Cardiogenic shock without a critically raised left ventricular end diastolic pressure: management and outcome in eighteen patients.

Eighteen patients in whom shock developed after acute myocardial infarction are described. There was electrocardiographic evidence of acute inferior infarction in 11, of inferolateral infarction in three, and of anteroseptal infarction in four. In all cases the right atrial pressure was the same as or exceeded the end expiratory pulmonary artery wedge pressure. Plasma volume expansion of 100-2500 ml was needed to produce an optimum pulmonary artery wedge pressure. Eleven patients needed additional inotropic support with dopamine. Despite the absence of a critical increase in pulmonary artery wedge pressure, potential or actual hypoxia was almost always present. Six patients needed endotracheal intubation and mechanical ventilation because they had severe hypoxia that was unresponsive to supplemental inspired oxygen. Life threatening arrhythmias were also common (ventricular fibrillation in seven patients and complete heart block in four). Five patients died. All surviving patients are well and only one requires treatment for heart failure.     

Acute arsenic toxicity--an opaque poison

We report a patient with fatal acute arsenic poisoning presenting as vomiting and diarrhea with the finding of intra-abdominal radiopacities on radiographs. These represent the classic features of acute arsenic toxicity and are detailed here as a reminder to others facing a similar puzzling patient with this potentially treatable poisoning.     

Ki-M8 monoclonal antibody reactive with an intracytoplasmic antigen of monocyte/macrophage lineage

A monoclonal antibody (MoAb), Ki-M8, that reacts specifically with cells of the monocyte/macrophage system is described. On light and electron microscopic immunohistochemistry, Ki-M8 recognizes intracytoplasmatically localized antigens of mol wt 30,000 and 32,000, increasingly expressed during differentiation of monocytes into macrophages. Ki-M8 antigen is detectable on almost all known tissue macrophages and monocyte/macrophage-related cell lines after appropriate stimulation. In functional terms Ki-M8 significantly impairs the generation of oxygen radicals during an induced respiratory burst. Applied to acute nonlymphoblastic leukemias, a clear-cut differentiation of the monocytic phenotype and differentiation is possible on the basis of Ki-M8 immunoreactivity. Ki-M8 represents a reagent specific for the monocyte/macrophage system with regard to antigen distribution in normal and neoplastic cells as well as with regard to its influence on a typical monocyte/macrophage-related function.     

Role of K+ channels in A2A adenosine receptor-mediated dilation of the pressurized renal arcuate artery

1. Adenosine A2A receptor-mediated renal vasodilation was investigated by measuring the lumenal diameter of pressurized renal arcuate arteries isolated from the rabbit. 2. The selective A2A receptor agonist CGS21680 dilated the arteries with an EC50 of 130 nM. The CGS21680-induced vasodilation was, on average, 34% less in endothelium-denuded arteries. 3. The maximum response and the EC50 for CGS21680-induced vasodilation in endothelium-intact arteries were not significantly affected by incubation with the K+ channel blockers apamin (100 nM), iberiotoxin (100 nM), 3,4-diaminopyridine (1 mM), glibenclamide (1 microM) or Ba2+ (10 microM). However, a cocktail mixture of these blockers did significantly inhibit the maximum response by almost 40%, and 1 mM Ba2+ alone or 1 mM Ba2+ in addition to the cocktail inhibited the maximum CGS21680-response by 58% and about 75% respectively. 4. CGS21680-induced vasodilation was strongly inhibited when the extracellular K+ level was raised to 20 mM even though the dilator response to 1 microM levcromakalim, a K(ATP) channel opener drug, was unaffected. 5. CGS21680-induced vasodilation was inhibited by 10 microM ouabain, an inhibitor of Na+/K(+)-ATPase, but ouabain had a similar inhibitory effect on vasodilation induced by 30 nM nicardipine (a dihydropyridine Ca2+ antagonist) or 1 microM levcromakalim. 6. The data suggest that K+ channel activation does play a role in A(2A) receptor-mediated renal vasodilation. The inhibitory effect of raised extracellular K+ levels on the A(2A) response may be due to K(+)-induced stimulation of Na+/K(+)-ATPase.