Effects of hypothermic perfusion of kidneys on tissue and mitochondrial phospholipids

The changes in the level of phospholipids in kidney tissue and isolated mitochondria from dog kidneys perfused hypothermically (6-8 degrees C) for 1, 3, and 5 days were compared. Following 1 day of perfusion there was no change in total tissue phosphatidylserine (PS), a 25% decrease in the level of phosphatidylethanolamine (PE), and a 16% decrease in phosphatidylcholine (PC). No further decrease was observed with longer perfusion times. In fact, an increase in the level of PE occurred between the third and fifth days. Mitochondria isolated from perfused kidneys also showed a slight decrease in PE and PC following 1 day, no further change at 3 days, and an increase at Day 5. The loss of tissue phospholipids does not appear related to the viability of perfused kidneys. The major loss occurs within 1 day of perfusion and kidneys perfused up to 3 days are fully viable. Five-day perfused kidneys are nonviable, but show no greater loss of phospholipids than the viable 1- or 3-day perfused kidneys.     

Defining reducible risk

In maternity care, costly high-technology interventions that have never been shown to be clinically effective continue to be used in the United States, while inexpensive and effective low-technology interventions continue to be underused. Three high-technology approaches to risk reduction—electronic fetal monitoring, cesarean section, and home uterine activity monitoring are contrasted with three low-technology approaches—prenatal care, smoking cessation, and nutrition supplementation. These technologies are examined in terms of current controversies over their safety, efficacy, and cost-effectiveness. Examination of these controversies illustrates how the medical technology industry, the regulatory process, and systems of social stratification contribute to social and cultural constructions of what are regarded as reducible birth risks.     

Glycine prevention of cold ischemic injury in isolated hepatocytes

Isolated hepatocytes suspended in a liver preservation solution (University of Wisconsin (UW) solution) and exposed to cold (5 degrees C) ischemia lose viability (LDH release) after 3 (76.5 +/- 2.6% extracellular LDH) and 4 days (90.3 +/- 5.7% extracellular LDH) storage when rewarmed (37 degrees C) in Krebs-Henseleit buffer. However, if 3 mM glycine is added to Krebs-Henseleit buffer the loss of LDH on rewarming was suppressed (% LDH = 24.4 +/- 2.2% and 33.2 +/- 3.0%, at 3 and 4 days, respectively). The protection by glycine could also be obtained by storing the hepatocytes in the UW solution containing 15 mM glycine and rewarming in the absence of glycine in Krebs-Henseleit buffer. There did not appear to be a relationship between the protection by glycine and glutathione concentration of the hepatocytes as shown by the lack of effect of a glutathione synthetase inhibitor (butathionine sulfoximine) on the protective effects of glycine. Other amino acids did not provide protection to hepatocytes exposed to cold ischemia. The mechanism of action of glycine is not known, but this compound may be important in improving cold storage of livers for transplantation.