Adult T cell leukemia/lymphoma with massive involvement of cardiac muscle and valves

An autopsy case of a 58-year-old woman with massive cardiac Involvement of adult T cell leukemia/lymphoma (ATLL) is reported. She developed cardiac failure due to aortic and mitral regurgitation with cardiac infiltration of ATLL cells, and underwent replacement of both aortic and mitral valves. Studies of the cut-surfaces revealed diffuse thickening of the subendocardial wall of the left chamber with widespread whitish-brown tumor infiltrates. In the regions surrounding the replaced aortic and mitral valves there was also massive tumor cell infiltration. The tumor cells infiltrating the cardiac muscle wall were T cell in origin and exhibited Leu-3a (CD4)-positive immunoreaction. Ultrastructurally, tumor cells contained markedly indented nuclei and some were attached directly to the muscle cells. These findings suggest that this was an unusual form of ATLL with widespread involvement of the heart.     

Demonstration of Ri-type adenosine receptors in bovine myocardium by radioligand binding

Summary Adenosine has been shown to have negative inotropic, chronotropic and dromotropic effects on the heart. The pharmacological profiles of these effects suggest that they are mediated via R_i (A₁) adenosine receptors, but a direct demonstration of these receptors is still missing. In the present study we report direct labelling of these receptors with (-)N⁶-[¹²⁵I]-p-hydroxyphenylisopropyladenosine ([¹²⁵I]HPIA). The radioligand bound in a saturable and reversible manner to a crude membrane preparation, the B _max-value was 30.5 fmol/mg protein and the K _D-value 1.1 nmol/l. A similar affinity of the ligand was obtained in kinetic and competition experiments. Competition experiments with a variety of adenosine analogues gave a pharmacological profile characteristic of R_i adenosine receptors with high affinities of N⁶-substituted derivatives and a marked stereospecificity for N⁶-phenylisopropyladenosine (PIA). Purification of the membrane preparation by density gradient centrifugation resulted in a 30-fold increase in the number of binding sites which was paralleled by a similar increase in the number of binding sites for [³H]ouabain. Guanine nucleotides decreased binding of [¹²⁵I]HPIA in a dose-dependent manner, but the IC₅₀-values were considerably higher than those reported in other tissues. Finally, binding of [¹²⁵I]HPIA appeared to be entropy-driven which has been shown to be characteristic of agonist binding to R_i adenosine receptors. These results suggest the presence of R_i adenosine receptors in ventricular myocardium which may be responsible for the mediation of the effects of adenosine and its analogues.Abbreviations [¹²⁵I]HPIA (-)N⁶-[¹²⁵I]-p-hydroxyphenylisopropyladenosine - (-)IHPIA (-)N⁶-iodo-p-hydroxyphenylisopropyladenosine - (+)/(-)PIA (+)/(-)N⁶-phenylisopropyladenosine - CHA N⁶-cyclohexyladenosine - NECA 5-N-ethylcarboxamidoadenosine - App(NH)p 5-adenylylimidodiphosphate - Gpp(NH)p 5-guanylylimidodiphosphate     

腺苷脱氨酶抑制剂对氧反常大鼠心脏的保护作用

本文观察到腺苷脱氨酶抑制剂EHNA对离体灌流大鼠心脏氧反常性损伤有明显的作用,此外还发现在缺氧期(无氧灌流30分钟)EHNA也表现出明显的保护作用,心脏收缩幅度的降低和静息张力的升高均显著低于对照组。表明在缺氧期也可能有自由基的产生。     

Changes in myocardial metabolism and ultrastructure of myocardial microvessels during pharmacological and cold cardioplegia under hypothermic conditions without perfusion

A combination of pharmacological and cold cardioplegia in with hypothermia without perfusion in open-heart surgery guarantee the reversible character of shifts in energy and free radical balance in the myocardium. However, this procedure can impair coronary micricirculation due to structural and functional changes in microvessel endothelium. Our results demonstrate that new cytoprotective approaches are extremely needed for cardiac protection during surgery.     

低心室容量负荷未能影响兔离体心肌的氧耗反应时间

为了解心肌容量负荷是否影响心肌的氧化磷酸化过程,采用兔离体灌流心肌线粒体氧耗反应时间测定方法,对一下正常心室容量负荷和低心室容量负荷时的心肌线粒体氧耗反应时间进行比较,结果提示心肌作功负荷变化未能影响心肌线粒体的能量代谢动态调节过程。     

Evidence against a role of nitric oxide in the indirect negative inotropic-effect of M-cholinoceptor stimulation in human ventricular myocardium

Nitric oxide (NO) has been reported to mediate several effects in response to muscarinic cholinergic stimulation in cardiovascular tissues. Recently, an attenuation of guinea pig cardiac myocyte contraction by NO has been described. The aim of the present study was to determine whether the indirect negative inotropic effect of M-cholinoceptor stimulation in human myocardium is in part due to an effect of endogenous NO. Therefore, the effect of carbachol was studied under control conditions and during inhibition of NO-synthase by pretreatment with N^G-monomethyl-l-arginine (NMMA). Functional experiments were performed in isolated, electrically driven (1 Hz, 37°C) left ventricular papillary muscle strips of human myocardium. Since cytokines have been reported to be increased in the serum of patients with heart failure and could induce NO-synthase activity in failing myocardium, we compared samples from nonfailing and terminally failing (classified as NYHA IV) hearts. The indirect negative inotropic effect of carbachol (10 mol/l) was studied in the presence of the \-adrenoceptor agonist isoprenaline (0.03 mol/l).After stimulation with isoprenaline, carbachol significantly (P < 0.05) reduced force of contraction. This effect was diminished in failing myocardium compared to nonfailing, probably due to the diminished inotropic response most likely due to the lower cAMP levels in response to \-adrenoceptor stimulation in the former condition. Pretreatment with NMMA (100 mol/l) altered the antiadrenergic effect of carbachol neither in nonfailing nor in failing preparations. Furthermore, inhibition of guanylyl cyclase, the target enzyme of NO, by preincubation with methylene blue (10 mol/l) for 30 min had no effect on the carbachol-induced decrease in force of contraction. Basal force of contraction, as well as the positive inotropic effect of isoprenaline remained unaffected by NMMA or methylene blue.The present study provides evidence that the indirect negative inotropic effect of M-cholinoceptor agonists is not due to an effect of NO in the human myocardium. Furthermore, the well known enhancement of cGMP in response to M-cholinoceptor stimulation appears not to be involved in this antiadrenergic effect.     

Effects of a leucocyte depleting arterial line filter on perioperative proteolytic enzyme and oxygen free radical release in patients undergoing aortocoronary bypass surgery

BACKGROUND: Proteolytic enzymes and oxygen free radicals released from activated leucocytes contribute significantly to the organ dysfunction associated with cardiopulmonary bypass. Leucocyte depletion during extracorporeal circulation should reduce the release of these toxic compounds and thereby improve postbypass myocardial and pulmonary function. Recently, a leucocyte-specific arterial line filter to achieve leucocyte depletion during clinical perfusion has become commercially available. The aim of this study, therefore, was to evaluate the influence of the leucocyte depleting arterial line filter on proteolytic enzyme release, oxygen free radical release and postbypass pulmonary and myocardial function in patients undergoing bypass surgery. METHODS: Forty patients undergoing elective aortocoronary bypass surgery were included into this prospective, randomized clinical study, 20 in the leucocyte depletion (LG-6 group, leucocyte-specific arterial line filter) and 20 in the control group (AV-6 group, standard arterial line filter). White cell count, differential white cell count, plasma elastase concentration, plasma malondialdehyde concentration and C-reactive protein were determined before, twice during and immediately after cardiopulmonary bypass, at the end of surgery and 6 and 20 h thereafter. RESULTS: White cell count, differential white cell count, malondialdehyde and C-reactive protein were not significantly different between LG-6 and control patients. Plasma elastase concentrations were significantly (P < or = 0.03) higher during and immediately after extracorporeal circulation in LG-6 group patients. Need for inotropic support, arterial pO2 after extracorporeal circulation and perioperative CK MB mass and troponin I release were not different between the two groups of patients. CONCLUSION: The use of a leucocyte depleting arterial line filter is associated with an increased release of the proteolytic enzyme elastase, but does not reliably and consistently achieve effective leucocyte depletion during clinical perfusion. In contrast to previous studies, we could not demonstrate any significant difference in postbypass pulmonary or myocardial function between patients perfused with the leucocyte-specific arterial line filter and control patients. Our data do not support the routine use of a leucocyte depleting arterial line filter during clinical perfusion in patients undergoing elective aortocoronary bypass surgery.     

Ultrasound Densitometric Analysis: Comparison Between an Online Digital Acquisition Acoustic Program and an Offline Analog Program

Videodensitometric analysis of myocardial contrast echocardiography is traditionally performed off line. Recently, an online contrast ultrasound analysis system, Acoustic Densitometry (Hewlett-Packard), was introduced. We compared pixel intensities acquired with Acoustic Densitometry to pixel intensities derived from videodensitometry. A tissue phantom was imaged in phase I using three transducer frequencies (2.5, 3.5, and 5.0 MHz). In phase II, an in vitro flowing tube model with various concentrations of Albunex® was imaged at two flow rates, 0.6 and 1.2 m/sec, and at two transducer frequencies, 2.5 and 3.5 MHz. The relationship between pixel intensities yielded by the two systems for identical ultrasound signals was determined with linear regression. Intensities derived with Acoustic Densitometry strongly correlated with those derived from the offline videodensitometry system. The intensities were related by a predictive multiplicative factor based on display characteristics of the two systems. These results suggest that semiquantitative, online perfusion analysis with Acoustic Densitometry is as sensitive as analysis offline with videodensitometry.