During past 7 years, 43 patients less than 2 years of age underwent closure of the ventricular septal defect. Durations of postoperative use of a respirator were 3 days or less in 30 patients (short-period group) and over 3 days in remaining 13 patients (long-period group). There was no operative death. Pre-, intra- and postoperative factors affecting prolonged respiratory care were analyzed between two groups. Results were as follows: There were statistically significant differences between short- and long-period groups on age (9.7 versus 6.5 months), body weight (6.3 versus 5.2kg) at surgery, necessity of preoperative respiratory care on respirator (0/30 versus 4/13), duration of cardiopulmonary bypass (108 versus 132min.), aortic clamp time (56 versus 70min.) and respiratory index at the first postoperative day (1.1 versus 1.7). These results revealed the necessity of far earlier surgical intervention in symptomatic patients before respiratory distress develops. Furthermore, shorter cardiopulmonary bypass and aortic clamp times should always be in mind for attaining smooth postoperative course.

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.