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Influence of brain injury on vasopressin-induced pial artery vasodilation: role of superoxide anion.

The present study was designed to investigate the effect of fluid percussion brain injury (FPI) on vasopressin-induced pial artery vasodilation and the role of superoxide anion generation in those observed effects. In the piglet, it was observed previously the FPI produces pial artery constriction associated with free radical generation. Anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. FPI of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Vasopressin in physiological and pharmacological concentrations (10 and 1,000 microU/ml) produced vasodilation that was reversed to constriction after FPI (15 +/- 1 vs. -8 +/- 1 and 25 +/- 1 vs. 13 +/- 1% for 10 and 1,000 microU/ml before and after injury, respectively). Vasopressin-induced dilation was associated with increased cerebrospinal fluid guanosine 3', 5'-cyclic monophosphate, and these biochemical changes were blunted by FPI (407 +/- 12 and 720 +/- 28 vs. 4 and 272 +/- 5 fmol/ml for control and 10 microU/ml before and after injury, respectively). In contrast, polyethylene glycol superoxide dismutase (PEG-SOD) and catalase pretreatment 30 min before FPI partially restored vasopressin-induced pial artery dilation (14 +/- 1 vs. 3 +/- 1 and 22 +/- 1 vs. 2 +/- 4% for 10 and 1,000 microU/ml before and after FPI, respectively). Similarly, biochemical changes associated with vasopressin dilation were also partially restored by PEG-SOD and catalase after FPI. These data show that vasopressin is reversed from a dilator to a vasoconstrictor after FPI and suggests the superoxide anion generation contributes to the alteration of vasopressin cerebrovascular effects after injury and that such altered vasopressin cerebrovascular effects contribute to pial vasoconstriction after FPI.

Animals↗

Traumatic brain injury does not alter cerebral artery contractility.

Previous studies have shown that traumatic brain injury (TBI) significantly reduces cerebral blood flow determined in vivo and reduces vascular reactivity in the pial circulation measured with cranial window preparations. We have now tested the hypothesis that TBI induces these changes by impairing intrinsic contractile activity of cerebral arteries. Anesthetized rats underwent moderate (2.2 atm) and severe (3.0 atm) midline fluid percussion TBI or sham injury following which posterior cerebral or middle cerebral arteries were isolated and isometric force generation was measured. Moderate (n = 5) and severe (n = 3) trauma had no effect on the magnitude of serotonin- or K+-induced force generation or sensitivity to serotonin in arteries isolated within 10 min of TBI. Functional disruption of the endothelium of posterior cerebral arteries isolated 10 min after moderate trauma or sham injury caused a reduction in the active tension response to serotonin that was similar in both groups. Blockade of cyclooxygenase with 5 microM indomethacin had no effect on serotonin-induced force generated by vessels with moderate trauma or in sham-treated rats. Acetylcholine induced an endothelium-dependent relaxation of posterior and middle cerebral arteries; the magnitude of the response was unaffected by moderate TBI. To determine whether prolonged in situ exposure of vessels to the traumatized cerebral milieu could reveal an alteration in intrinsic contractility, posterior cerebral arteries were isolated 30 min after TBI; again, no differences in the tension or relaxation responses were observed. It is concluded that midline fluid percussion TBI did not affect contraction or relaxation of proximal middle or posterior cerebral arteries in rats.

Acetylcholine↗

Brain injury impairs ATP-sensitive K+ channel function in piglet cerebral arteries.

BACKGROUND AND PURPOSE: Traumatic injury is the leading cause of death for infants and children, and mortality is increased with head injury. Previous studies have shown that pial arteries constricted and that responses to several nitric oxide (NO)-dependent dilator stimuli were blunted after fluid percussion injury (FPI) in newborn pigs. Membrane potential of vascular muscle is a major determinant of vascular tone, and activity of K+ channels is a major regulator of membrane potential. Recent data show that the NO releasers sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) and 8-bromo-cGMP elicit dilation via ATP-sensitive K+ channel (KATP) activation. The present study was designed to investigate the effect of FPI on KATP channel function. METHODS: Chloralose-anesthetized newborn pigs equipped with a closed cranial window were connected to a percussion device that consisted of a saline-filled cylindrical reservoir and a metal pendulum. Brain injury of moderate severity (1.9 to 2.1 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Pial artery diameter was measured with a video microscaler. Data were analyzed by repeated measures ANOVA. An alpha level of P < .05 was considered significant. RESULTS: FPI blunted dilation to cromakalim (10(-8), 10(-6) mol/L), a KATP agonist (10 +/- 1% and 27 +/- 2% versus 3 +/- 1% and 7 +/- 2% before and after FPI, respectively, n = 8). Similarly, FPI blunted dilation to calcitonin gene-related peptide, an endogenous KATP activator. FPI also blunted dilator responses to SNP, S-nitroso-N-acetylpenicillamine, and 8-bromo-cGMP (10(-6) to 10(-8) mol/L) (10 +/- 1% and 20 +/- 1% versus 2 +/- 1% and 8 +/- 2% for SNP before and after FPI; 9 +/- 1% and 16 +/- 1% versus 2 +/- 1% and 4 +/- 1% for 8-bromo-cGMP before and after FPI, respectively, n = 8). In contrast, responses to papaverine and brain natriuretic peptide were unchanged after FPI. CONCLUSIONS: These data show that KATP channel function is impaired after FPI. Furthermore, these data suggest that impaired function of mechanisms distal to NO synthase contribute to altered cerebral hemodynamics after FPI.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

New ultrasonic femoropopliteal and tibiofemoral tests in the study of patency of the deep venous system.

In phlebology, every new noninvasive examining method is of great importance. Now there are new femoropopliteal and tibiofemoral tests, described originally by Odisio in Argentina and, in a modified form applying ultrasound, introduced in Europe by Krcilek and Barták. An experiment with 25 patients was performed to verify the conclusive evidence of the tests. The diagnosis of deep venous thrombosis was examined here by clinical and femoropopliteal and tibiofemoral tests according to Odisio. Finally the diagnosis was verified by the Doppler ultrasonic method. The principle of the femoropopliteal test is the palpative perception, when the fingertips of the left hand applied to the inguen somewhat medially from the femoral artery detect the deep venous wave caused by a repeated percussion of the right hand in the fossa poplitea. Getting some experience enables one to practice simple examinations leading to verification of a suspected diagnosis of femoral thrombosis. Replacing the palpating hand by a sonde of an ultrasonic detector gave substantial precision to examinations in the test modification. Similarly the diagnosis of deep venous thrombosis of the calf was verified by the percussional tibiofemoral test, when the right hand repeatedly percussed on the calf in the course of crural veins, while the left hand palpated the transmission of the wave to the inguen. Both modifications of the femoropopliteal and tibiofemoral tests were verified by the classical ultrasonic examination method. The results were compared with those from a control group of 25 patients without clinical and phlebogic symptoms of disease of the lower limbs.

Adult↗

Musculoskeletal demands on flamenco dancers: a clinical and biomechanical study.

The flamenco dancer acts on the floor like a drummer. The percussive footwork and vibration patterns created during dancing impose unusual demands on the musculoskeletal system. This study investigated the clinical and biomechanical aspects of this task. Using the electrodynogram and skin-mounted accelerometers, foot pressures as well as hip and knee vibrations were recorded in 10 female dancers after a thorough clinical evaluation. A health questionnaire was also distributed to 29 dancers. Foot pressures and acceleration data reveal the percussive nature of the dance. Some clinical findings, like calluses, are related to pressure distribution. Urogenital disorders, as well as back and neck pain, may be related to the vibrations generated by the flamenco dance form. The hip joint seems to absorb most of the impacts. "Vibration-pressure" diagrams are suggested as a useful tool for evaluating a dancer's biomechanical behavior, as well as the effect of floors and footwear on this behavior.

Adult↗

The acute effects of body position strategies and respiratory therapy in paralyzed patients with acute lung injury.

BACKGROUND: Routine turning of critically ill patients is a standard of care. In recent years, specialized beds that provide automated turning have been introduced. These beds have been reported to improve lung function, reduce hospital-acquired pneumonia, and facilitate secretion removal. This trial was designed to measure the physiological effects of routine turning and respiratory therapy in comparison with continuous lateral rotation (CLR). METHODS: The study was a prospective, quasi-experimental, random assignment, trial with patients serving as their own controls. Paralyzed, sedated patients with acute respiratory distress syndrome were eligible for study. Patients were randomized to receive four turning and secretion management regimens in random sequence for 6 h each over a period of 24 h: (1) routine turning every 2 h from the left to right lateral position; (2) routine turning every 2 h from the left to right lateral position including a 15-min period of manual percussion and postural drainage (P&PD); (3) CLR with a specialized bed that turned patients from left to right lateral position, pausing at each position for 2 min; and (4) CLR with a specialized bed that turned patients from left to right lateral position pausing at each position for 2 min, and a 15-min period of percussion provided by the pneumatic cushions of the bed every 2 h. RESULTS: Nineteen patients were entered into the study. There were no statistically significant differences in the measured cardiorespiratory variables. There was a tendency for the ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration (PaO2/FIO2) to increase (174 +/- 31 versus 188 +/- 36; P = 0.068) and for the ratio of deadspace to tidal volume (Vd/Vt) to decrease (0.62 +/- 0.18 versus 0.59 +/- 0.18; P = 0.19) during periods of CLR, but these differences did not achieve statistical significance. There were statistically significant increases in sputum volume during the periods of CLR. The addition of P&PD did not increase sputum volume for the group as a whole. However, in the four patients producing more than 40 ml of sputum per day, P&PD increased sputum volume significantly. The number of patient turns increased from one every 2 h to one every 10 min during CLR. CONCLUSION: The acute effects of CLR are undoubtedly different in other patient populations (spinal cord injury and unilateral lung injury). The link between acute physiological changes and improved outcomes associated with CLR remain to be determined.

Adult↗

Atypical clinical features of pediatric appendicitis.

BACKGROUND: The diagnosis of appendicitis remains challenging in children. Delays in diagnosis, or misdiagnosis, have important medical and legal implications. The typical, or classic, presentation of pediatric appendicitis has been modeled after adult disease; however, many children present atypically with subtle findings or unusual signs. OBJECTIVES: To determine the frequency of atypical clinical features among pediatric patients with appendicitis and to investigate which atypical features are the strongest negative predictors for appendicitis among patients being evaluated for appendicitis. METHODS: Children and adolescents with suspected appendicitis were enrolled over 20 consecutive months. Pediatric emergency physicians completed standardized data collection forms on eligible patients. Final diagnosis was determined by pathology or follow-up telephone call. Typical and atypical findings were defined strictly a priori. RESULTS: Seven hundred fifty-five patients were enrolled. The median age was 11.9 years (interquartile range [IQR]: 8.5, 14.9 yr); 36% of patients were diagnosed with appendicitis. Among patients with appendicitis, the most common atypical features included absence of pyrexia (83%), absence of Rovsing's sign (68%), normal or increased bowel sounds (64%), absence of rebound pain (52%), lack of migration of pain (50%), lack of guarding (47%), abrupt onset of pain (45%), lack of anorexia (40%), absence of maximal pain in the right lower quadrant (32%), and absence of percussive tenderness (31%). Forty-four percent of patients with proven appendicitis had six or more atypical characteristics. The median number of atypical features for patients with proven appendicitis was five (IQR: 4.0, 7.0). The greatest negative predictors, on the basis of likelihood ratios, were as follows: white blood cell count (WBC) of <10,000 per cubic millimeter (likelihood ratios [LR], 0.18), absolute neutrophil count (ANC) of <7,500 per cubic millimeter (LR, 0.35), lack of percussive tenderness (LR, 0.50), lack of guarding (LR, 0.63), and no nausea or emesis (LR, 0.65). CONCLUSIONS: Appendicitis in pediatric patients is difficult to diagnose because children present with a wide variety of atypical clinical features. Forty-four percent of patients with appendicitis presented with six or more atypical features. Two atypical features are the strongest negative predictors of appendicitis in children: WBC of <10,000 per cubic millimeter and an ANC of <7,500 per cubic millimeter.

Adolescent↗

Mounding phenomenon: an experimental study in vitro.

"Mounding" is a local contracture of skeletal muscle that is induced by tapping the muscle directly. We studied the mounding phenomenon in vitro on rat muscles that were percussed by a rotating hammer. In the bulged portion of muscle, there were scattered areas where the sarcomere length was shortened. After muscle was depolarized by the application of KCl-Ringer solution or relaxing solution, the mounding phenomenon was preserved. Agents that abolish the function of T-tubule or T-SR junction did not alter the phenomenon, either. However, after the function of intracellular membrane system such as the sarcoplasmic reticulum (SR) was destroyed by Brij 58, the mounding disappeared. Thus, the mounding is a local contracture that is probably induced by calcium ion liberated from the SR by percussion.

Animals↗

The effect of age on motor and cognitive deficits after traumatic brain injury in rats.

Age is one of the most important predictors of outcome after human traumatic brain injury. This study used fluid percussion brain injury to investigate the effects of aging on outcome after brain injury in rats. Three-month-old (n = 8) and 20-month-old (n = 11) rats were injured at a low level (1.7-1.8 atm) of fluid percussion brain injury or received a sham injury (n = 6 for both age groups). Body weight and motor function (beam balance and beam walking) were assessed before injury and for the first 5 days after injury. Cognitive outcome was assessed with the Morris water maze on Days 11 to 15 after injury. Injury did not produce significant weight loss in either age group. At the low level of brain injury used in this study, the 3-month-old rats did not demonstrate any significant motor deficits on the beam-balance or beam-walking tasks. However, the 20-month-old rats displayed significant beam-balance deficits on each of the 5 postinjury test days and significant beam-walking deficits for the first 3 postinjury days. Although Morris water maze performance was impaired in both age groups, the magnitude of impairment was greater in the aged animals. These data demonstrate that traumatic brain injury in the aged animal is marked by increased motor and cognitive deficits, in the absence of pronounced compromise of the animal's general health.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Two cases of diskitis attributable to anaerobic bacteria in children.

Diskitis, an inflammation of the intervertebral disk, is generally attributable to Staphylococcus aureus and rarely Staphylococcus epidermidis, Kingella kingae, Enterobacteriaciae, and Streptococcus pneumoniae. In many cases, no bacterial growth is obtained from infected intervertebral discs. Although anaerobic bacteria were recovered from adults with spondylodiscitis, these organisms were not reported before from children. The recovery of anaerobic bacteria in 2 children with diskitis is reported. Patient 1. A 10-year-old male presented with 6 weeks of low back pain and 2 weeks of low-grade fever and abdominal pain. Physical examination was normal except for tenderness to percussion over the spine between thoracic vertebra 11 and lumbar vertebra 2. The patient had a temperature of 104 degrees F. Laboratory tests were within normal limits, except for erythrocyte sedimentation rate (ESR), which was 58 mm/hour. Blood culture showed no growth. Magnetic resonance imaging with gadolinium contrast revealed minimal inflammatory changes in the 12th thoracic vertebra/first lumbar vertebra disk. There was no other abnormality. A computed tomography (CT)-guided aspiration of the disk space yielded bloody material, which was sent for aerobic and anaerobic cultures. Gram stain showed numerous white blood cells and Gram-positive cocci in chains. Cultures for anaerobic bacteria yielded heavy growth of Peptostreptococcus magnus, which was susceptible to penicillin, clindamycin, and vancomycin. The patient was treated with intravenous penicillin 600 000 units every 6 hours for 3 weeks, and then oral amoxicillin, 500 mg every 6 hours for 3 weeks. The back pain resolved within 2 weeks, and the ESR returned to normal at the end of therapy. Follow-up for 3 years showed complete resolution of the infection. Patient 2. An 8-year-old boy presented with low back pain and low-grade fever, irritability, and general malaise for 10 days. He had had an upper respiratory tract infection with sore throat 27 days earlier, for which he received no therapy. The patient had a temperature of 102 degrees F, and physical examination was normal except for tenderness to percussion over the spine between the second and fourth lumbar vertebrae. Laboratory tests were normal, except for the ESR (42 mm/hour). Radiographs of the spine showed narrowing of the third to fourth lumbar vertebra disk space and irregularity of the margins of the vertebral endplates. A CT scan revealed a lytic bone lesion at lumbar vertebra 4, and bone scan showed an increase uptake of (99m)technetium at the third to fourth lumbar vertebra disk space. CT-guided aspiration of the disk space yielded cloudy nonfoul-smelling material, which was sent for aerobic and anaerobic cultures. Gram stain showed numerous white blood cells and fusiform Gram-negative bacilli. Anaerobic culture grew light growth of Fusobacterium nucleatum. The organism produced beta-lactamase and was susceptible to ticarcillin-clavulanate, clindamycin, metronidazole, and imipenem. Therapy with clindamycin 450 mg every 8 hours was given parenterally for 3 weeks and orally for 3 weeks. Back pain resolved within 2 weeks. A 2-year follow-up showed complete resolution and no recurrence. This report describes, for the first time, the isolation of anaerobic bacteria from children with diskitis. The lack of their recovery in previous reports and the absence of bacterial growth in over two third of these studies may be caused by the use of improper methods for their collection, transportation, and cultivation. Proper choice of antimicrobial therapy for diskitis can be accomplished only by identification of the causative organisms and its antimicrobial susceptibility. This is of particular importance in infections caused by anaerobic bacteria that are often resistant to antimicrobials used to empirically treat diskitis. This was the case in our second patient, who was infected by F nucleatum, which was resistant to beta-lactam antibiotics. The origin of the anaerobic bacteria causing the infection in our patient is probably of endogenous nature. The presence of abdominal pain in the first child may have been attributable to a subclinical abdominal pathothology. The preceding pharyngitis in the second patient may have been associated with a potential hematogenous spread of F nucleatum. P magnus has been associated with bone and joint infections. This report highlights the importance of obtaining disk space culture for aerobic and anaerobic bacteria from all children with diskitis. Future prospective studies are warranted to elucidate the role of anaerobic bacteria in diskitis in children.

Child↗

Characteristics of acupuncture meridians and acupoints in animals.

In recent years, an increasing number of studies has been conducted on the biophysical characteristics of the meridians and acupoints in humans and animals. The authors aim to further illustrate the objective existence and superficial locations of the meridians in various species of animals. Twelve sheep, ten goats, thirteen pigs, eleven cats, eight rabbits and seven donkeys were used to measure low impedance lines (LILs) and high percussion sound lines (HPSLs) on the skin surface of the animals, along the vertical planes of the dorsal line, using electrical impulses and high percussion sound. The results of these studies are given.

Acupuncture Points↗

Electrophysiological analysis of warming up phenomenon in myotonia.

The after discharges following grip and percussion in myotonia of 4 cases with myotonic dystrophy were evaluated in repetitive percussion or grip, in cold exposure and in warm exposure electromyographically. By repetition, the after discharges reduced markedly. After 2 or 3 trials, after discharges disappeared or became short duration. During local cooling (15 degrees C-20 degrees C), the amplitude and the prolongation in the duration of after discharges were marked, although these enhanced after discharges were reduced by repetition even in cooling. During local warming (40 degrees C-42 degrees C), the after discharges became less marked or disappeared. Both the warming of muscle and the repetitive movements reduced the duration of abnormal after discharges. These effect might be explained on the same mechanism which was the change of the ion transport in muscle membrane, and could be called as warming up phenomenon together. The degree of these after discharges are close related to the degree of myotonic phenomenon. Myotonia is the disorder of primarily the electrical excitabilities, not the contractile properties. So the method of evaluation of after discharges electromyographically is very valuable compared to the measurement of the relaxation process which was used popular in evaluation of myotonia in the past.

Action Potentials↗

Changes in local cerebral blood flow, glucose utilization, and mitochondrial function following traumatic brain injury in rats.

The pathophysiology of secondary brain damage following experimental traumatic brain injury was investigated by measuring local cerebral blood flow (lCBF), local cerebral glucose utilization (lCGU), and activity of succinate dehydrogenase (SDH), which is a mitochondrial enzyme of the tricarboxylic acid cycle, in the rat brain after moderate lateral fluid percussion injury. Measurements used autoradiography for lCBF and lCGU with [14C]iodoantipyrine and [14C]2-deoxyglucose, respectively. Regional SDH activity was determined using quantitative imaging of formazan produced from 2,3,5-triphenyl tetrazolium chloride by SDH. lCBF decreased at 1 hour after injury and was significantly lower than the preinjury level in almost all regions of both hemispheres at 6 and 24 hours, and remained low at 2 weeks. lCGU increased 1 hour after injury but was significantly decreased at 6 and 24 hours, and at 2 weeks in most regions of both hemispheres. The ipsilateral hemisphere showed a significant decrease in the activity of SDH in the cortices, hippocampus, thalamus, and caudate/putamen, most conspicuously 72 hours after injury, whereas no significant decrease was observed in the contralateral hemisphere at any time. Necrosis in the injured cortex and reduction of the number of neurons in the ipsilateral hippocampus were observed 2 weeks after injury. The present study showed that a decrease in lCBF and mitochondrial dysfunction occur with glucose hypermetabolism around 1 hour after lateral fluid percussion injury, and that lCBF, lCGU, and mitochondrial function all deteriorate after 6 hours. This suggests that lCBF and cellular metabolism may change dynamically during the several hours following traumatic brain injury, and afterwards neuronal damage may result in an irreversible change in the areas with depressed glucose hypermetabolism in the early period after injury in combination with mitochondrial dysfunction.

Animals↗

Transient suppression of event-related evoked potentials produced by mild head injury in the cat.

Studies in humans have shown that sensory stimuli, presented in the context of certain tasks, can elicit a late positive component (LPC), namely P300, in the scalp-recorded evoked potential believed to reflect neural activity related to attentional processes. A similar LPC has been reported in cats and monkeys. In this study, the LPC of the auditory evoked potential (AEP) in the cat was used to detect impairment in attention to a relevant stimulus after low levels of cerebral concussion produced by a fluid percussion device. A hollow screw (for fluid percussion) and stainless steel screws (for AEP recording) were surgically placed in the skull. After recovery from surgery, animals were trained in the paradigm to obtain an LPC. Pupillary dilation was conditioned to tones. A random sequence of two discriminable tones was presented. The lower tone had a probability of 0.1 and was followed by a tail shock (tone-shock). After 400 to 1000 tone-shock presentations, animals attended to the lower tone stimulus as inferred by selective pupillary dilation. In the AEP an early positive component at 50 to 120 msec related to an alerting response was enhanced, and an LPC at 250 to 450 msec appeared in response to the paired tone-shock. Animals were then subjected to cerebral concussion. Complete recovery of normal reflexes, motor coordination, and orienting response was seen within 2 hours after injury. The LPC was suppressed for a period of at least 3 days, suggesting that low magnitudes of brain injury can disrupt higher-order neural activities. This disruption can persist despite recovery of other neurological functions.

Animals↗

Effect of posttraumatic hypoventilation on cerebral energy metabolism.

Cerebral energy metabolism was studied in cats subjected to fluid-percussion brain trauma followed immediately by 30 minutes of controlled hypoventilation for the purpose of simulating a more realistic model of human head injury. The cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRGl) were measured, with simultaneous phosphorus-31 magnetic resonance spectroscopy quantifications of cerebral tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi). Hypoventilation alone did not produce marked changes in CMRGl, tissue pH, or PCr:Pi ratios. When hypoventilation was combined with trauma, marked alterations in CBF, CMRGl, PCr:Pi ratio, and tissue pH were seen, indicating relative ischemia. The alterations of cerebral energy metabolism produced by combining trauma and hypoventilation are more severe than those caused by fluid-percussion trauma alone, and may provide a more realistic model of human head injury.

Animals↗

Production and clearance of lactate from brain tissue, cerebrospinal fluid, and serum following experimental brain injury.

Lactate dynamics in the brain, cerebrospinal fluid (CSF), and serum were studied in 20 chloralose-anesthetized cats following fluid-percussion trauma. Brain lactate and brain tissue pH were measured by hydrogen-1 and phophorus-31 magnetic resonance spectroscopy. The CSF, arterial, and cerebrovenous serum lactate levels as well as serum glucose concentration were quantified. In the six sham-operated control animals, brain, CSF, cerebrovenous, and arterial lactate levels as well as brain pH remained at normal values. In the five animals in the mild-trauma group (1.6 atm), brain and CSF lactate levels were moderately elevated, although the brain pH and serum lactate content remained at control values. Severe trauma (3.1 atm) in nine cats produced an 82% increase in the brain lactate index and a reduction in brain tissue pH (7.02 +/- 0.02 to 6.95 +/- 0.02; mean +/- standard error of the mean), indicating brain tissue acidosis caused by excessive lactate accumulation. Brain lactate levels reached a peak 1 1/2 hours after severe trauma, then steadily decreased to normal levels by 8 hours posttrauma. Maximum increases of CSF and arterial lactate levels (from 1.4 +/- 0.2 to 4.1 +/- 0.4 and from 1.6 +/- 0.2 to 4.1 to 0.6 mmol/liter, respectively) were observed 15 minutes after trauma, and the values decreased during the next 2 hours. The response was biphasic, with a secondary rise observed in both CSF and serum lactate levels during the remaining 4 hours of the experiment. The difference between the arterial and venous lactate levels (A-Vlact) gradually increased and reached a peak 2 hours postinjury (from -0.05 +/- 0.10 to -0.41 +/- 0.09 mmol/liter). The results of this study show that the production of lactate in brain tissue, CSF, and blood increased in proportion to the severity of the injury. The observation that lactate levels in blood and CSF are maximum immediately following impact while brain lactate and A-Vlact are gradually increasing suggests that the brain-tissue production of lactate fails to account for the rapid appearance of lactate in CSF and blood. It is speculated that the initial elevation of CSF lactate values reflects the systemic response of trauma, and the secondary rise of CSF lactate levels following severe trauma is due to slow seepage of lactate produced by brain tissue into the CSF space. These studies are the first to describe the temporal profile of brain lactate production and eventual clearance by CSF and blood in fluid-percussion injury.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Possible protective effect of endogenous opioids in traumatic brain injury.

Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.

Animals↗

Relationship between body and brain temperature in traumatically brain-injured rodents.

Recent work has shown that mild to moderate levels of hypothermia may profoundly reduce the histological and biochemical sequelae of cerebral ischemic injury. In the present study, the authors examined the effect of fluid-percussion injury on brain temperature in anesthetized rats and the effect of anesthesia on brain temperature in uninjured rats. The relationship between the brain, rectal, and temporalis muscle temperatures during normothermia, hypothermia, and hyperthermia was studied following a moderate magnitude of fluid-percussion brain injury (2.10 to 2.25 atmospheres) in rats. The results showed that mean brain temperature in 10 anesthetized injured rats, in 21 anesthetized uninjured rats, and in 10 unanesthetized uninjured rats was a mean (+/- standard error of the mean) of 36.04 degrees +/- 0.20 degrees C, 36.30 degrees +/- 0.08 degrees C, and 37.95 degrees +/- 0.09 degrees C, respectively. There was no significant difference in temperature under general anesthesia between injured and uninjured rats (p greater than 0.05). In the absence of brain injury, mean brain temperature was significantly lower in anesthetized rats than in unanesthetized rats (p less than 0.001). In anesthetized brain-injured rats, temporalis muscle temperature correlated well with brain temperature over a 30 degrees to 40 degrees C range, even when brain temperature was rapidly changed during induction of hypothermia or hyperthermia (r = 0.9986, p less than 0.0001). In contrast, rectal temperature varied inconsistently from brain temperature. These observations indicated that: 1) brain injury itself does not influence brain temperature in this model; 2) anesthesia alone decreases brain temperature to levels producing cerebral protection in this model; and 3) external monitoring of temporalis muscle temperature can provide a reliable indirect measure of brain temperature in the course of experimental brain injury. The authors believe that it is essential to monitor or control brain temperature in studies of experimental brain injury.

Animals↗