In order to gain further insight into the relationship between high-density lipoprotein (HDL) metabolism and plasma triglyceride transport, measurements were made of HDL cholesterol concentration, apoprotein (apo) AI and AII metabolism, very-low-density-lipoprotein (VLDL) apo B metabolism, and heparin-elutable adipose tissue lipoprotein lipase (LPL) activity in seventeen subjects with a wide range of plasma triglyceride concentrations (0.8-25 mmol/l). The fractional catabolic rate (FCR) of VLDL apo B was directly related to LPL activity (r = +0.80), providing evidence that the activity of the enzyme in adipose tissue is a determinant of the rate of lipolysis of VLDL in man. HDL cholesterol concentration was a positive function of both VLDL apo B FCR (r = +0.74) and LPL activity, a finding consistent with previous evidence for the origin of a proportion of HDL cholesterol from 'surface remnants' liberated during VLDL catabolism. THe FCRs of both apo AI and apo AII were inversely related to VLDL apo B FCR (AI, r = -0.52; AII, r = -0.69) and to LPL activity. The synthetic rate of ap AII, but not that of apo AI, was positively correlated with VLDL apo B synthesis (r = +0.7 1). Thus, the metabolism of the major proteins of HDl in man appears to be closely associated with VLDL metabolism.

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Temporal gradients of amnesic effects from different doses of COa were determined for rats and mice and compared with one obtained in a comparable previous study using electroconvulsive shock (ECS) as the amnesic agent. At 25-sec. exposure to CO 2 , rats showed significant retrograde amnesia (RA) when treatment was delayed up to 4 min. after punishment, but not after 5, while ECS produced amnesia up to 30 sec. but not after 1 min. Tests using shorter exposures to CO 2 and stronger current of ECS showed that this difference could not be accounted for by intensity of treatment. This and other differences suggest that the two treatments may produce RA via different mechanisms.

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