MVC). Mean arterial blood pressure was studied during static endurance contractions of the elbow flexor and extensor muscles at forces corresponding to 10% and 40% MVC. Mean value for endurance time at 10% MVC was significantly longer for flexion [111.3 (SD 56.1) min] than for extension [18.1 (SD 7.5) min;n = 7]. At 40% MVC the difference in mean endurance time disappeared [2.3 (SD 0.7) min for elbow flexion and 2.3 (SD 0.7) min for elbow extension]. Mean arterial blood pressure exhibited a continuous and progressive increase during the 10% MVC contractions indicating that the 15% MVC concept would not appear to be valid. The terminal blood pressure value recorded at the point of exhaustion in the 10% MVC elbow extension experiment was identical to the peak pressure attained in the 40% MVC contraction. For the elbow flexors the terminal pressor response was slightly but significantly lower at 10% MVC [122.3 (SD 10.1) mmHg, 16.3 (SD 1.4) kPa] in comparison with 40% MVC [130.4 (SD 7.4) mmHg, 17.4 (SD 1.0) kPa]. When the circulation to the muscles was arrested just prior to the cessation of the contraction, blood pressure only partly recovered and remained elevated for as long as the occlusion persisted, indicating the level of pressure-raising muscle chemoreflexes. Based on blood pressure recordings obtained during the occlusion, it is suggested that the slight reduction in terminal pressor response seen in the 10% MVC elbow flexion experiment was due to a reduced chemoreflex drive characteristic of a slow twitch muscle group during prolonged low force contractions.     

Declining density of intimal smooth muscle cells and age as preconditions for atheronecrosis in the basilar artery

The aging basilar artery has some differences and some similarities when compared with the aorta and coronary arteries. As the non-necrotic intimal thickness increases over time, the number of smooth muscle cells reaches a steady state around age 25–30 years in the coronaries and aorta, but continues to increase in the basilar artery, even to 90 years of age. The numbers of cells per unit of tissue (the cell density) declines with age, and the patterns of decline are quantitatively similar in all three arterial segments. All arteries so far examined behave alike in showing that atheronecrosis emerges in those specimens that have sufficiently low density of intimal smooth muscle cells. These results identify low intimal cell density as a criterion for recognizing arteries that are prone to atheronecrosis. One possible explanation is that depopulation of the fibrotically thickened and aged intima, by spreading apart the smooth muscle cells with expanding matrix materials, could be the conditioning factor that brings about the intrusion of atheronecrosis.     

Bilateral Occlusion of Carotid Artery in Awake Hypertensive Rats (SHR-SP) as a Model of Global Cerebral Ischemia

Bilateral occlusion of carotid arteries in awake hypertensive rats (SHR-SP) was used as a model of global brain ischemia (duration of occlusion — until appearance of seizures). In normotensive rats (WKY), no seizures developed over 60 min. We revealed swelling of mitochondria in dendrites of hippocampal CA1 pyramidal cells, which was more pronounced in SHP-SP than in WKY rats. Blood pressure and heart rate in SHR-SP rats increased starting from the first minutes of occlusion, while in WKY rats these parameters remained unchanged. We proved that bilateral occlusion of the carotid arteries in awake SHR-SP rats can be used as an adequate model of global cerebral ischemia. Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 146, No. 12, pp. 627–630, December, 2008     

Computerised analysis of auscultatory sounds associated with vascular patency of haemodialysis access

Vascular access for renal dialysis is a lifeline for about 120 000 individuals in the United States. Stethoscope auscultation of vascular sounds has some utility in the assessment of access patency, yet can be highly skill-dependent. The objective of the study was to identify acoustic parameters that are related to changes in vascular access patency. The underlying hypothesis is that stenoses of haemodialysis access vessels or grafts cause vascular sound changes that are detectable using computerised data acquisition and analysis. Eleven patients participated in the study. Their vascular sounds were recorded before and after angiography, which was accompanied by angioplasty in most patients. The sounds were acquired using two electronic stethoscopes and then digitised and analysed on a personal computer. Vessel stenosis changes were found to be associated with changes in acoustic amplitude and/or spectral energy distribution. Certain acoustic parameters correlated well (correlation coefficient=0.98, p<0.0001) with the change in the degree of stenosis, suggesting that stenosis severity may be predictable from these parameters. Parameters also appeared to be sensitive to modest diameter changes (>20%), (p<0.005, Wilcoxon rank sum test). These results suggest that computerised analysis of vascular sounds may be useful in vessel patency surveillance. Further testing using longitudinal studies may be warranted.     

磁共振成像及氧化铁粒子标记在干细胞治疗脑缺血大鼠中的应用

目的 探讨磁共振成像及氧化铁粒子标记在干细胞治疗脑卒中模型中的应用价值.方法 线栓法建立9只大鼠大脑中动脉缺血模型,进行神经行为学评分、磁共振影像学和病理学评价,并对上述3项指标进行相关性分析.用超顺磁性氧化铁体外标记骨髓间充质干细胞,并另筛选18只脑缺血大鼠,分别接受缺血对侧皮层(n.6)、缺血同侧纹状体(n=6)的标记干细胞移植,并设对照组(n=6).分别在脑缺血后1 d、细胞移植后第1天、第7天及第14天进行磁共振扫描,观察各时间点的标记干细胞显示情况,并对各组之间梗死体积的变化进行统计学分析.结果 神经行为学评分、磁共振影像学和病理学评价对大鼠脑缺血模型评价的相关性好.磁共振各序列均可显示局部移植的标记干细胞,梯度回波序列最敏感,T2像空间分辨力高.磁共振成像可显示局部移植标记干细胞随时间推移而产生的分布变化.干细胞治疗各组之间脑梗死体积变化无明显差异.结论 磁共振成像是大鼠脑缺血模型评价的理想工具,配合氧化铁粒子标记干细胞可活体状态下了解干细胞移植后的分布变化.     

Angiotensin II and renal prostaglandin release in the dog. Interactions in controlling renal blood flow and glomerular filtration rate

The relationship between angiotensin II and renal prostaglandins, and their interactions in controlling renal blood flow (RBF) and glomerular filtration rate (GFR) were investigated in 18 anaesthetized dogs with acutely denervated kidneys. Intrarenal angiotensin II infusion increased renal PGE₂ release (veno-arterial concentration difference times renal plasma flow) from 1.7 ± 0.9 to 9.1 ±0.4 and 6-keto-PGFja release from 0.1 ±0.1 to 5.3 ± 2.1 pmol min^-1. An angiotensin II induced reduction in RBF of 20% did not measurably change GFR whereas a 30% reduction reduced GFR by 18 ± 8%. Blockade of prostaglandin synthesis approximately doubled the vasocon-strictory action of angiotensin II, and all reductions in RBF were accompanied by parallel reductions in GFR. When prostaglandin release was stimulated by infusion of arachidonic acid (46.8± 13.3 and 15.9± 5.4 pmol min^-1 for PGE₂, and 6-keto-PGFja, respectively), angiotensin II did not change prostaglandin release, but had similar effects on the relationship between RBF and GFR as during control. In an ureteral occlusion model with stopped glomerular filtration measurements of ureteral pressure and intrarenal venous pressure permitted calculations of afferent and efferent vascular resistances. Until RBF was reduced by 25–30% angiotensin II increased both afferent and efferent resistances almost equally, keeping the ureteral pressure constant. At greater reductions in RBF, afferent resistance increased more than the efferent leading to reductions in ureteral pressure. This pattern was not changed by blockade of prostaglandin synthesis indicating no influence of prostaglandins on the distribution of afferent and efferent vascular resistances during angiotensin II infusion. In this ureteral occlusion model glomerular effects of angiotensin II will not be detected, and it might well be that the shift from an effect predominantly on RBF to a combined effect on both RBF and GFR induced by inhibition of prostaglandin synthesis is located to the glomerulus. We therefore postulate that renal prostaglandins attenuate the effects of angiotensin II on glomerular surface area and the filtration barrier, and not on the afferent arterioles as previously suggested.     

早期脑血管病的微循环表现

通过对血液微循环观测，分析微循环障碍与早期脑血管病发生率的相关性。方法：采用微循环显微镜观察人体甲襞微循环的微血管和微血流的动态变化。结果：微循环障碍患者，表现明显微血管痉挛性和淤滞性改变，由于微循环灌注减少，加重组织缺血缺氧，微血栓形成。结论：微血管及微血流的异常影响人体机能代谢的变化，导致微血管内皮损伤、血液的凝固性增强，而外周血流及血管的异常改变，同样可影响脑血流量及供血。提示微循环障碍与早期脑血管病密切相关。对早期预防、诊断具有重要参考价值。