ABSTRACT
Return of blood flow after periodic ischemia is often accompanied by myocardial injury, commonly known as lethal reperfusion injury (RI). Experimental studies have shown that 50% of muscle die of ischemia and another 50% die because of reperfusion. It is characterized by myocardial, vascular, or electrophysiological dysfunction that is induced by the restoration of blood flow to previously ischemic tissue. This phenomenon reduces the efficiency of the present modalities used to combat the ischemic myocardium. Moreover, despite an improved understanding of the pathophysiology of this process and encouraging preclinical trials of multiple agents, most of the clinical trials to prevent RI have been disappointing and leaves us at ground zero to explore newer approaches.
ABSTRACT
BACKGROUND: Esophageal motility and lower esophageal sphincter (LES) pressure change with rapid changes in intraabdominal pressure (IAP); the response of these to slow change in IAP is not known. AIMS: To study esophageal body motility and LES pressures in patients with cirrhosis with tense ascites in the basal state and after paracentesis. METHODS: Twenty four patients with cirrhosis of liver and tense ascites and 13 with cirrhosis without ascites (controls) were studied. Basal intragastric (IGP) and LES pressures, and esophageal body response to water swallows, were recorded using a water perfusion system; IAP was measured in patients with ascites. In patients with ascites, the study was repeated twice: after paracentesis of two liters of fluid and after adequate control of ascites. RESULTS: Basal IGP (p = 0.002) and duration of esophageal contraction (p = 0.01) were lower in controls, but basal LES pressures were similar in the two groups. After control of ascites, IAP (p = 0.02) and IGP (p = 0.005) decreased; amplitude and duration of distal esophageal contraction decreased (p < 0.05). The frequency of high-amplitude waves also decreased (p = 0.04). LES pressure remained unaltered. CONCLUSIONS: Esophageal contraction duration is increased in the presence of ascites, and decreases after control of ascites; LES pressure is not affected by ascites.