Observations on the use of the aVR-V6 relationship to recognize limb lead error.

Electrocardiograms are subject to technical errors that confound interpretation, and although some are readily apparent, others are overlooked by experienced physicians. Thus, failure to recognize a recording error can lead to faulty clinical actions. By exploiting the reciprocal relationship of leads aVR and V6, this article provides a simple and useful way to quickly and confidently determine whether a tracing was properly recorded.

Influence of fructose-1,6-diphosphate on endotoxin-induced lung injuries in sheep.

Background: Fructose-1,6-diphosphate (FDP) is reported to have a salutary effect in endotoxin shock and sepsis. This investigation describes the effect of FDP on pulmonary and systemic hemodynamics, lung lymph protein clearance, and leukocyte count in sheep infused with Escherichia coli endotoxin.

Materials And Methods: Anesthetized sheep (n = 18), some of which underwent thoracotomy to cannulate lymphatic nodes, were used in this study.

Osborn (J) wave appearance on the electrocardiogram in relation to potassium transfer and myocardial metabolism during hypothermia.

The genesis of the J wave during hypothermia has been attributed to injury current, delayed ventricular depolarization and early repolarization, tissue anoxia, and acidosis. To our knowledge, no studies have addressed the appearance of the J wave in relation to the myocardial K+ transfer and metabolism during hypothermia. Dogs (n = 9) were progressively cooled, blood samples were taken from the aorta and coronary sinus, and myocardial tissue samples were obtained for adenosine triphosphate (ATP), creatine phosphate (CP), and glycolytic intermediate determination.

Einthoven's triangle: lead errors and an algorithm for solution.

The three bipolar leads (I, II, and III) of the 12-lead electrocardiogram are subject to technical errors that not only confound interpretation but may lead to faulty clinical actions. While some errors are readily recognized, even experienced electrocardiographers overlook others. This paper reviews the nature of limb lead errors and offers what we think is a generally useful method to deduce the observed, but erroneous, lead configurations.

Fructose diphosphate attenuates the acetaminophen-induced liver injury in the rat evidence for involvement of nitric oxide.

We have previously shown that fructose-1,6-diphosphate (FDP) stimulates the synthesis of nitric oxide probably by stimulating the hepatic inducible nitric oxide synthase (iNOS). The aim of the present study was to evaluate the hepatoprotective role of FDP in acetaminophen-induced liver injury and whether this hepatoprotective effect is mediated by nitric oxide. Liver injury was induced in adult Sprague-Dawley rats by the administration of acetaminophen (1.

Fructose-1,6-diphosphate suppresses T-lymphocyte proliferation, promotes apoptosis and inhibits interleukins-1, 6, beta-actin mRNAs, and transcription factors expression.

The overall objective of this study was to determine the role fructose 1,6-diphosphate (FDP), a naturally occurring glycolytic intermediate, plays in activated T-lymphocytes. The hypothesis is twofold. First, we propose that FDP inhibits T cell proliferation to a greater extent than fructose-1-phosphate (F1P), fructose-6-phosphate (F6P) and mannose-6-phosphate (M6P); second, we argue that FDP suppresses immune activation by inhibiting inflammatory cytokine expression, inhibiting expression of key transcription factors, and by inducing apoptosis in immune cells.

Fructose-1,6-diphosphate alone and in combination with cyclosporine potentiates rat cardiac allograft survival and inhibits lymphocyte proliferation and interleukin-2 expression.

Background: Fructose-1,6-diphosphate (FDP) reduces postischemic reperfusion injury and is used alone and in combination with cyclosporine A (CsA) as an immunosuppressant.

Methods: Wistar-Furth rat hearts were grafted to Lewis rats. Activated T-cell proliferation, viability, and interleukin-2 expression were determined.

Prevention of alpha-naphthylthiourea-induced pulmonary edema with fructose-1,6-diphosphate.

Neutrophil-derived oxygen free radicals have been implicated in the pathogenesis of noncardiogenic pulmonary edema. Fructose-1,6-diphosphate (FDP) has been shown to inhibit oxygen free radicals production by activated neutrophils. Thus, we investigated whether FDP would attenuate formation of pulmonary edema in anesthetized dogs injected with alpha-naphthylthiourea (ANTU).