Although remote ischemic preconditioning (RIPC) is an organ-protective maneuver from subsequent ischemia reperfusion injury (IRI) by application of brief ischemia and reperfusion to other organs, its mechanism remains unclear. However, it is known that RIPC reduces the heart, brain, and liver IRI, and that nitric oxide (NO) is involved in the mechanism of this effect. To identify the role of NO in the protective effect of RIPC in renal IRI, this study examined renal function, oxidative status, and histopathological changes using N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor. Remote ischemic preconditioning was produced by 3 cycles of 5 minutes ischemia and 5 minutes reperfusion . Blood urea nitrogen, creatinine (Cr), and renal tissue malondialdehyde levels were lower, histopathological damage was less severe, and superoxide dismutase level was higher in the RIPC + IRI group than in the IRI group. The renoprotective effect was reversed by L-NAME. Obtained results suggest that RIPC before renal IRI contributes to improvement of renal function, increases antioxidative marker levels, and decreases oxidative stress marker levels and histopathological damage. Moreover, NO is likely to play an important role in this protective effect of RIPC on renal IRI.
Traumatic tricuspid regurgitation is a rare complication of blunt cardiac injury and frequently misdiagnosed during the initial assessment. Unfortunately, it may be diagnosed after deterioration of right ventricle function, which may be fatal to the patient. Here, we report a case of a patient with blunt chest injury complicated by a diagnosis of traumatic severe tricuspid regurgitation after deterioration of the right ventricle function even after the patient was subjected to serum cardiac enzyme normalization. The patient was a driver and admitted to the hospital owing to multiple traumatic injuries. Echocardiography was performed suspicious of blunt cardiac injury, which revealed no abnormal findings. Initial cardiac enzyme levels were high, but after serial follow-up, the levels improved. However, on day 4 of hospitalization, hemodynamic deterioration occurred owing to severe tricuspid regurgitation and delayed right ventricle dysfunction. Immediate tricuspid valve replacement was performed, however, the patient had a pronged recovery period. We believe that it is important to take into account the nature of the accident and the presentation of clinical signs and symptoms and not be blinded by laboratory test results alone; it is also important to consider performing repeated serial echocardiographic examinations for blunt cardiac injury patients.
Rationale: Emergence is not simply the reverse process of induction. Many dynamic situations could occur in this period by distinct neurobiology as recent studies indicated. Herein we report a rare case of failure of emergence from general anesthesia after cervical spine surgery.Patient concerns: Despite the perioperative vital signs and laboratory results were unremarkable, the patient could not recover his mental status and spontaneous breathing during emergence. 20 minutes after cessation of anesthetic drug administration, his blood pressure suddenly began to decrease requiring transfusion and vasopressor.Diagnosis: After thorough inspection of intraoperative alterations of hemodynamic and metabolic values, which showed no significant changes except possible signs of delayed volume loss, cerebrovascular bleeding was most suspected as the cause of the event. Computed tomography was performed and infratentorial hemorrhage after cervical spine surgery was checked.Interventions: Decompression operation was required for removing the hemorrhage. However, the patient's family refused further management considering his limited life expectancy.Outcomes: The patient expired on postoperative day 5.lessons: Failure to awaken is a relatively rare event. It could be confused with simple delayed emergence, which is often caused by residual drug effect. However, when it occurs, the result could be devastating. Therefore, appropriate recognition and prompt response are required to decrease the mortality and morbidity of the patient. Abbreviations: ABGA = arterial blood gas analysis, BIS = bispectral index, BP = blood pressure, BT = body temperature, Ce = effect-site concentration, CI = cardiac index, Cp = plasma concentration, CSF = cerebrospinal fluid, CT = computed tomography, CVP = central venous pressure, ECG = electrocardiography, Hct = hematocrit, HR = heart rate, PRBC = packed red blood cells, RCH = remote cerebellar hemorrhage, ScvO 2 = central venous oxygen saturation, SpO 2 = oxygen saturation, SVV = stroke volume variation, TCI = target-controlled infusion.
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