颈中交感神经节阻滞治疗急性脑梗塞的临床疗效观察

目的　观察颈中交感神经节阻滞治疗脑梗塞的临床效果。方法　将 6 4例脑梗塞患者按就诊次序随机分为两组 :(1)颈中交感神经阻滞组 (下简称阻滞组 ) :34例。 (2 )对照组 :30例。两组在脑梗塞常规用药上相同 ,阻滞组采用气管旁颈 6横突法 ,隔日阻滞 1次 ,共 6次。 2周后进行疗效评定。结果　阻滞组总有效率 (88 2 3 % )明显高于对照组 (6 0 % )。结论　颈中交感神经节阻滞是一种创伤较小的侵入性交感神经阻断技术 ,对缺血性脑血管病疗效确切     

Recovery of T cell subsets after autologous bone marrow transplantation is mainly due to proliferation of mature T cells in the graft

In 22 patients with malignancies, treated with high-dose chemoradiotherapy and autologous bone marrow transplantation (BMT), peripheral blood T cell subsets and functions were studied. In ten cytomegalovirus (CMV)-negative patients, CD4+ and CD8+ T cells (representing T cells of the helper/inducer phenotype and T cells of the suppressor/cytotoxic phenotype, respectively), recovered slowly and simultaneously. In 12 CMV-positive patients, however, CD8+ T cells recovered more rapidly than CD4+ T cells and rose to increased counts. No T cells with an immature phenotype (CD1+, OKT6+) were observed. Lymphocyte stimulation by herpes simplex virus infected fibroblasts (and by CMV-infected fibroblasts in CMV-positive patients) in contrast remained high and even increased after BMT in both groups. These data indicate that T cell recovery after autologous BMT is mainly due to proliferation of mature T cells present in the BM graft and not to generation of new T cells from T cell precursors.     

Impaired thickening of nonischemic myocardium during acute regional ischemia in the dog

To study the regional function of nonischemic myocardium after the onset of regional ischemia, graded circumflex coronary arterial stenosis was induced in 18 open-chest anesthetized dogs. Two-dimensional echocardiographic views were obtained at each degree of occlusion in a cross-sectional plane marked by two to three metal beads sewn to the left ventricular epicardium. Percent systolic thickening was measured at 16 equally spaced points around the left ventricle and correlated with microsphere-determined regional myocardial blood flow. Baseline thickening averaged 44.9 +/- 6.4%. During transmural ischemia percent systolic thickening decreased to -16.1 +/- 4.0% in the ischemic region and also decreased in adjacent nonischemic regions (to 2.4 +/- 2.4% in segments closest to the ischemic region [adjacent 1] and to 15.5 +/- 3.9 in segments further away [adjacent 2]), but was unchanged in segments directly opposite the ischemic region (remote region). During subendocardial ischemia, percent systolic thickening fell only in the ischemic and adjacent 1 regions (1.4 +/- 5.2% and 24.9 +/- 5.0%, respectively). Dipyridamole, 0.21 to 0.42 mg/min iv, given to seven dogs during transmural ischemia, caused a three- to fivefold increase in flow to the nonischemic and no change in flow to the ischemic region; function was not altered in any region. Propranolol, 0.1 mg/kg iv, was given to five dogs during transmural ischemia to depress contractility in the remote region. Percent systolic thickening fell in the remote (from 50.0 +/- 7.7% to 34.6 +/- 5.6%), but increased in adjacent 1 (from -0.25 +/- 3.7% to 15.2 +/- 3.9%) and in adjacent 2 (from 17.4 +/- 2.8% to 33.4 +/- 3.9%) regions, and remained unchanged in the ischemic region. We conclude the following: During transmural ischemia percent systolic thickening is markedly impaired in nonischemic myocardium immediately adjacent to the ischemic region, and is impaired to a lesser degree in regions located relatively far from the ischemic border. Dysfunction therefore overestimates the extent of regional ischemia after total coronary occlusion. During subendocardial ischemia function ceases in the ischemic region and functional impairment of nonischemic myocardium is restricted to immediately adjacent regions. Dysfunction of adjacent regions is not caused by "relative ischemia" related to increased local oxygen demands or to a steal phenomenon. Mechanical tethering of nonischemic myocardium adjacent to ischemic regions, secondary to changes in left ventricular shape during contraction, may contribute to the impairment of systolic thickening in adjacent regions during transmural ischemia.     

Computer graphics for digitally formatted images

The increasing use of digitally formatted imaging systems requires high-quality interactive gray-scale computer raster graphics systems for the management, display, and analog film recording of digital image and alphanumeric information. These systems are a combination of computer hardware and software and implement a set of graphics protocols. This paper describes a set of interactive graphics protocols that has been developed for clinical use.     

胃肠道、食管、腹膜后、腹腔干、颈部多发血管瘤1例

湘雅三医院消化科近年收治1例胃肠道、食管、腹膜后、腹腔干及颈部多发血管瘤患者,对其给予食管、胃血管瘤套扎及鱼肝油酸钠注射治疗,出院后随访,患者一般情况可.因本病罕见,现将其报告如下.     

Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion. Further studies showed that heparin-induced thrombocytopenia sera also produced a marked increase in procoagulant activity. In contrast, sera from patients with quinine- or quinidine-induced thrombocytopenia did not generate platelet-derived microparticles nor generate increased procoagulant activity. However, quinine/quinidine-induced thrombocytopenia sera produced a significant increase in the binding of IgG to platelets in a drug-dependent fashion, whereas sera from patients with heparin-induced thrombocytopenia demonstrated no drug-dependent binding of IgG to platelets. We also observed increased levels of circulating microparticles in patients with acute heparin-induced thrombocytopenia compared with control patients. Our observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-induced thrombocytopenia.