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Biomedical subjects

L Cherian

Publications and source records attributed to L Cherian.

At least 37 records · Page 2Linked to original sources
PubMed1996

Secondary insults increase injury after controlled cortical impact in rats.

Secondary ischemic insults are common after severe head injury and contribute to poor neurological outcome. To study the increased vulnerability of the traumatized brain to secondary insults, bilateral carotid occlusion was produced after a controlled cortical impact injury in rats. The injury produced by either the impact injury or the bilateral carotid occlusion was mild to moderate when studied individually. The 1 and 3 m/sec impact injuries alone caused no detectable contusion at the impact side and minimal neuronal loss in the hippocampus. The 5 m/sec impact injury alone resulted in a small contusion with a median volume of 5.4 mm3. The 40-min period of bilateral carotid occlusion alone caused no cortical injury and no neuronal loss in the CA1 region of the hippocampus. When the 40 min of bilateral carotid occlusion was produced 1 h after the impact injury, there was an increase in the damage produced. The contusion volume was significantly larger after the 3 and 5 m/sec impact injuries and the hippocampal neuronal loss was significantly greater after the 1 and 3 m/sec impact injuries. When varying durations of bilateral carotid occlusion were produced 1 h after a 3 m/sec impact injury, contusion volume was significantly larger after bilateral carotid occlusion duration of 40 min, and CA1 neuronal loss was significantly greater after bilateral carotid occlusion durations of 30 and 40 min. When 40 min of bilateral carotid occlusion was produced at different time intervals after a 3 m/sec injury, the increased contusion volume was maximal when bilateral carotid occlusion occurred at 4 h after the impact injury, and the increased neuronal loss in the CA3 region of the hippocampus was maximal when bilateral carotid occlusion occurred at 1 h after the impact injury. By 24 h after the impact injury, 40 min of bilateral carotid occlusion had minimal consequences, similar to the effect in sham-injured animals. These results mimic the clinical situation where secondary insults of a severity that would not cause permanent neurological damage in a normal person are associated with a marked worsening of neurological outcome after head injury and where the injured brain is most susceptible to secondary insults in the first few hours after injury.

Animals↗
PubMed1996

Activation of ornithine decarboxylase and accumulation of putrescine after traumatic brain injury.

Activation of ornithine decarboxylase (ODC), the initial enzyme in polyamine synthesis, and accumulation of putrescine are thought to mediate pathological processes in the ischemic and traumatized brain. Past studies have separately investigated either ODC or polyamines after head injury. The purpose of the present study was to quantify both ODC activity and polyamines in the rat parietal cortex before and after controlled cortical impact injury. Adult, male rats underwent a right craniectomy and were subjected to a 5 m/sec, 2-mm deformation impact injury. Rats were sacrificed 1, 4, 8, and 24 h postimpact and tissues from the injured (right) and contralateral (left) hemisphere were analyzed for ODC and polyamines. ODC activity was determined by measuring the decarboxylation of [14C]ornithine to putrescine. Putrescine, spermidine, and spermine were determined by high performance liquid chromatography. Cortical impact induced a 10- to 20-fold increase in ODC activity and a 4- to 5-fold increase in putrescine in the ipsilateral cortex. Spermidine and spermine did not significantly increase in the ipsilateral (right) cortex compared to controls (right cortex). In contrast, there was a slight increase in spermidine content in the contralateral (left) cortex after injury. The delayed increase in ODC activity and accumulation of putrescine may mediate pathophysiological changes observed after head injury.

Animals↗
PubMed1996

Ileal inhibition and modulation of carbachol-stimulated proximal small intestinal motor functions in humans.

Carbohydrates within the distal small intestine inhibit endogenously stimulated proximal gastrointestinal motor activity and induced an interdigestive-like pattern in humans. In order to further investigate the intermediary mechanisms of the ileal inhibitory effects, we intubated eight healthy volunteers with an oroileal multilumen tube and stimulated small intestinal motility exogenously with a continuous intravenous infusion of the cholinergic agonist carbachol. Additionally, the ileum was perfused for 15-min intervals with either carbohydrates (total load: 18 g) or normal saline as volume control. Ileal carbohydrate perfusion inhibited the carbachol-stimulated motility pattern significantly (p < 0.001) and induced phase-III-like motor activity; ileal saline had no effect. These data suggest that a direct inhibition of cholinergic systems may be involved in the ileal inhibitory effects on proximal small intestinal motility.

Adult↗
PubMed1996

Changes in phospholipids and acetylcholinesterase during early phase of injury to spinal cord--an experimental study in rats.

Injury to spinal cord was produced in rats by the clip compression technique by placing the aneurysm clip extradurally for 30 seconds. The traumatised spinal segment and the adjoining upper segment were used for biochemical estimations. Motor function of the injured rats was evaluated using the inclined plane. Phospholipid phosphorus values were significantly decreased in the injured spinal segment at 24 hrs. AchE activity was also decreased in the traumatised segment one week after injury. Dexamethasone and verapamil reversed the changes in AchE activity at the end of one week. At the one week assessment period, aneurysm clipped rats showed a decrease in the maximum angle in the inclined plane. Dexamethasone and verapamil treated rats showed improvement in the neurologic function, neurologic recovery was better in the dexamethasone treated group.

Acetylcholinesterase↗
PubMed1995

Regional cerebral blood flow after controlled cortical impact injury in rats.

Regional cerebral blood flow (rCBF) and laser-Doppler perfusion were measured in rats after controlled cortical impact injury (CCII), a model of traumatic brain injury. Male Long-Evans rats were anesthetized with isoflurane and surgically prepared with arterial and venous cannulae. CCII was induced after a craniectomy by deforming the right parietal cortex to a depth of 2 mm with a metal cylinder traveling at a velocity of 5.2 m/s. Laser-Doppler perfusion was monitored from the surface of the left frontal cortex. rCBF, using 14C-isopropyliodoamphetamine, and laser-Doppler perfusion were measured in three groups of rats consisting of a sham group (n = 6), a group 30 min after CCII (n = 6), and a group 4 h after CCII (n = 5). CCII was characterized by cortical ischemia (rCBF < 20 mL.100 g-1.min-1) surrounding the site of impact. The occipital cortex, a cortical region distant from the impact site, was also ischemic in some, but not all, injured rats. In the 30-min group, the ischemic zone showed very sharp boundaries with cortical areas of hyperperfusion surrounding the ischemic zone. In the 4-h group, the ischemic boundaries were not as sharp and the hyperperfusion surrounding the ischemic zone was no longer present. The caudate-putamen, hippocampus, and thalamus showed significant reductions in rCBF ranging from 50% to 30% of control 30 min and 4 h postinjury, respectively. We conclude that complex changes in rCBF occur shortly after CCII and persist for at least 4 h. During this time several brain regions, especially the cortical areas, may suffer damage due to the ischemia.

Animals↗
PubMed1994

Lateral cortical impact injury in rats: cerebrovascular effects of varying depth of cortical deformation and impact velocity.

Intracranial pressure (ICP), blood pressure (BP), cerebral perfusion pressure (CPP), and cortical perfusion (LDF) of the contralateral parietal cortex were measured after cortical impact injury in 36 rats. Changes in these physiologic parameters were compared using analysis of variance to a group of 11 rats who received a sham impact. In one series of experiments, the velocity and duration of the impact injury were kept constant, and the severity of the injury was determined by varying the depth of cortical deformation from 2 to 3 mm. The peak pressure inside the skull was directly related to the depth of cortical deformation, and was 93 +/- 16, 182 +/- 18, and 268 +/- 57 mm Hg with the 2, 2.5, and 3 mm deformation, respectively, when the impact velocity was 5 m/sec. With the 2 mm depth injury, there was a transient decrease in BP (p < 0.05) and a 12% decrease in LDF after the impact. With the 2.5 mm depth injury, a small transient increase in ICP and decrease in BP and a 30% decrease in LDF occurred (p < 0.05). ICP then gradually increased throughout the 8 h experiment, becoming significantly greater than the sham-injured animals by 5 h after the impact. LDF gradually returned toward normal throughout the experiment. With the 3 mm depth injury, a marked transient increase in ICP (p < 0.05) and BP (p < 0.05) occurred immediately after the impact. The increase in BP lasted < 5 min, and subsequently the BP decreased to approximately 50 mm Hg for the rest of the experiment. The initial marked increase in ICP lasted 15 min and then remained 5-10 mm Hg higher (p < 0.05) than in the sham-injured animals for the rest of the experiment. LDF decreased by an average of 50% (p < 0.05) immediately after the impact and remained lower than that of the sham-injured animals for the rest of the experiment. In another series of experiments, the depth of cortical deformation was kept constant at 2.5 mm, and the severity of the injury was determined by varying the velocity from 1 to 5 m/sec. The peak ICP was significantly related to the impact velocity, averaging 45 +/- 12, 66 +/- 9, and 182 +/- 18 mm Hg with the 1, 3, and 5 m/sec impact injuries, respectively. The 1 m/sec impact had no effect on ICP and only a transient decrease in BP.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMed1994

Lateral cortical impact injury in rats: pathologic effects of varying cortical compression and impact velocity.

Direct lateral cortical impact through the intact leptomeninges using a pneumatically driven piston produces increasingly severe pathophysiologic derangements with increasing cortical deformation. We studied the histopathologic correlates of cortical impact injury produced by 2 mm, 2.5 mm, and 3 mm deformation in the rat at 5 m/sec. Additionally, the effect of impact velocity at a 2.5 mm deformation was assessed at 1 m/sec, 3 m/sec, and 5 m/sec. The brains were examined 14 days after injury. Cortical contusion maximum cross-sectional area, volume, and the percentage CA1 and CA3 hippocampal neuronal loss correlate with cortical deformation and impactor velocity. Contusion volume increased with increasing cortical deformation. Deformations of 2, 2.5, and 3 mm at 5 m/sec produced contusion volumes of 4.59, 8.9, and 21.68 mm3, respectively. At a fixed cortical deformation of 2.5 mm, contusion volume increased with increasing impact velocity. Impact velocities of 1, 3, and 5 m/sec produced contusion volumes of 5.79, 7.42, and 8.9 mm3, respectively. Hippocampal CA3 neuronal loss increased with increasing cortical deformation. Deformations of 2, 2.5, and 3 mm at 5 m/sec produced neuronal loss of 29%, 48.3%, and 79.5%, respectively. At a fixed cortical deformation of 2.5 mm, hippocampal CA3 neuronal loss increased with increasing impact velocity. Impact velocities of 1, 3, and 5 m/sec produced neuronal loss of 18.25%, 33.75%, and 48.3%, respectively. Hippocampal CA1 neuronal loss was also seen and paralleled cortical deformation and impact velocity. Cortical deformation and impact velocity are critical parameters in producing cortical contusion and must be considered when comparing results using this model.

Animals↗
PubMed1994

Calorie sources and recovery from central nervous system ischemia.

OBJECTIVES: Glucose is the primary substrate for the energy requirements of the nervous system. Nevertheless, administration of glucose to critically ill patients with central nervous system trauma may have adverse effects on their neurologic recovery. The purpose of this study was to evaluate the effects of other sources of nonprotein calories on spinal cord lactate accumulation and on electrophysiologic recovery after a period of severe spinal cord ischemia. DESIGN: Two randomized, blinded studies were performed: one of glycolytic energy substrates (fructose, xylitol, sorbitol, glycerol) and one of ketogenic energy substrates (beta-hydroxybutyrate, acetate, butyrate). SETTING: College teaching hospital laboratory. SUBJECTS: New Zealand albino rabbits (weight 3.5 to 4.5 kg). INTERVENTIONS: After infusion of the randomly assigned treatment, temporary ischemia was produced in the lumbosacral spinal cord by occluding the abdominal aorta with a balloon catheter. MEASUREMENTS AND MAIN RESULTS: Blood concentrations of glucose, lactate, pyruvate, and ketone bodies and spinal cord dialysate concentration of lactate were measured before and after infusion of the assigned treatment, and during ischemia and during the first 2 hrs after reperfusion. Spinal somatosensory evoked potentials were recorded during ischemia to assure a similar severity of ischemia in all animals and during the first 2 hrs after reperfusion as a measure of electrophysiologic recovery. Infusion of the glycolytic nutrients xylitol and fructose increased blood glucose and lactate concentrations, and resulted in increased lactate accumulation in the spinal cord during ischemia and resulted in a significantly poorer recovery of the spinal somatosensory evoked potential than infusion of saline. Infusion of sorbitol and glycerol did not have these adverse effects in the doses administered. None of the ketogenic nutrients increased blood glucose concentration or increased lactate accumulation in the spinal cord during ischemia when compared with infusion of saline. Infusion of butyrate and acetate caused arterial hypotension and resulted in a poorer recovery of the spinal somatosensory evoked potential than saline. Infusion of beta-hydroxybutyrate did not have an adverse effect on blood pressure or on evoked potential recovery. CONCLUSIONS: Glycerol, sorbitol, and beta-hydroxybutyrate deserve further evaluation as potential nonprotein calorie sources in patients with neurologic injury. Xylitol and fructose are not suitable since these substrates resulted in hyperglycemia and increased lactate accumulation in the central nervous system, and had detrimental effects on electrophysiologic recovery after ischemia. The short-chain fatty acids (acetate and butyrate) also had adverse effects on electrophysiologic recovery after ischemia, probably because of their hypotensive effects when given intravenously, rather than from the effects of their metabolism.

Analysis of Variance↗
PubMed1993

[The terminal ileum as a co-regulator of cyclic interdigestive pancreatic secretion in man].

Nutrients present in the ileum of humans can modulate endogenously stimulated pancreatic secretion. To determine whether cyclic interdigestive pancreatic secretion can also be influenced by nutrients in the ileum, six fasting volunteers were intubated with an oro-ileal multi-lumen tube for perfusing test and marker solutions, aspiration of duodenal contents and recording of motility. At the beginning of the interdigestive cycle, the ileum was perfused intermittently with solutions of carbohydrates, proteins or lipids in the physiological amounts observed in the ileum after a meal; saline solution was perfused as a control. After saline, protein and calcium perfusion, the expected periodic increase in chymotrypsin secretion was observed during phase II of the interdigestive cycle (p < 0.05 vs phase I). In contrast, carbohydrates and lipids inhibited the phase-II-associated increase in pancreatic secretion. These findings indicate that the ileum may be involved in the regulation of human interdigestive pancreatic secretion.

Adult↗
PubMed1993

[The synthetic somatostatin analog octreotide: effect on interdigestive pancreas secretion and gastrointestinal motility in man].

The aim of the present study was to determine the effects of a therapeutical dose of the long-acting cyclic somatostatin analogue octreotide (SMS 201-995) on cyclical interdigestive small intestinal motor function and exocrine pancreatic secretion in humans. Five fasting healthy subjects swallowed a gastroduodenal multi-lumen tube assembly and received continuous infusions of saline and octreotide (720 ng/kg/hr) for at least one interdigestive motor cycle or two hours. Upper gastrointestinal motility was recorded continuously by standard manometry. Duodenal chymotrypsin outputs were measured at 15 minutes intervals using polyethylene glycol as a dilution marker. Octreotide significantly decreased the length of the interdigestive motor cycle to one third of the control period (p < 0.01). Phase II proportion was reduced to less than 5% of the cycle length (controls: 66%; p < 0.01). The propagation velocity of octreotide-induced motor activity fronts was significantly slower compared with migrating motor complexes during the control period (controls: 6.8 +/- 0.4 cm/min, octreotide: 2.3 +/- 0.4 cm/min; p < 0.05). Overall duodenal chymotrypsin output was markedly inhibited by octreotide (5% of controls; p < 0.01). Moreover, during octreotide administration coupling between interdigestive motor activity and pancreatic exocrine enzyme secretion was disrupted. In conclusion short administration of a therapeutical dose of octreotide exerts similar effects on upper intestinal interdigestive human motor secretory parameters as naturally occurring molecular forms of somatostatin at pharmacological doses.

Adult↗
PubMed1993

Evaluation of a microsensor intracranial pressure transducer.

This report describes the results of a laboratory evaluation of a new device for monitoring intracranial pressure (ICP), consisting of a miniature pressure transducer mounted on a pressure sensing diaphragm. In in vitro tests, 6 microsensor transducers were monitored for drift at pressures of 10 mmHg and 20 mmHg. The maximal drift of any of the transducers was 1 mmHg over 9 days. In in vivo tests, the ICP measurement obtained with the microsensor transducer correlated well with pressures recorded from a catheter in the cisternal magna with a Statham transducer over a wide range of ICP values (n = 511, r = 0.998, P < 0.001). If these laboratory findings can be duplicated in clinical studies, this microsensor transducer may be a useful alternative to the ventriculostomy catheter and other currently used devices for monitoring ICP.

Animals↗
PubMed1992

Evaluation of drug effects on spinal cord injury--an experimental study in monkeys.

Contusion injury is produced experimentally in anaesthetised monkeys by weight drop method. A group of animals having laminectomy alone served as sham controls. Drugs were administered 30 min after injury initially. Naloxone and nifedipine were administered as single dose administration immediately after injury. Dipyridamole and DMSO were administered daily for a period of 1 week. Acetylcholinesterase (AchE) was estimated in 2 spinal tissue segments, S1-at the site of injury and S2-the segment above the site of injury, at the end of 1 week after sacrificing the animals. Contusion injury produced significant decrease in specific activity of AchE in the traumatised segment of the experimental animals. The non-traumatised adjacent segment did not show any significant change. Nifedipine, naloxone and DMSO produced a decrease in AchE activity in S1 and S2 segments. Monkeys developed paraplegia after contusion injury. A score 2+ was observed after 1 week as compared to the score of 4+ of sham controls. Single dose administration of naloxone seemed to reverse the motor deficit by getting a score of 3+; other drugs did not produce any beneficial effect on motor deficit.

Animals↗
PubMed1991

Ganglioside or sialic acid attenuates ethanol-induced decrements in locomotion, nose-poke exploration, and anxiety, but not body temperature.

1. This laboratory has previously reported that pretreatment with ganglioside, or even with its constituent, sialic acid (SA), can attenuate certain intoxicating effects of ethanol. It was important to see if these findings could be replicated, particularly by using other measures of ethanol effects. Herein we report that pretreatment with either gangliosides or SA attenuated ethanol-induced decrements in locomotion, nose-poke exploration, and anxiety, but not body temperature. 2. An ethanol dose of 4 gm/kg caused a temperature drop of about 3 degrees C, which was unaffected by any pretreatment. The onset to sleep, however, was delayed an average of 18 or 36 secs in mice pretreated with ganglioside or SA, respectively. Ethanol-only (4 gm/kg) depressed mean cumulative locomotor activity to 31% of normal, whereas the depression was 83% of normal with beef brain ganglioside pretreatment. At 2 gm/kg ethanol alone decreased nose poking in a hole-board test to 29% of normal, but the depression was only 55-63% of normal with SA or ganglioside pretreatment. In a staircase climbing anxiety test, this dose of ethanol had no effect by itself, but both ganglioside and SA pre-treatment increased climbing by 22%. Ethanol did depress rearing to only 11% of normal, whereas rearing was 51 and 99% of normal with SA and ganglioside pretreatment, respectively. In a dark-preference test, ethanol-only caused mice to spend 64% of the time in the light, compared to 31% for controls. Time in the light was only 39 and 46% with ganglioside and SA pretreatment, respectively. 3. Blood levels of ethanol were not significantly affected by pretreatment. 4. When given alone, gangliosides significantly stimulated locomotion and staircase climbing. SA significantly decreased rearing in the staircase test. Both gangliosides and SA tended to increase nose poking, number of crossings in the dark-preference test, and time in a lighted compartment. Thus, it is possible that some of the attenuation of intoxication is attributable to non-specific stimulant properties of gangliosides and SA.

Animals↗
PubMed1990

Effect of acute injections of ethanol on lipid and protein-bound sialic acid in mice of different ages.

Mice of different age groups (weanling, young adult and aged) were tested for changes in brain lipid- and protein-bound sialic acid (SA) 2 h after ethanol (2 g/kg, i.p.), either as a single dose or after binge dosing of five repeated doses of ethanol spaced 2 h apart. The results clarify our earlier demonstrations that acute ethanol can reduce whole brain SA. Ethanol generally decreased SA of both gangliosidic and glycoprotein origin, with the effect varying with number of doses and mouse age. Single-dose ethanol decreased both lipid-bound and protein-bound SA in young adults and decreased lipid-bound SA in aged mice. There was no effect on lipid-bound SA in weanlings, but weanlings did have a 72% decline in protein-bound SA. Repeated injections in young adults did not cause the SA decrease seen with acute injection. In both weanling and aged mice, however, repeated injections did cause large decreases in both lipid- and protein-bound SA. Small, but statistically significant, changes also occurred in free SA. Ethanol increased free SA in singly-dosed young adults and in multiply-dosed aged adults, while causing a distinct decrease in singly-dosed weanlings.

Age Factors↗
PubMed1990

Feedback regulation of human pancreatic secretion. Effects of protease inhibition on duodenal delivery and small intestinal transit of pancreatic enzymes.

To determine the effects of luminal protease inhibition on duodenal delivery and the intraluminal fate of pancreatic enzymes, six healthy subjects were intubated with an oro-ileal multilumen tube assembly. By using nonabsorbable markers, cumulative trypsin, chymotrypsin, lipase, and amylase activities were measured as delivered to duodenum, midjejunum, and distal ileum, with or without simultaneous duodenal perfusion of the protease inhibitor camostat at graded doses. Compared with saline, camostat (a) inhibited trypsin activity in the entire small intestinal lumen by up to 99%, and significantly reduced chymotrypsin activity by up to 89%; (b) significantly increased duodenal deliveries of lipase activity, amylase activity and volume; (c) did not influence plasma cholecystokinin concentrations; and (d) significantly increased jejunal and ileal deliveries of lipase but not amylase activity. Small intestinal transit and motility were not affected by camostat. In additional in vitro studies, camostat significantly reduced the spontaneous decline in lipase activity in fresh human duodenal juice incubated at 37 degrees C. These findings demonstrate that duodenal deliveries of lipase and amylase activities increase when intraluminal protease activity is decreased; they suggest that this increase is not caused by slower proteolytic destruction of enzyme protein but by stimulation of pancreatic secretion. Thus, luminal protease-mediated feedback regulation of pancreatic secretion may be operative in humans. Because plasma cholecystokinin concentrations were not affected, these effects may in part be independent of cholecystokinin. The data further suggest that proteolytic digestion plays a major role in the rapid loss of luminal lipase activity on small intestinal transit.

Adult↗
PubMed1989

Ethanol-induced hydrolysis of brain sialoglycoconjugates in the rat: effect of sialic acid in antagonizing ethanol intoxication.

Several reports indicate that acute ethanol promotes the cleavage of brain sialoglycoconjugates (SGC). We attempted to confirm this effect by monitoring cleavage of sialic acid (SA) that had been radiolabeled by pretreatment with the specific precursor of SA, N-[3H]acetyl-D-mannosamine, injected intracerebroventricularly into rats 20 h prior to ethanol injection (2 or 3 g/kg, given four times in a simulated "binge drinking" protocol). Analysis of the residual labeled material revealed a significant reduction of radiolabel (p less than 0.01), as compared to saline controls. A dose of 3 g/kg diminished the total labeled SGC by half. Brain sialidase activity was not affected by the ethanol treatment. Since ethanol intoxication is associated with enhanced SA cleavage, one hypothesis needing testing is that loss of SA might help to cause intoxication. If so, pretreatment with SA might antagonize intoxication, presumably by offsetting loss due to cleavage of SA. Consistent with our earlier results, we found that when sialic acid was given i.p. (25 mg/kg), 1, 6, or 24 h prior to ethanol injection (4 g/kg, i.p.), the sleep time was reduced by 35-40% and the performance on rotorod was significantly enhanced (p less than 0.01). When ethanol was replaced by pentobarbital (40 mg/kg), the sleep time was increased (approximately 30%) at 6 h after injection with either 25 or 100 mg/kg sialic acid, whereas at the 24 h postinjection it was decreased (approximately 20%) at both doses. The results suggest that sialic acid is a key component in mediating ethanol effects and perhaps also, in a different way, anesthetic effects.

Alcoholic Intoxication↗
PubMed1989

Changes in noradrenaline and histamine in monkey spinal cords traumatised by weight drop, compression and subsequent decompression.

Levels of noradrenaline (NA) and histamine (H) in the spinal cord of monkeys at 8, 24 and 48 hr following 200 g/cm contusion injury, 50 g of compression injury at 8 hr and decompression for 16 and 40 hr following 8 hr of compression were studied in the traumatised and in an adjacent non-traumatised segment. The NA level doubled in the traumatised and non-traumatised segments at 8 hr contusion injury followed by a slow decline to control values at 24 and 48 hr of contusion injury. There was no change in NA content of the spinal cord segments at 8 hr of compression injury. Decompression for 16 hr following 8 hr of compression increased NA content of the traumatised segment. H levels decreased in the traumatised and non-traumatised segments at 24 and 48 hr of contusion injury. Compression for 8 hr elevated H in the traumatised and non-traumatised segments. On decompression H level was further increased in the traumatised segment.

Animals↗