Fatty acid supply and organ phospholipid turnover in two canine shock models

Serum free fatty acid (FFA) flux is decreased in shock. The question arose whether the limited availability of FFA would result in a fuel deficit in organs containing no stored lipid and also in the slower turnover of organ phospholipids. The fasting dog's lung, stomach, heart, and liver contained little or no triglyceride, while skeletal muscle, diaphragm, and occasionally intestine had large lipid stores. The replacement rate of lipid fuels and the turnover rate of the fatty acyl moieties of phospholipids were determined by radioactive tracer methods in several organs of dogs in shock due to controlled cardiac tamponade or hemorrhage and their respective controls. In the normotensive controls one-third of the FFA available was directly oxidized; the rest was temporarily incorporated into phospholipids and triglycerides. This incorporation represents replacement of lipid fuels in the organs. Both shock models caused a similar decrease in the total FFA flux and a similar pattern of redistribution among organs. Organs other than heart, lung, and diaphragm replenished their lipid stores slowly in shock. This could cause a fuel deficit in liver and stomach, neither of which have large triglyceride stores. FFA incorporation into phospholipids was slower than esterification into triglycerides in all organs except diaphragm and skeletal muscle both in shock and in normotension. The rate of phospholipid turnover decreased significantly in shock in liver, intestine, and stomach, but increased in heart and lung. Thus liver and stomach are the organs most likely to be affected by the decreased availability of FFA in shock.