Evaluation of atypical human immunodeficiency virus immunoblot reactivity in blood donors

Blood donors reactive by enzyme-linked immunosorbent assay for antibody to the human immunodeficiency virus (HIV) who showed atypical patterns of viral core protein reactivity on Western blot were monitored for several months. Characterization of their antibodies was performed by 1) use of recombinant HIV proteins; 2) determination of cross-reactivity to HTLV-I, HTLV-II, and HTLV-IV: 3) assessment of immune status; and 4) identification of potentially interfering autoantibodies. Nineteen of 20 donors maintained the same HIV antibody reactivity throughout the follow-up period; the other donor became fully antibody-positive. Eighteen of 20 donors' sera showed clear reactivity with HIV recombinant core proteins. Ten of 19 donor samples demonstrated cross-reactivity to HTLV-IV; 3 of these 10 also cross-reacted with HTLV-I. The immune status of all donors was normal, although the medical histories and HLA antibody screens suggested possible autoimmune reactivity in 9 of 18 donors. During follow-up interviews, three donors reported possible risk factors for HIV infection that had not been acknowledged at the time of blood donation. We conclude that exclusion of donors with these atypical serologic test results is warranted while further studies to determine significance are being conducted.     

Thoracic epidural anesthesia time-dependently modulates pulmonary endothelial dysfunction in septic rats

Introduction  

Increasing evidence indicates that epidural anesthesia improves postoperative pulmonary function. The underlying mechanisms, however, remain to be determined. Because pulmonary nitric oxide has been identified to play a critical role in pulmonary dysfunction in sepsis, we hypothesized that thoracic epidural anesthesia (TEA) modulates endothelial dysfunction via a nitric oxide-dependent pathway.     

Myocardial ischaemia in patients with impaired left ventricular function undergoing coronary artery bypass grafting--milrinone versus nifedipin

BACKGROUND AND OBJECTIVE: Myocardial ischaemia and infarction are major complications immediately after coronary artery bypass grafting. They may be due to incomplete surgical revascularization, perioperative anaesthetic management or vasospasm of arterial grafts, e.g. the internal mammary artery. Infusions of nifedipine or milrinone have been advocated to prevent spasm of the mammary artery. The study compared the incidence of myocardial ischaemia after continuous infusion of either nifedipine (0.2 microg kg(-1) min(-1)) or milrinone (0.375 microg kg(-1) min(-1)) in patients with compromised left ventricular function scheduled for elective coronary artery bypass graft. METHODS: After Institutional Review Board approval, this double-blinded randomized clinical study enrolled 30 adult patients with compromised left ventricular function (ejection fraction < 0.4) scheduled for elective coronary artery bypass grafting after written informed consent had been obtained. Ischaemia was detected by Holter electrocardiographic monitoring. The incidence of myocardial cell death was monitored by serial determinations of the creatine kinase-MB (CK-MB) and troponin-I. RESULTS: New ST elevation > or = 0.2 mV or new ST depression < or = 0.1 mV occurred in five of 15 patients in the milrinone group (33.3%) and in 13 of 15 patients (86.6%) in the nifedipine group (P < 0.05). There were increases in CK-MB and troponin-I in both groups. Twenty-four hours postoperatively, CK-MB (P = 0.003) and troponin-I (P = 0.001) were significantly higher in the nifedipine group. CONCLUSIONS: Perioperative continuous infusion of milrinone, compared with nifedipine, results in a significantly lower incidence of myocardial ischaemia and myocardial cell damage after elective coronary artery bypass grafting.     

Naloxone prevents increased atrial natriuretic peptide release during regional myocardial ischaemia and stunning in awake dogs

Background. Atrial natriuretic peptide (ANP) release is increasedin patients with ischaemic left ventricular dysfunction. A beneficialeffect of naloxone on recovery from myocardial stunning wasshown previously. The aim of this study was to investigate theeffects of naloxone on ANP release during regional myocardialischaemia and stunning in awake dogs. Methods. Ten dogs were chronically instrumented for measurementof heart rate, left atrial, aortic, and left ventricular pressure(LVP), LV dP·dt_max/min^–1, and myocardial wall-thickeningfraction. An occluder around the left anterior descending artery(LAD) allowed induction of reversible ischaemia in the LAD-perfusedmyocardium. Each dog underwent two ischaemic episodes (randomizedcrossover fashion; separate days): 10 min of LAD occlusion (1)after application of naloxone (63 µg kg^–1), and(2) without naloxone. ANP levels were measured at baseline (BL)and at predetermined time points until complete recovery ofmyocardial stunning occurred. Results. LAD ischaemia-induced release of ANP (peak level: 182(30) vs 27 (7) pg ml^–1 BL) only in the control group withoutnaloxone. Between 1 and 180 min of reperfusion, ANP levels weresignificantly higher only in the control group (P<0.05). Conclusion. Pre-ischaemic application of naloxone prevents thisischaemia-induced ANP-release in conscious dogs. Br J Anaesth 2002; 88: 87–93     

Recurrent venous thrombosis and markers of inflammation

Inflammatory processes may play a key role in venous thrombosis, by inducing a procoagulant state through the action of cytokines and chemokines on monocytes and endothelial cells. Plasma concentrations of three inflammatory mediators, interleukin 6 (IL-6), interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1), that mediate the cross-talk between inflammation and coagulation, were measured in 182 subjects with recurrent venous thrombosis and 350 healthy subjects recruited through a general practice. Elevated levels of IL-6 (>90th percentile of the control group) were detected in 25.8% of the patients with venous thrombosis in comparison with 10% (by definition) of the controls [odds ratio 2.4 (95%CI 1.5-3.8)]. In 21.5% of the patients elevated plasma levels of IL-8 (>90th percentile) were determined [odds ratio 2.0 (95%CI 1.2-3.5)]. Elevated levels of MCP-1 (>90th percentile) were detected in 24.1% of the patients [odds ratio 1.9 (95%CI 1.2-3.2)]. This is the first large clinical study showing that an increase in inflammatory mediators is associated with venous thrombosis. Future prospective studies are necessary to clarify the causal nature of the inflammatory process with respect to venous thrombosis.