Abstract
We recently demonstrated that calcitonin gene-related peptide (CGRP) released from sensory neurons reduces spinal cord injury (SCI) by inhibiting neutrophil activation through an increase in the endothelial production of prostacyclin (PGI2). Carperitide, a synthetic -human atrial natriuretic peptide (ANP), reduces ischemia/reperfusion (I/R)-induced tissue injury. However, its precise therapeutic mechanism(s) remains to be elucidated. In the present study, we examined whether ANP reduces I/R-induced spinal cord injury by enhancing sensory neuron activation using rats. ANP increased CGRP release and cellular cAMP levels in dorsal root ganglion neurons isolated from rats in vitro. The increase in CGRP release induced by ANP was reversed by pretreatment with capsazepine, an inhibitor of vanilloid receptor-1 activation, or with (9S,10S,12R)2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12epoxy-1H-diindolo[1,2,3-fg:3,2,1-kl]pyrrolo[3,4-i][1,6]-benzodiazocine-10-carboxylic acid hexyl ester (KT5720), an inhibitor of protein kinase A (PKA), suggesting that ANP might increase CGRP release from sensory neurons by activating PKA through an increase in the cellular cAMP level. Spinal cord ischemia was induced in rats using a balloon catheter placed in the aorta. ANP reduced mortality and motor disturbances by inhibiting reduction of the number of motor neurons in animals subjected to SCI. ANP significantly enhanced I/R-induced increases in spinal cord tissue levels of CGRP and 6-keto-prostaglandin F1. a stable metabolite of PGI2. ANP inhibited I/R-induced increases in spinal cord tissue levels of tumor necrosis factor and myeloperoxidase. Pretreatment with 4-chloro-3-methoxycinnamanilide (SB366791), a specific vanilloid receptor-1 antagonist, and indomethacin reversed the effects of ANP. These results strongly suggest that ANP might reduce I/R-induced SCI in rats by inhibiting neutrophil activation through enhancement of sensory neuron activation.
Highlights
To clarify the relation between ATP and prostaglandinE2 (PGE2) in the immunologic system, we investigated the acute and chronic effects of PGE2 on activation of purinergic signaling in monocytes by measuring the ATP-induced elevation of intracellularCa2+ ([Ca]i) in fura-2-loaded THP-1 monocytes
IFNγ plays a critical role in host defense by promoting Th1 phenotype and bacterial clearance
Low IFNγ levels are were washed, loaded with fura-2-AM, and transferred into a quartz associated with the Th2 phenotype consistent with critical illness cuvette and placed in the thermostat-regulated sample chamber of anergy [2]
Summary
To clarify the relation between ATP and prostaglandinE2 (PGE2) in the immunologic system, we investigated the acute and chronic effects of PGE2 on activation of purinergic signaling in monocytes by measuring the ATP-induced elevation of intracellularCa2+ ([Ca]i) in fura-2-loaded THP-1 monocytes. Several experimental studies suggest that thrombolysis therapy acts directly on thrombi or emboli and enhances microcirculatory reperfusion In this retrospective study we investigated the extent of blood coagulation and fibrin formation via the plasma D-dimer level, an indicator of endogenous fibrinolytic activity, in patients who underwent inhospital and out-of-hospital cardiac arrest from nontraumatic causes. Methods MEDLINE, EMBASE, CINAHL, and the Cochrane Library were searched, and studies were included if they reported on ICU patients > 16 years old who were evaluated for CINMA clinically and electrophysiologically, and they contained sufficient data to quantitatively measure the association between CINMA and clinically relevant exposures and/or outcomes. Our aim was to evaluate the role of the cardiac markers NT-proBNP, Troponin T (TnT) and myoglobin as predictors of inhospital and 6-month all-cause mortality in patients admitted to a general adult ICU with severe sepsis/septic shock. Aging is associated with decreased cardiopulmonary and renal reserve as well as the development of progressive organ failure
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