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Bacterial sepsis has become the most frequent infectious complication of transfusion. Although Yersinia enterocolitica is a common enteropathogen usually causing relatively mild disease, it is nevertheless a prominent cause of life-threatening post-transfusion infection. To gain a better understanding of the clinical presentation and prognosis of this rare occurrence, we performed a systematic and detailed review of 55 published cases, which we present here after a description of the mechanisms underlying the contamination of red blood cell preparations by Y. enterocolitica. The symptoms are rapid-onset septic shock sometimes heralded by atypical symptoms, such as explosive diarrhea, with an overall fatality rate of 54.5%. Although the pathophysiology involves transfusion of preformed bacterial endotoxin, timely administration of effective antibiotics seems to improve the prognosis. Increased vigilance of the blood supply could help mitigate this transfusion hazard, although cost-effective strategies are difficult to define for this highly serious but infrequent event.
Bacterial sepsis has become the most frequent infectious complication of transfusion. Although Yersinia enterocolitica is a common enteropathogen usually causing relatively mild disease, it is nevertheless a prominent cause of life-threatening post-transfusion infection. To gain a better understanding of the clinical presentation and prognosis of this rare occurrence, we performed a systematic and detailed review of 55 published cases, which we present here after a description of the mechanisms underlying the contamination of red blood cell preparations by Y. enterocolitica. The symptoms are rapid-onset septic shock sometimes heralded by atypical symptoms, such as explosive diarrhea, with an overall fatality rate of 54.5%. Although the pathophysiology involves transfusion of preformed bacterial endotoxin, timely administration of effective antibiotics seems to improve the prognosis. Increased vigilance of the blood supply could help mitigate this transfusion hazard, although cost-effective strategies are difficult to define for this highly serious but infrequent event.
Pressor effects of the vasoconstrictor hormone arginine vasopressin (AVP), observed when systemic AVP concentrations are less than 100 pM, are important for the physiological maintenance of blood pressure, and they are also the basis for therapeutic use of vasopressin to restore blood pressure in hypotensive patients. However, the mechanisms by which circulating AVP induces arterial constriction are unclear. We examined the novel hypothesis that KCNQ potassium channels mediate the physiological vasoconstrictor actions of AVP. Reverse transcriptase polymerase chain reaction revealed expression of KCNQ1, KCNQ4, and KCNQ5 in rat mesenteric artery smooth muscle cells (MASMCs). Whole-cell perforated patch recordings of voltage-sensitive K ϩ (K v ) currents in freshly isolated MASMCs revealed 1,3-dihydro-1-phenyl-3,3-bis(4-pyridinylmethyl)-2H-indol-2-one (linopirdine)-and 10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone (XE-991)-sensitive KCNQ currents that were electrophysiologically and pharmacologically distinct from other K v currents. Suppression of KCNQ currents by AVP (100 pM) was associated with significant membrane depolarization, and it was abolished by the protein kinase C (PKC) inhibitor calphostin C (250 nM). The KCNQ channel blocker linopirdine (10 M) inhibited KCNQ currents in MASMCs, and it induced constriction of isolated rat mesenteric arteries. The vasoconstrictor responses were not additive when combined with 30 pM AVP, and they were prevented by the L-type Ca 2ϩ channel blocker verapamil. Ethyl-N-[2-amino-6-(4-fluorophenylmethylamino)pyridin-3-yl] carbamic acid (flupirtine) significantly enhanced KCNQ currents, and it reversed constrictor responses to 30 pM AVP. In vivo, i.v. administration of linopirdine induced a dose-dependent increase in mesenteric artery resistance and blood pressure, whereas flupirtine had the opposite effects. We conclude that physiological concentrations of AVP induce mesenteric artery constriction via PKCdependent suppression of KCNQ currents and L-type Ca 2ϩ channel activation in MASMCs.Membrane voltage (V m ) determines the open probability of L-type Ca 2ϩ channels in vascular smooth muscle cells (VSMCs), and K ϩ channels represent a primary effector for adjusting V m . To the extent that Kϩ channels are open in resting VSMCs, the outward flux of K ϩ through these channels (measured as K ϩ current) will tend to stabilize the resting V m at negative (hyperpolarized) voltages and prevent opening of voltage-sensitive Ca 2ϩ channels. In contrast, reduction of outward K ϩ currents in VSMCs results in a shift to more positive V m (membrane depolarization) leading to activation of L-type Ca 2ϩ channels and entry of Ca 2ϩ into the cell. Elevation of the cytosolic Ca 2ϩ concentration in this manner can trigger VSMC contraction and vasoconstriction.KCNQ channels (Kv7 family) are voltage-sensitiveThis work was supported by the National Heart Lung and Blood Institute Grant R01 HL070670 (to K.L.B.) and the American Heart Association Grant 0715618Z (to A.R.M.).The chemical st...
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