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We experienced a case of cardiac arrest which occurred after prosthetic replacement of the femoral stem. The patient died three hours and fifty minutes after the end of operation, following hypouresis, pulmonary edema and hypoxia. According to the autopsy, extensive and severe fat embolism was documented in the lung and kidney, and this is considered to be the cause of the death. When prosthetic replacement of the femoral head is performed, we have to keep in mind the danger of fat embolism.

We have tested the two enantiomers of trans-azetidine-2,4-dicarboxylic acid, (2S,4S)-azetidine-2,4-dicarboxylic acid ((2S,4S)-ADA) and (2R,4R)-azetidine-2,4-dicarboxylic acid ((2R,4R)-ADA) for activity at the human metabotropic glutamate receptors mGlu1b, mGlu2, mGlu4a and mGlu5a expressed in mammalian cells. In Chinese hamster ovary (CHO) cells expressing human mGlu2 receptors, 500 microM (2S,4S)-ADA inhibited forskolin-stimulated cAMP accumulation by 33 +/- 3% while 100 microM (1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid induced an inhibition by 66 +/- 5%. The (2R,4R)-ADA enantiomer was inactive at human mGlu2 receptors. In CHO cells expressing human mGlu4a receptors, 10 microM L-AP4 inhibited forskolin-stimulated cAMP levels by 37 +/- 4% whereas both ADA enantiomers of trans-azetidine-2,4-dicarboxylic acid (500 microM) had no such effect. In CHO cells expressing human mGlu1b receptors and L cells expressing human mGlu5a receptors, both enantiomers, applied at 500 microM or 1 mM, were ineffective in stimulating inositolmonophosphate accumulation and did not affect quisqualate-stimulated inositolmonophosphate accumulation. We conclude that (2S,4S)-azetidine-2,4-dicarboxylic acid is a weak human mGlu2 receptor agonist and that (2R,4R)-azetidine-2,4-dicarboxylic acid is inactive at human mGlu2 receptors. Trans-azetidine-2,4-dicarboxylic acid has no significant agonistic effect on human mGlu4a receptors and neither agonistic nor antagonistic effects on human mGlu1b and mGlu5a receptors.

Forty-five hypertensive patients for elective abdominal surgery were investigated regarding the effects of PGE1 on the cardiovascular responses to tracheal intubation. Administration of PGE1 at the dose of 0.10 or 0.20 micrograms.kg-1.min-1 for 10 minutes before tracheal intubation significantly reduced the blood pressure responses immediately after the intubation and 2 minutes later. The increases in heart rate were not altered with and without the administration of PGE1. So the increases in rate pressure products were markedly reduced with PGE1 compared with the control values. Plasma concentration of catecholamines was measured before and after tracheal intubation. Norepinephrine was elevated markedly immediately after the intubation and this change was not affected by the infusion of PGE1. These results demonstrate that PGE1 ameliorates the pressure responses by the release of norepinephrine and thus reduces the increases in rate pressure products immediately after tracheal intubation.