The rates in Japan of cardiac arrest and death during anesthesia and surgery due to all etiologies as well as those totally attributable to anesthesia are comparable to those of other developed countries.
Taken together, these data uncover a novel effect of iron restriction on renal damage and hypertension through the inhibition of renal mineralocorticoid receptor signaling.
Iron accumulation is associated with the pathophysiology of chronic kidney disease (CKD). Renal fibrosis is a final common feature that contributes to the progression of CKD; however, little is known about the association between renal iron accumulation and renal interstitial fibrosis in CKD. Here we investigate the effects of iron chelation on renal interstitial fibrosis in a rat model of CKD. CKD was induced by 5/6 nephrectomy in Sprague-Dawley rats. At 8 weeks after operation, 5/6 nephrectomized rats were administered an oral iron chelator, deferasirox (DFX), in chow for 8 weeks. Other CKD rats were given a normal diet. Sham-operative rats given a normal diet served as a control. CKD rats exhibited hypertension, glomerulosclerosis and renal interstitial fibrosis. Iron chelation with DFX did not change hypertension and glomerulosclerosis; however, renal interstitial fibrosis was attenuated in CKD rats. Consistent with these findings, renal gene expression of collagen type III and transforming growth factor-β was increased in CKD rats compared with the controls, while iron chelation suppressed these increments. In addition, a decrease in vimentin along an increase in E-cadherin in renal gene expression was observed in CKD rats with iron chelation. CKD rats also showed increased CD68-positive cells in the kidney, whereas its increase was attenuated by iron deprivation. Similarly, increased renal gene expression of CD68, tumor necrosis factor-α and monocyte chemoattractant protein-1 was suppressed in CKD rats with iron chelation. Renal iron accumulation seems to be associated with renal interstitial fibrosis in a rat model of CKD.
Iron restriction prevented further deterioration of preexisting renal damage. The beneficial effects of iron restriction on renal damage seem to be associated with inhibition of renal mineralocorticoid receptor signaling.
The quality of chest compression (CC) is influenced by the surface supporting the patient. The present study compared chest compression depth with and without a rigid backboard on an operating table with a pressure-distributing mattress. We hypothesized that the presence of a backboard would result in an increased depth of chest compression on the operating table with a pressure-distributing mattress. In a randomized crossover trial, we simulated in-hospital cardiac arrest in a Resusci Anne SkillReporter model placed on a standard operating table with a 6-cm-thick pressure-distributing mattress. A total of 25 male doctors performed CC 30 times, with or without the rigid backboard. Mean chest compression depth increased from 4.9 ± 0.4 to 5.4 ± 0.3 mm (P < 0.0001) when a backboard was present. Mean proportion of compressions >50 mm increased significantly with the presence of a backboard (53.6% ± 32.3%-81.8% ± 15.0%, P < 0.0001). Applying a backboard significantly increased CC depth during cardiopulmonary resuscitation of a manikin model on an operating table with a pressure-distributing mattress.
VD (LVOT-AR) has good intra-procedural inter-technique consistency and clinical robustness. Greater than mild post-TAVI AR, but not mild post-TAVI AR, is associated with late mortality.
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