We have investigated the force required to remove lumbar extradural catheters from 88 parturients to determine the effects of patient positioning at removal, relative to the position at insertion. Parturients were allocated randomly to one of four groups: LS (lateral insertion, sitting withdrawal), LL (lateral insertion, flexed lateral withdrawal), SL (sitting insertion, lateral withdrawal) or SS (sitting insertion, sitting withdrawal). In both positions, the lumbar spine was kept maximally flexed. The force required to remove the catheter was measured at withdrawal. We found that the withdrawal force was influenced by the relationship between the position at removal and that at insertion, and we recommend that for ease of removal, patients should be placed in the same position as they were at the time of insertion. Compared with all other groups, the withdrawal force in patients in group LS was significantly greater (P < 0.05).

The feasibility of day case laparoscopic cholecystectomy was assessed in unselected patients using a standard anaesthetic protocol. Postoperative pain and nausea were assessed at 6 and 24 h postoperatively (visual analogue scale, range 0-10). Thirty-two patients were studied (23 female, 9 male, mean age 49.6 years). The mean duration of surgery was 68 min. At 6 h after surgery, 10 patients (31%) had no pain at rest. For the group as a whole, the median pain score was 3 at rest (range 0-6), 4 on movement (0-9), and 5 on coughing (0-9) and eight patients (25%) were nauseated. At 24 h, 15 (46.9%) had no pain at rest. For the group as a whole, the median pain score was 1 at rest (0-7), 3 (0-6) on movement and 3 on coughing (0-9). The same eight patients were nauseated. Ten patients (31.3%) were judged fit for discharge at 6 h, and 28 (87.5%) by 24 h. There was no statistical difference in mean age or duration of surgery in those judged fit for early discharge compared to the study group as a whole. Nausea was an important factor in those unfit for discharge at 24 h. Selection criteria might improve these figures. From the results of our study, 24 h admission is a more realistic goal and will be suitable for most patients requiring laparoscopic cholecystectomy.

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An inherited metabolic disorder in a strain of New Zealand White rabbits, characterized by marked hypercholesterolemia (394 ± 1 0 0 mg/dl), with moderately elevated or normal triglyceride levels is described. Low density lipoprotein (LDL), intermediate density lipoprotein (IDL) and very low density lipoprotein (VLDL) cholesterol levels were increased. VLDL and IDL, and to a lesser extent LDL, had increased free cholesterol and esterified cholesterol content, and triglyceride content was reduced. Kinetic studies with 131 I and 125 l-labelled rabbit lipoproteins showed a marked increase in production rates of VLDL apo B and LDL apo B. LDL cholesterol levels were directly related to LDL apo B production rate (r = 0.938, p < 0.001). Both in hypercholesterolemic and normal rabbits injected with labelled VLDL, the specific activity-time curves of VLDL apo B and LDL apo B did not intersect, indicating that LDL apo B was in part derived from sources other than VLDL. No defect was demonstrated in receptormediated catabolism of LDL by cultured skin fibroblasts from hyperlipidemic animals. The fractional catabolic rate of LDL apo B was subnormal, but increased when the expanded LDL apo B pool size was reduced by exchange transfusion; the low fractional catabolism may therefore be attributable, at least in part, to saturation of LDL receptors consequent upon the increased pool size of LDL. The hyperlipidemia in this strain of rabbits may be unique in that the underlying mechanism appears to be overproduction of VLDL and LDL. (Arteriosclerosis 7:105-112, March/April 1987) E xperimental induction of hyperlipidemia with consequent atherosclerosis-like lesions was first documented in cholesterol-fed rabbits more than seventy years ago. 1 This and subsequent dietary studies have provided insights into the pathogenesis of atherosclerosis in humans. More recently two genetic disorders associated with atherosclerosis have been described in laboratory animals. One, in the Watanabe heritable hyperlipidemic (WHHL) rabbit, is associated with pronounced hyperlipidemia in normally fed rabbits 2 and results from a defect in receptor-mediated catabolism of low density lipoprotein (LDL), intermediate density lipoprotein (IDL), and very low density lipoprotein (VLDL). 3 There is secondary overproduction of LDL. 4 ' 5 IDL and LDL levels in plasma are greatly increased. The disorder, which is associated with arterial lesions similar to human atherosclerosis, is in most respects analogous to familial hypercholesterolemia in man. The second disorder is the result of selected inbreeding to produce animals that develop pronounced hyperlipidemia and arterial lesions in response to cholesterol feeding ("hyper-responders"), reflecting a genetic predisposition to the metabolic effects of this diet. 6 Pronounced hypercholesterolemia in a chow-fed New Zealand White rabbit was observed by one of us (ALV). The rabbit was mated with a normal female; four of the first litter of seven were hypercholesterolemic. The disorder has been transmitted vertically t...