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Psychopharmacological properties of crude extract and essential oil of Lippia multiflora (Lm), a verbenacea of african traditional pharmacopea were investigated in rat using classical methods. The extract of Lm is constituted by an infusion of dried leaves. The essential oil is obtained by hydrodistillation of the dried leaves of Lm with a yield of 0.6%. A dilution of 1% is realised with distilled water and the dose of 2 ml/kg of this solution was chosen for this study. The wistar rats of both sexes weighting between 150 and 250 g are used. Animal's behaviour is observed macroscopically for 12 hours. The spontaneous motor activity is appreciated by method of Martin et al. slightly modified. The number of squares jumped by animals in a rectangular cage is determined in ten minutes. The traction test which measures the time necessary for restoration of posterior paws of rat on metallic bar and the duration of pentobarbital sleeping are used for evaluation of muscle relaxant and sedative effects, respectively. The effects of the two preparations of Lm on apomorphin stereotypies and hypothermia are used to investigate the eventual neuroleptic or antidepressant activity. Analgesic property is evaluated by using acetic acid method. The results are expressed as mean +/- SEM. Data are analysed by using the Dunnett's test. A probability level of 0.05 or less was considered to be stalistically significant. The two preparations of Lm at the doses used are well tolerated by rats. No macroscopic difference is observed in behavioural of control and treated groups. Crude extract and essential oil:--does not modify a spontaneous motor activity: control: 45.00 +/- 5.63; crude extract of Lm: 31.00 +/- 5.63; essential oil of Lm: 28.00 +/- 7.62; diazepam 4 mg/kg: 23.80 +/- 5.27 (P < 0.05);--caused an increase of the time necessary for the restoration of paws on the metallic bar in the traction test: control 1.20 +/- 0.25 sec; crude extract of Lm 5.60 +/- 0.57 sec (P < 0.01), essential oil of Lm. 3.60 +/- 0.57 sec (P < 0.01) diazepam 3.60 +/- 0.57 sec (P < 0.01). The differences between the results obtained with crude extract, essential oil and diazepam are significant;--caused a reduction of abdominal cramps induced by acetic acid, control: 26.80 +/- 0.41; crude extract of Lm: 17.00 +/- 1.45 (P < 0.01); essential oil of Lm: 9.20 +/- 1.91 (P < 0.01) and acetylsalicylic acid (Aspegic*) 25 mg/kg 5.40 +/- 1.25 (P < 0.01). The differences is significant between essential oil and crude extract (P < 0.05) but no significant difference is observed between essential oil and acetylsalicylate of lysin. No activity of the two preparations is observed on apomorphin stereotypia and hypothermia comparatively with haloperidol 4 mg/kg and clomipramin 16 mg/kg respectively. Those results confirm the tranquillizer and analgesic activities of Lm and reveal that the crude extract would be more muscle relaxant and the essential oil more analgesic.
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PMID:[Psychopharmacological properties of crude extract and essential oil of Lippia multiflora]. 1168 58

This study was undertaken to measure the effects of mild hypothermia on cerebral blood flow and metabolism and cardiovascular responses to hypoxia in the fetal sheep. Near-term fetal sheep were chronically instrumented with laser Doppler flowmetry in the parietal cortex for measurement of relative changes in cerebral blood flow, as well as with arterial and sagittal sinus catheters for measurement of oxygen extraction by the brain and a cooling coil around the fetal thorax. Fetuses were studied during cooling alone, cooling with superimposed maternal hypoxia to achieve a fetal arterial Po2 of 1.33 to 1.60 kPa, or hypoxia alone. In response to cooling alone [1.6 degrees +/- 0.1 degrees C (mean +/- SEM) decrease in brain temperature], fetal blood pressure and heart rate both increased significantly whereas cerebral blood flow decreased 14 +/- 4%, commensurate with a 24 +/- 8% decline in cerebral metabolic rate. Administration of moderate hypoxia during cooling resulted in a significant increase in cerebral blood flow, decreased heart rate, and no further increase in blood pressure. In response to hypoxia alone, fetal blood pressure was significantly increased, heart rate was decreased, and cerebral blood flow increased by 24 +/- 8%, whereas cerebral metabolic rate decreased by 38 +/- 13%. Arteriovenous oxygen extraction was unchanged by cooling alone but increased significantly in response to hypoxia administered during cooling. We therefore conclude that oxygen delivery to the fetal sheep brain remains coupled to metabolic rate during hypothermia and that hypothermia does not impair the compensatory cardiovascular responses of the fetus to acute moderate hypoxia.
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PMID:Effect of mild hypothermia and hypoxia on blood flow and oxygen consumption of the fetal sheep brain. 1286 1

The aim of this study was to evaluate effect of a short-acting neuroleptic (acepromazine) on capture stress response in roe deer (Capreolus capreolus). Sixteen roe deer were captured by drive-nets in the winters of 1998, 1999, and 2001. Roe deer were divided into two groups: animals in the treatment group received an intramuscular injection of acepromazine (0.093 mg/kg +/- 0.003 SEM; n = 8) while animals in the control group (n = 8) did not receive tranquilizer. Heart rate and body temperature, as well as hematologic and biochemical indicators of stress, were used to evaluate effect of the neuroleptic over 3 hr. Heart rate decreased over time after capture in both groups (P < 0.05), but stabilized sooner in the treated roe deer (75 min after capture) than in the controls (105 min after capture). Body temperature decreased over 45 min and then stabilized in both groups (P < 0.05). Comparisons of blood parameters revealed significantly lower red blood cell count (RBC), lymphocyte count, hemoglobin concentration, packed cell volume (PCV), and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH) activities in tranquilized animals compared with controls (at least P < 0.05). A reduction in PCV, lymphocyte count, and serum cortisol concentrations (at least P < 0.05) and an increase in serum creatinine levels (P < 0.05) were recorded over time in control animals, while a reduction in RBC and hemoglobin concentration (at least P < 0.05) and an increase in serum urea concentrations (P < 0.05) over time were observed in the treated group. Finally, a decrease in serum lactate and potassium levels and an increase in CK, AST, ALT, and LDH activities were recorded over time in both groups. Results obtained showed the suitability of using acepromazine in capture operations in order to reduce stress response and prevent its adverse effects in roe deer. The beneficial effect was not only due to the sedative effect of acepromazine, but also to peripheral vasodilatation.
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PMID:Effects of acepromazine on capture stress in roe deer (Capreolus capreolus). 1291 Jul 65

The post-thrombotic brain has recently been reported to have an enhanced vulnerability to a second embolic insult. Although postischemic hypothermia is neuroprotective in global and focal ischemia models, the effect of mild hypothermia on outcome after thromboembolic insults has not been evaluated. This study therefore determined whether brain hypothermia (33 degrees C) was neuroprotective against repeated thromboembolic insults. Photochemically induced non-occlusive common carotid artery thrombosis (CCAT) leading to platelet embolization to the brain was induced in anesthetized rats ( n=35). Thirty minutes after CCAT, brain temperature was maintained at normothermic (37 degrees C) or hypothermic (33 degrees C) levels for 4 h followed by a slow rewarming period (1.5 h). Three days later, rats underwent a secondary CCAT insult under normothermic conditions and were allowed to survive for an additional 3 days prior to perfusion fixation and quantitative histopathological assessment. Compared to normothermic animals, mild hypothermia after the first embolic insult produced a significant reduction ( P>0.05) in overall infarct volume. Hypothermia reduced total infarct volume from 7.55+/-2.32 mm(3) (mean +/- SEM) in normothermic rats to 2.56+/-0.88 mm(3) in hypothermic animals undergoing repeated insults. Histopathological analysis also demonstrated less evidence for focal hemorrhage in the cooled groups. These data demonstrate that mild hypothermia is protective in a thromboembolic stroke model. In addition, post-thrombotic hypothermia decreases the histopathological vulnerability of the post-thrombotic brain to secondary embolic insults. These findings may be important in the prevention of stroke in patients at risk.
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PMID:The beneficial effect of mild hypothermia in a rat model of repeated thromboembolic insults. 1496 24

Thermal homeostasis is important for the well-being of laboratory rodents during experimental investigations involving chemical restraint. Anaesthesia-induced hypothermia may alter physiological processes, prolong recovery times, or result in death. Therefore, active warming may be needed to prevent excess heat loss from the rodent to the environment. Three methods of active warming were evaluated in typical rodent procedural areas and recovery cages: a forced-air warming system, infra-red heat emitter and circulating-water blanket. The first experiment involved recording the temperature of the immediate environment of the three devices, with and/or without the accompanying plastic drape, to simulate a surgical situation. In the second experiment, temperatures were recorded within cages that simulated a recovery situation with the same modalities. Forced-air warmer blankets (FAWB) were either wrapped around or placed underneath standard polycarbonate rodent cages and the results were compared with cage temperatures warmed by the heat emitter and circulating-water blanket. Temperatures were recorded at 0, 20, 40, and 60 min for each warming treatment, to determine mean temperature (+/- SEM) and the magnitude of increase (+/- SEM) between 0 and 60 min. All three devices showed an increase in temperature, but the FAWB with a plastic drape heated the procedural area microenvironment (Experiment 1) quickly and to a final temperature of 38.6 degrees C (101.5 degrees F) at 60 min, compared with 25 degrees C (77 degrees F) for the heat emitter and 28 degrees C (82.4 degrees F) for the circulating-water blanket. The magnitude of increase was significantly different for each treatment, but the FAWB with a plastic drape climbed 16.3 degrees C (29.3 degrees F) in 60 min. In Experiment 2, the FAWB wrapped around a cage, covered with a plastic drape, heated recovery cages to 32.5 degrees C (90.5 degrees F) compared to the heat emitter 26.4 degrees C (79.5 degrees F) and circulating-water blanket with drape 26.3 degrees C (79.3 degrees F). The magnitude of increase in the microenvironmental temperature was significantly higher for the FAWB, with the plastic drape wrapped around the recovery cage, compared to the other treatments. In both experiments, forced-air warming proved superior to the more traditional thermal support treatments in heating the microenvironments quickly and to an optimum ambient temperature. Forced-air warming devices should be considered when thermal support is required for rodent procedural areas and recovery cages.
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PMID:A comparison of a forced-air warming system to traditional thermal support for rodent microenvironments. 1497 89

During the last decades there has been a debate regarding whether transvascular protein transport is an active (transcytosis) or a passive (porous) process. To separate cooling-sensitive transcytosis from passive transport processes between blood and peritoneal fluid, we induced hypothermia in rats in vivo, reducing their body temperature to 19 degrees C. Control rats were kept at 37 degrees C. Either human albumin, or IgG, or IgM, or LDL, radiolabeled with (125)I, was given intra-arterially together with (51)Cr-EDTA. During tracer administration, a 2-hour peritoneal dialysis dwell was performed. Clearance of the tracers to dialysate, and the permeability-surface area coefficient (PS) for (51)Cr-EDTA and glucose were assessed. During cooling, mean arterial blood pressure (MAP) was reduced to 40% of control and plasma viscosity increased by 48.5%, while peritoneal blood flow was reduced to 10%. At 19 degrees C, clearance of albumin to dialysate fell from 9.30 +/- 1.62 (SEM) to 3.13 +/- 0.28 microl/min (p < 0.05), clearance of IgG from 6.33 +/- 0.42 to 2.54 +/- 0.12 microl/min (p < 0.05), clearance of IgM from 3.65 +/- 0.33 to 1.10 +/- 0.12 microl/min (p < 0.05), and clearance of LDL from 3.54 +/- 0.20 to 0.73 +/- 0.06 microl/min (p < 0.05). The fall in PS for (51)Cr-EDTA was from 0.320 +/- 0.01 to 0.075 +/- 0.003 ml/min (p < 0.05), and that for glucose from 0.438 +/- 0.02 to 0.105 +/- 0.01 ml/min (p < 0.05). Tissue cooling reduced large solute transport largely in proportion to the cooling-induced reductions of MAP (to 40%), and the concomitant increase in viscosity (to 67%), i.e. to approximately 20-30% (0.40 x 0.67) of control, though LDL clearance was reduced further. The fall in small solute PS, in excess of the viscosity effect, mirrored the fall in peritoneal blood flow occurring during hypothermia. In conclusion, the good correlation of predicted to calculated changes suggests that the overall transendothelial macromolecular passage in vivo occurs passively, and not due to active processes.
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PMID:Transvascular passage of macromolecules into the peritoneal cavity of normo- and hypothermic rats in vivo: active or passive transport? 1501 May 75

The objective of this study was to investigate energy metabolism of the gut and liver as well as serum inflammatory cytokines following exploratory laparotomy at moderate hypothermia. Two groups of rats were studied, (n=6-8/group); laparotomy at normothermia for 120 min and laparotomy at hypothermia (32-33 degrees C) for 120 min. Study 1: Intestinal glucose, succinate, lactate, phosphocreatine, and ATP as well as hepatic glucose, succinate, lactate, and ATP were measured in terms of micromole per gram using magnetic resonance spectroscopy. Study 2: Serum levels of TNF-alpha, IL-1beta, LPS-inducible chemokine (LIX), and sICAM-1 were measured by ELISA. Histology of the gut and liver were interpreted. Data are expressed as mean and SEM. In Study 1, laparotomy at hypothermia caused an increase in intestinal glucose levels (0.78+/-0.03 vs. 1.29+/-0.11, P=0.0012) with a decrease in hepatic lactate levels (0.82+/-0.04 vs. 0.44+/-0.06, P<0.001). There were no differences in the other metabolites between the two groups. In Study 2, there were no differences in serum TNF-alpha, IL-1beta, LIX, or sICAM-1 between the two groups. Histological features of the gut and liver among groups were comparable. In conclusion, the intestine and liver react to hypothermia differently. However, levels of high-energy phosphates in both organs are not affected by hypothermia suggesting adequate energy for the organs. It is unlikely that hypothermia induces either systemic inflammatory response or hypoxic damage to the intestine and liver in this model.
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PMID:The effects of moderate hypothermia on energy metabolism and serum inflammatory markers during laparotomy. 1632 33

Exposure to stressors that elicit fear and feelings of hopelessness can cause severe vagal activation leading to bradycardia, syncope, and sudden death. These phenomena though documented, are difficult to diagnose, treat clinically, and prevent. Therefore, an animal model incorporating these cardiovascular conditions could be useful. The present study examined 'sinking' during a 2-h swim stress, a phenomenon that occurs in 50% of rats during 25 degrees C water exposure. Concurrent measurements of body temperature, immobility, heart rate (HR), and PR interval (a measure of vagal activity) were made. Neither decreases in immobility nor variations in hypothermia during swim were correlated with sinking. Bradycardia was more severe in sinking rats (average minimum HR+/-SEM; 143+/-13 vs 247+/-14; p<0.01), and PR interval was elevated (p<0.0001). To examine potential modulation of vagal activity during stress, corticotropin-relasing factor (CRF) receptor antagonists (antalarmin, R121919 and astressin B), a glucocorticoid receptor antagonist (RU486), and a peripherally acting cholinergic antagonist (methylatropine nitrate) were administered. The centrally acting CRF antagonist, antalarmin (32 mg/kg), produced elongation of the PR interval (p<0.0001), robust bradycardia (135+/-18; p<0.001), and increased sinking (92%; p<0.05), and methylatropine nitrate (3.2 mg/kg) blocked these effects. Corroborating these data, two different CRF antagonists, R121919 (30 mg/kg) and astressin B (intracerebroventricular (i.c.v.), 0.03 mug/rat) increased sinking to 100%. RU486 (20 mg/kg) blocked HPA axis negative feedback and decreased percent sinking to 25%. From these studies, we concluded that sinking during a 2-h water exposure was a result of extreme vagal hyperactivity. Furthermore, stress-induced CRF release may serve to protect against elevated cardiac vagal activity.
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PMID:Facilitation of cardiac vagal activity by CRF-R1 antagonists during swim stress in rats. 1671 Mar 22

Perinatal hypoxic-ischemic injury of the basal ganglia is a significant cause of disability in premature infants. Prolonged, moderate cerebral hypothermia has been shown to be neuroprotective after experimental hypoxia-ischemia; however, it has not been tested in the preterm brain. We therefore examined the effects of severe hypoxia and the potential neuroprotective effects of delayed hypothermia on phenotypic striatal neurons. Preterm (0.7 gestation) fetal sheep received complete umbilical cord occlusion for 25 min followed by cerebral hypothermia (fetal extradural temperature reduced from 39.4+/-0.3 degrees C to 29.5+/-2.6 degrees C) from 90 min to 70 h after the end of occlusion. Hypothermia was associated with a significant overall reduction in striatal neuronal loss compared with normothermia-occlusion fetuses (mean+/-SEM, 5.5+/-1.2% vs. 38.1+/-6.5%, P<0.01). Immunohistochemical studies showed that occlusion resulted in a significant loss of calbindin-28 kd, glutamic acid decarboxylase isoform 67 and neuronal nitric oxide synthase-immunopositive neurons (n=7, P<0.05), but not choline acetyltransferase-positive neurons, compared with sham controls (n=7). Hypothermia (n=7) significantly reduced the loss of calbindin-28 kd and neuronal nitric oxide synthase, but not glutamic acid decarboxylase-immunopositive neurons. In conclusion, delayed, prolonged moderate head cooling was associated with selective protection of particular phenotypic striatal projection neurons after severe hypoxia in the preterm fetus. These findings suggest that head cooling may help reduce basal ganglia injury in some premature babies.
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PMID:Induced cerebral hypothermia reduces post-hypoxic loss of phenotypic striatal neurons in preterm fetal sheep. 1696 98

Because various immune functions are impaired at temperatures only 1 degrees to 3 degrees C less than normal, we tested the hypothesis that mild hypothermia during anesthesia impairs resistance to dermal infections. Guinea pigs were anesthetized for 6 hours with 1% inspired halothane. Their core temperatures were maintained at either 39 degrees C (normal for guinea pigs, n = 12) or 36 degrees C (n = 12). Two hours after induction of anesthesia, three doses each of Staphylococcus aureus (10(8), 10(7), and 10(6) organisms) were injected intradermally at nine sites on each animal's back. Core temperatures were not controlled after recovery from the anesthetic, and animals in each group were maintained in the same environment. Four days after anesthesia, each injection site was excised to obtain a count of viable bacteria. Subcutaneous oxygen partial pressure values, averaged over time, were 53 +/- 3 mm Hg (mean +/- SEM) in the hypothermic group and 62 +/- 4 mm Hg in the normothermic group (p = 0.06). Capillary perfusion, as assessed by laser Doppler flowmetry, was comparable in the two groups. One day after injection of 10(8) bacteria, the area of induration was 89 +/- 11 mm(2) in the hypothermic group but only 61 +/- 6 mm(2) in the normothermic group (p < 0.05). On postanesthetic day 4, the area of induration was 72 +/- 6 and 59 +/- 6 mm(2) in the hypothermic and normothermic groups, respectively (p > 0.05). After inoculation with 10(8) bacteria, the fraction recovered was 1.0 +/- 0.2 in the hypothermic groups and 0.6 +/- 0.2 in the normothermic group (p < 0.05). After inoculation with 10(7) and 10(6) bacteria, the fraction recovered was less than 0.2, and no difference was found between the hypothermic and normothermic animals. Thus mild hypothermia during halothane-induced anesthesia slightly impairs resistance to dermal infection.
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PMID:Mild hypothermia during halothane-induced anesthesia decreases resistance to Staphylococcus aureus dermal infection in guinea pigs. 1716 11


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