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• W2021709498 abstract "In Response: In the case we reported,1 the patient's arterial blood pressure remained at approximately 60/40 mm Hg for about 40 minutes and responded poorly to norepinephrine and phenylephrine. The cardiac output was increased (8.0 L/min) and the systemic vascular resistance (SVR) was low (369 dynes · s · cm−5), with a heart rate of >100 bpm. Hemoglobin-oxygen saturation, temperature, electrolytes, and acid-base status were normal. Thus, our patient's hemodynamics were typical of the vasoplegic syndrome (severe and persistent hypotension, tachycardia, normal or increased cardiac output, decreased SVR, and poorly responsive to volume infusions and vasoconstrictive drugs)2,3 and differed from postreperfusion syndrome (PRS) in etiology, symptoms, and treatment (Table 1).Table 1: Differences Between VS and PRSWe accept that vasoplegic syndrome is related to ischemia reperfusion injury of intestine and graft liver, which is why we cited articles related to ischemia reperfusion injury. Further studies are needed to explore the precise mechanism of vasoplegic syndrome during liver transplantation. Patients with vasoplegic syndrome tend to have increased morbidity and mortality.4,5 The conventional treatment, vasopressin and methylene blue administration, has been based on an understanding of the pathophysiology of vasomotor dysfunction after graft reperfusion, which includes cAMP-dependent vasoconstriction, cGMP/ nitric oxide–dependent vasoconstriction, vasopressin deficiency, and hyperpolarization-dependent vasoconstriction.5,6 Methylene blue can be used as a last-resort pharmacologic agent to treat vasopressor-refractory vasoplegic syndrome.5 Compared with vasoplegic syndrome, PRS is defined as a decrease in mean arterial blood pressure of >30% below the baseline value for at least 1 minute, occurring during the first 5 minutes after reperfusion.7,8 The sudden influx of cold, acidic, hyperkalemic blood from the grafted liver into the systemic circulation, hypothermia, hypocalcemia, minor air and thrombus embolization, and release of vasoactive substances or inflammatory mediators from the grafted liver and ischemia–reperfusion gut may lead to the development of PRS by decreasing SVR or due to myocardial dysfunction.7,8 Based on previous studies, treatment of PRS includes volume expansion, correction of abnormal acid-base status, vasopressor and inotropic agents, prophylactic ischemia reperfusion injury agents, and maintaining normal body temperature.7,8 Patients with vasoplegic syndrome seen after cardiac surgery, septic shock, and liver transplantation have different proinflammatory cytokine responses and pathophysiology processes, which may lead to the variety of cases reported by different authors, but share the hemodynamic characteristics of low SVR and high cardiac output, the mechanisms of nitric oxide, and cGMP overproduction.4–6 Zhongping Cao Guocai Tao Department of Anesthesia Southwest Hospital The Third Military Medical University Chongqing, China [email protected]" @default.
• W2021709498 created "2016-06-24" @default.
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• W2021709498 date "2010-03-01" @default.
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• W2021709498 title "Is It Possible to Distinguish Between Vasoplegic Syndrome and Postreperfusion Syndrome During Liver Graft Reperfusion?" @default.
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