Knee-chest vs horizontal side position during induction of spinal anaesthesia in patients undergoing lumbar disc surgery

In the prone knee-chest position the spread of plain 0.5% bupivacaine in the cerebrospinal fluid and associated haemodynamic changes may be different compared with the horizontal position. A randomized comparison was performed in 40 ASA I-II patients, aged 24-61 yr, undergoing lumbar disc surgery. Subarachnoid injection (27-gauge needle) at the L2-3 interspace with 3 ml of 0.5% bupivacaine was performed with the patient in the operative knee-chest position (prone knee-chest group, n = 20) or in the horizontal side position (supine side horizontal group, n = 20). Patients in the supine side horizontal group were turned into the horizontal supine position for 20 min, and subsequently they were placed in the operative knee-chest position. In three patients in the prone knee-chest group, the spinal needle was replaced by a larger needle (25-gauge). The final cephalad extension of sensory analgesia on skin tested by pinprick was T5 (median) in the prone knee-chest group and T6 in the supine side horizontal group. Recovery was also similar, on average 210 min from injection in both groups. The mean decrease in systolic arterial pressure was somewhat greater in the prone knee-chest group (30 mm Hg) than in the supine side horizontal group (13 mm Hg). The need for ephedrine occurred earlier in the supine side horizontal group (three patients, all within 10 min from local anaesthetic injection) than in the prone knee-chest group (six patients, all after 15 min). Four of the latter patients also required administration of an anticholinergic for bradycardia compared with two patients in the supine side horizontal group. Light sedation was given to five patients in the prone knee-chest group and to four in the supine side horizontal group because of numbness and aching in the shoulders. We conclude that spinal block was similar in the two groups but there was a tendency to more frequent episodes of haemodynamic deterioration in the knee-chest position.     

Assessment of accelerography with the TOF-GUARD: a comparison with electromyography

The effects of age were studied on a new animal model of tardive dyskinesia, i.e., the quantification of oral dyskinesia in rats repeatedly treated with reserpine. Adult and old rats received two injections of reserpine (0.5 or 1.0 mg/kg s.c.) or vehicle, separated by 48 h. One, 10, 25 and 40 days after the second injection of reserpine or vehicle, the animals were observed for quantification of the behavioral parameters of oral dyskinesia: tongue protrusion and vacuous chewing movement frequencies and duration of twitching of the facial musculature. Phenomenologically, control old rats and reserpine-treated adult animals showed very similar oral dyskinesia. When compared to control adult rats, the significant increase in tongue protrusion frequency induced by reserpine treatment was more persistent in the old rats than in the adult animals. Because it is well known that age increases the persistence of tardive dyskinesia, our data provide further support for the validation of reserpine-induced oral dyskinesia as an animal model of tardive dyskinesia. In addition, the possibility is raised that a common pathophysiological mechanism may underlie tardive dyskinesia and age- and reserpine-induced oral dyskinesia.     

Glomerular basement membrane changes in aging nondiabetic and diabetic guinea pigs

Glomerular hyperplasia and thickening of the glomerular basement membrane increase with age in humans and animals. This glomerulopathy can be enhanced by hyperglycemic conditions such as diabetes mellitus. When diabetic guinea pigs were examined by fluorescent microscopy, deposits of a substance similar to immunoglobulin G (IgG) were seen. Comparison with nondiabetic age-matched control animals suggest that glomerulopathy is related to aging, and can be further enhanced by hyperglycemia.     

Downregulation of the Ras activation pathway by MAP kinase phosphorylation of Sos

Formation of a complex of the nucleotide exchange factor Sos, the SH2 and SH3 containing adaptor protein Grb2/Sem-5 and tyrosine phosphorylated EGF receptor and Shc has been implicated in the activation of Ras by epidermal growth factor (EGF) in fibroblasts: related mechanisms for activation of Ras operate in other cell types. An increase in the apparent molecular weight of Sos has been reported to occur after several minutes of receptor stimulation due to phosphorylation by mitogen-activated protein (MAP) kinases. We report here that treatment of human peripheral blood T lymphoblasts with phorbol esters causes a similar shift in mobility of Sos. This modification of Sos does not alter its ability to bind Grb2, but correlates with strong inhibition of the binding of the Sos/Grb2 complex to tyrosine phosphorylated sequences, either a tyrosine phosphopeptide in cell lysates or p36 in intact cells. This effect, along with the mobility shift of Sos, can be mimicked in vitro by phosphorylation of Sos by the mitogen-activated protein kinase, ERK1. A novel negative feedback mechanism therefore exists whereby activation of MAP kinases through Ras results in the uncoupling of the Sos/Grb2 complex from tyrosine kinase substrates without blocking the interaction of Sos with Grb2.     

Nitric oxide synthase pathway may mediate human natural killer cell cytotoxicity

The present study provides evidence that the human natural killer (NK) cell effector mechanism causing target cytolysis has a requirement for L-arginine. In a deficient medium (DM) containing only salts, buffer system and glucose, NK cell-mediated cytotoxicity was found to decrease by 70% as compared to that obtained in a complete medium (CM). However, adding L-arginine to such DM could restore the activity of NK cells to the normal level. Many other components of CM, such as serum, glutamine and vitamins did not improve NK cell-mediated killing in DM. When all amino acids except L-arginine were added to DM only a partial recovery of NK cell functional cytolysis was seen. L-arginine enhanced the NK cell activity in a dose-dependent manner. Additionally, the inhibitor of both inducible and constitutive nitric oxide synthase, N-monomethyl-L-arginine (L-NMMA) inhibited NK cytolytic activity in DM supplemented with L-arginine indicating participation of nitric oxide (NO). The results also show that the stimulatory effect of L-arginine on human NK cell-mediated cytotoxicity was accompanied by an increase in NO formation as determined by accumulation of nitrite and citrulline. L-NMMA gave a dose-dependent reduction in NO generation as well. The nitrite and citrulline production dose-dependently correlated with not only the concentration of L-arginine in the cultivation medium, but also the enhanced NK cell-mediated cytolysis. Taken together, these findings could define a L-arginine/NO-linked effector mechanism in human NK cells. Nitrite and citrulline were not formed when NK cell-mediated target cell killing took place in a L-arginine-free DM supplemented with additives. Thus, it appears as if human NK cells may cause target cell killing via both NO-dependent and -independent processes.     

Hepatic resection for colorectal liver metastases

The lack of other effective treatment for colorectal liver metastases makes hepatic resection a primary treatment consideration. Between January 1980 and December 1990, 26 selected patients with liver colorectal metastases who underwent hepatic resection were reviewed. The age, sex, site of primary lesion, histological grade, lymph node involvement, location, size, and number of hepatic metastases, type of hepatic resection, and preoperative CEA blood levels were documented. Complete removal with histologically negative resection margins were accomplished in 24 patients. The extent of resection performed was hepatic lobectomy in 12 patients. Segmentectomy in eight patients, and wedge resection in four patients. The 5-year survival rate was 30.5 per cent. Patients with metachronous metastases showed a better survival rate than those with synchronous lesions--46.6% versus 13.6% respectively (P = 0.08). None of the other factors studied showed a significant effect on survival. All patients were followed from the time of hepatic resection to the time of this study or death. During a median follow-up of 30.9 months, 20 patients developed recurrence of their disease (60 per cent in the liver). There was no perioperative mortality. Morbidity arose in 66.6 per cent of patients, with a majority of the complications being minor. We conclude that hepatic resection can be performed safely enough to be recommended in selected patients.