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PubMed2006

[An improved operation approach for bipedal rat model construction].

OBJECTIVE: To explore an improved operation approach to make up the ethical deficiency of classical bipedal rat model. METHODS: 20 SD rats were randomly divided into an improved group and a traditional group averagely. Improved group were operated with plexus brachialis nerve amputation, while traditional group with forelimbs amputation close to shoulder joint. Forelimb and shoulder joint movements were observed and electromyography of the peripheral muscles around shoulder joint were recorded to make certain the paralytic scope. Operation duration and axillary artery hurt probability of both the improved and traditional operation were compared to evaluate the operation risk of improved approach. Mean total upright time on 2 d, 1 w, 2 w, 4 w and 6 w post-operation and upright posture on 6 w post-operation were recorded to evaluate the human-upright-posture-simulating effect of bipedal rats operated with improved approach. RESULTS: Compared with classical amputation approach, improved approach exhibited simpler operation procedure, shorter operation duration and lower axillary artery hurt probability. Electromyography revealed that all forelimb muscles and most shoulder-peripheral muscles were denervated, forelimbs of the improved bipedal rats were absolutely paralyzed and shoulder joint reserved only slight abduction function. The mean total upright time of improved bipedal rats was longer than the classical ones after 2 w post-operation, while upright posture showed no difference with classical bipedal rats. CONCLUSIONS: The improved operation approach not only simplified operation procedures, but also achieved even better effect than classical amputation operation and exempted bipedal rat model from the ethical shadow.

Animals↗
PubMed2006

Perinatal corticosteroid effect on amygdala and hippocampus volume during brain development in the rat model.

Exposure of the fetus to corticosteroid during brain development has been suggested to cause permanent change in brain structure and has been associated with long term cognitive, behavioral and emotional impairment. We evaluated the effect of perinatal corticosteroid, at a dose similar to that which human fetuses are exposed, on cerebral cortex, corpus collosum, hippocampus, dentate gyrus and amygdala in a rat model. Rat pups were given betamethasone at day 1 (P1). Brain sections from the rat pups at postnatal day 45 (P45) were then analyzed. No differences were noted in the volumes of cerebral cortex, corpus collosum, hippocampus, dentate gyrus, or three nuclei of the amygdala compared to the control and sham groups. We concluded that a single course of betamethasone, at a comparable dose to that which the human fetus is exposed in clinical practice, had no effect on these regional brain volumes at this stage of development.

Amygdala↗
PubMed2003

Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of metastatic lung tumors in a rat model.

OBJECTIVES: The objectives of the study were to test the hypothesis that hyperbaric levels of oxygen enhance the sensitivity of a sarcoma cell line to doxorubicin (Adriamycin) both in vitro and in vivo in a rat model of pulmonary metastases and to test the feasibility of arterialization of mixed venous blood by direct injection of aqueous oxygen into the pulmonary artery in a rat model. METHODS: Rat sarcoma (MCA-2) cells were incubated in the presence of increasing concentrations of doxorubicin (0.1-2.0 micromol/L). A dose-dependent toxicity relationship at 12 hours of treatment was examined with and without pretreatment with hyperbaric oxygen (3.7 atm absolute for 1.5-3.5 hours). In vivo, Sprague-Dawley rats (n = 24) were injected intravenously with 10(6) MCA-2 cells, and the lung tumors were allowed to mature for 14 days. At that time the animals were divided into four groups: control (no treatment), doxorubicin at 2 mg/kg, hyperbaric oxygen (oxygen at 2 atm absolute for 30 minutes), and hyperbaric oxygen plus doxorubicin. Seven days after treatment, the numbers of lung nodules were counted and the lung weights were determined. In additional rats (n = 7), aqueous oxygen (1 mL oxygen/g saline solution) was infused into the pulmonary artery to determine whether arterialization of mixed venous blood was comparable to pulmonary artery oxygenation with a hyperbaric chamber (n = 7). RESULTS: Hyperbaric oxygen plus doxorubicin produced significantly greater cytolysis of MCA-2 cells (P <.01) than did doxorubicin alone. Hyperbaric oxygen plus doxorubicin also significantly decreased the number of lung metastases and the lung weight relative to doxorubicin alone (P <.01 and P <.01, respectively). The feasibility of arterialization of mixed venous blood (>100 mm Hg) with aqueous oxygen infusion was demonstrated. CONCLUSIONS: Hyperbaric oxygen enhanced the chemotherapeutic effect of doxorubicin both in cell culture and in the rat model. Aqueous oxygen infusion can be used to oxygenate mixed venous blood at levels similar to those obtained with the use of a hyperbaric chamber.

Animals↗
PubMed2006

Impact of Lotensin and Salviae on the changes of TGF-beta1 and its receptors in a rat model of chronic cyclosporine-induced nephropathy.

OBJECTIVES: Transforming growth factor-beta(1) (TGF-beta(1)) and its receptors, type 1 (TR-1) and type 2 (TR-2) play important roles in chronic cyclosporine (CsA)-induced nephropathy. Lotensin is known as an angiotensin-converting enzyme inhibitor and may reduce chronic CsA-induced nephropathy. Recently it is reported that Salviae (a Chinese medicine), which can improve microcirculation and decrease the expression of TGF-beta(1) has the same effect as that of lotensin. Therefore, in this study we assessed the effects of Lotensin or Salviae on the chronic CsA-induced upregulation of TGF-beta(1), TR-1, and TR-2 in a rat model. MATERIALS AND METHODS: Sodium-depleted rats were administered CsA by gastric gavage and a new rat model of chronic CsA-induced nephropathy was established. Rats with chronic CsA-induced nephropathy were treated by lotensin or Salviae. The proteins of TGF-beta(1), TR-1, and TR-2, and the mRNA of TR-1 and TR-2 in the kidneys of CsA-treated rats, were measured by immunohistochemistry (IHC) and in situ hybridization (ISH). The results were investigated semiquantitatively by image analysis. RESULTS: Lotensin or Salviae individually attenuated CsA-induced nephropathy in the rat models, and downregulated the protein expressions of TGF-beta(1), TR-1, and TR-2, and the mRNA transcripts of TR-1 and TR-2 in the rat model. CONCLUSION: Our studies show that treatment with lotensin or Salviae is useful in preventing chronic CsA-induced nephropothy.

Activin Receptors, Type I↗
PubMed2004

Rosiglitazone increases extravasation of macromolecules and endothelial nitric oxide synthase in skeletal muscles of the fructose-fed rat model.

Reduced extravasation of macromolecules in skeletal muscle has recently been documented in the fructose-fed rat model, corroborating a hypothesis that a functional obliteration of muscle regional microcirculation might lead to hypertension and restrict access of nutrients and hormones to their target cells. The goal of this study was to assess the impact of a treatment with rosiglitazone on the reduced muscle vasopermeability observed previously in the fructose-fed rat model. Fructose-fed Sprague-Dawley rats were gavaged with rosiglitazone (10 micromol kg(-1) per day; n = 21) or the vehicle only (n = 19) for 3 consecutive weeks before assessing the extravasation of Evans Blue (EB) dye in vivo in distinct muscle groups. Relative to control group, rosiglitazone reduced mean arterial blood pressure (Delta = -16.7%, P < 0.001), plasma insulin (Delta= -39.1%, P < 0.05) and plasma triglyceride (Delta= -32.8 %, P < 0.01) concentrations in a significant manner. Plasma VEGF concentrations were significantly lower in the rosiglitazone-treated animals compared to the control animals (32.7 +/- 0.8 pg ml(-1) versus 46.1 +/- 1.2 pg ml(-1), P < 0.001). While no changes were observed in the lungs or the kidneys, fructose-fed rats treated with rosiglitazone had a 30-50% increase (P < 0.005) in the extravasation of EB regardless of the skeletal muscle group studied (rectus femoris, soleus, gastrocnemius lateralis, vastus lateralis and tibialis cranalis). In homogenates of skeletal muscles (vastus lateralis) of fructose-fed rats, rosiglitazone resulted in a significant increase in NO synthase (NOS) activity (Delta = +41.9 %, P < 0.003) as well as endothelial NOS immunoreactive mass (Delta = +37.8 %, P < 0.01) compared to the control animals. There was no change in the immunoreactive level of the nNOS isoform, the most abundant muscle isoform, or in the immunoreactive levels of VEGF. In conclusion, rosiglitazone appears to restore a vascular dysfunction previously documented in the skeletal muscle microcirculation, as evidenced by improved skeletal muscle vasopermeability and upregulation of the muscle endothelium-NO system in the fructose-fed rat model. These effects on muscle per se might also result in a partial improvement of the insulin resistance phenomenon by improving the distribution of nutrients and insulin to skeletal muscle. This effect appears to be independent of circulating levels of VEGF since changes in plasma concentrations of this permeability factor were lower in the rosiglitazone-treated group.

Animals↗
PubMed2004

The role of C-reactive protein in ischemia/reperfusion injury and preconditioning in a rat model of myocardial infarction.

For the first time the involvement of C-Reactive protein (CRP) in early (acute) and delayed ischemic (IPC) and pharmacological (chemical) preconditioning (CPC) in an in vivo model of rat myocardial infarction was presented. Acute IPC was produced by three 5 minute occlusion (ischemia) periods interspersed with 5 minute reperfusion, followed by 30 minute occlusion of the left coronary artery and 2 hour reperfusion injury. Acute CPC was produced by a k-opioid receptor agonist U50488H (5 mg/kg) applied i.v. 15 minutes before 30 minute ischemia/ 2 hour reperfusion. Delayed preconditioning was produced by 30 minute ischemia/ 2 hour reperfusion, induced 24 hour after either ischemic or pharmacological preconditioning. The myocardial ischemia/reperfusion injury was evaluated on the basis of total and cardiac creatine kinase isoenzyme activity, functional recovery of the heart (ECG), infarct size (% IS/RA) and mortality at the end of the experiments. The results obtained showed that: k-opioid receptor agonist U50488H mimics both the acute and delayed IPC in the above experimental protocol; Both acute IPC and most probably CPC act by opening of K(ATP) channels (the effects were blocked by nonspecific ATP-sensitive K channel blocker glybenclamide), and via activation of protein kinase C (a selective protein kinase C inhibitor chelerythrine blocked the efects); C-reactive protein (CRP) was significantly elevated by 54% in non-preconditioned acute ischemia/reperfusion injury. The elevation was more pronounced (82% increase) 24 hour after non-preconditioned ischemia/reperfusion injury. It reflected very well the increase in cardiac isoenzymes, infarct size and mortality of the rats, and can be used as a marker of the severity of myocardial injury in this model; The increase of CRP was prevented by both IPC and CPC in early, and especially in late preconditioning. This confirms the involvement of CRP as a marker in cardiac ischemic/reperfusion injury. It was concluded that in addition to the established involvement of adenosine, bradykinin, opioid and other receptors, a suppression of myocardial CRP/complement production might be involved in the biological mechanism of preconditioning. This could be a promising perspective in clinical interventions against ischemia/reperfusion injuries of the heart.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2003

A rat model of syngeneic bone marrow transplantation during breast cancer therapy.

The purpose of this study was to develop a breast cancer model in rats, in which myeloablative chemotherapy and syngeneic bone marrow transplantation (SBMT) could be evaluated systematically for therapeutic effect. The Wistar-Furth (WF) DMBA-4 breast cancer cell line transplanted into naive WF rats produced rapidly growing tumors that were lethal within 2 months. SBMT was performed following preparation with a regimen (Bu-Cy), consisting of busulfan 16 mg/kg by gastric gavage on days -3 and -2 followed by 250 mg/kg of cyclophosphamide i.p. on day -1. Marrow was prepared from the femurs of donors and infused i.v. into the recipient on day 0. In all, 15 rats treated with Bu-Cy without marrow died, while 22 of 25 transplanted rats survived. In total, 16 rats with measurable tumors showed tumor responses following transplantation, but tumors recurred and survival was minimally prolonged. Of nine rats transplanted before clinical tumors were detected, five became long-term survivors that resisted further tumor challenge. It was concluded that the DMBA-4 breast cancer in WF rats could serve to evaluate SBMT following myeloablative doses of chemotherapy at various tumor loads. At large tumor loads therapy was not curative, but at low tumor burdens cures were possible and resistance to subsequent tumor challenge was demonstrated. The model may be useful for further studies of stem cell infusion in rodent tumor systems.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

Decreased raphe unit activity in a rat model of endogenous depression.

One theory about the pathogenesis of endogenous depression is that decreased serotonergic (5-HT) neurotransmission is involved in producing the disorder. A key component of brain 5-HT neurotransmission is the discharge rate of 5-HT neurons in the dorsal raphe nucleus (DRN), a major aggregation of 5-HT neurons. We tested the hypothesis that the discharge rate of 5-HT neurons in the DRN was decreased in a new animal (rat) model of human endogenous depression. In this model, rats are treated neonatally with the antidepressant chlorimipramine. When adult, these animals exhibit several behavioral, REM sleep, and treatment response features of the human disorder. We found in a single unit measurements in adult, pentobarbital-anesthetized rats that, compared with 'non-depressed' control rats, the 'depressed' rats had a lower discharge rate of 5-HT neurons in the DRN. This correlation is consistent with the theory that 5-HT neurotransmission is diminished in endogenous depression.

Animals↗
PubMed2005

Alendronate inhibits spine fusion in a rat model.

STUDY DESIGN: A posterolateral lumbar fusion model in rats. OBJECTIVE: To study the effects of alendronate on posterolateral lumbar fusion in rats. SUMMARY OF BACKGROUND DATA: To our knowledge, there are no studies that show a significant inhibition of manual palpation-assessed spine fusion by alendronate. METHODS: A total of 75 Sprague-Dawley rats underwent intertransverse fusion with 7-tailbone autograft at L4-L5. Animals received saline (control), alendronate equivalent to human dose (dose1, 5 microg/kg/day), or 10 times the human dose (dose10, 50 microg/kg/day) via subcutaneous osmotic pumps starting the day of surgery. Eight weeks after surgery, animals were euthanized, and fusion was assessed by manual palpation. Radiographic area and optical density of fusion masses were calculated. Histomorphometry was used to assess the percentage area of fusion masses occupied by bone or marrow tissues. RESULTS: Manual palpation fusion rates were lower in alendronate groups (50% and 40%, respectively) than in the control group (95%, P = 0.002). Interobserver and intraobserver kappa values were high (0.97-1.00). There were dose-dependent and statistically significant (P < 0.001) increases in fusion mass area and optical density with increasing alendronate dose. Fusion masses in dose10 animals had significantly higher percent area of bone tissue (P = 0.01) and lower percent area of marrow elements (P < 0.001) when compared to control animals. CONCLUSIONS: Alendronate inhibits spine fusion in rats. Fusion masses in alendronate-treated animals appeared radiographically larger and denser than those in control animals despite lower fusion rates. Quantitative histomorphometry confirmed that alendronate inhibited bone graft resorption and incorporation. We recommend that patients undergoing spine arthrodesis should not take alendronate until fusion is achieved.

Alendronate↗
PubMed1995

Evidence for the efficacy of TRAM flap delay in a rat model.

The dilemma in selecting a variant of the transverse rectus abdominis musculocutaneous (TRAM) flap for autogenous tissue breast reconstruction is to balance maximal flap perfusion against the sacrifice of abdominal-wall integrity. A surgical delay has been suggested as one very simple fascia-sparing technique that simultaneously augments flap volume, but no randomized clinical studies have been performed to prove whether there is any benefit whatsoever following such a maneuver. Because large groups of nearly identical subjects may be more readily available for comparison in an animal model, the rat TRAM flap provides an inexpensive method to further investigate the delay phenomenon in this setting. Staged procedures were performed in 15 Sprague-Dawley rats initially causing a delay by division of one or both dominant vessels (cranial epigastric) supplying the rectus abdominis muscles. Either 2 or 4 weeks later, TRAM flaps were elevated based only on the subservient (caudal epigastric) pedicle. A control group of 7 rats with immediate formation of a TRAM flap had a mean survival of 46.3 +/- 15.37 percent of their original flap surface area. After a 2-week delay, viability was 50.2 +/- 17.54 percent for ipsilateral and 39.4 +/- 7.57 percent for flaps with prior bilateral dominant pedicle division. Neither was significantly different from control (p = 0.68 and 0.38, respectively). However, the ipsilateral 4-week delayed group had 67.8 +/- 8.96 percent flap survival, which represented a significant enhancement when compared with the undelayed control TRAM flaps (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Muscles↗
PubMed1988

Cyclosporine disposition in the hyperlipidemic rat model.

Since cyclosporine is heavily bound to plasma lipoproteins, its pharmacokinetic profile was evaluated in the Zucker hyperlipidemic rat model (N = 4) and compared to Zucker lean (N = 4) and Sprague-Dawley (N = 4) rat models. Following a single i.v. dose (5 mg/kg) of cyclosporine, serial blood samples, collected by tail bleed, were assayed for cyclosporine concentration by radioimmunoassay. Pharmacokinetic analysis was performed by standard non-compartmental methods. Half-lives between the three groups were not different. However, Zucker obese rats demonstrated a significantly smaller volume of distribution at steady-state (2.8 +/- 1.1 L/kg; p less than 0.01) versus the Zucker lean (5.4 +/- .9 L/kg) and Sprague-Dawley rats (5.6 +/- .7 L/kg). Likewise, the total body clearance was markedly reduced in the obese (0.24 +/- .09 L/h/kg; p less than 0.01) versus lean (0.51 +/- .04 L/h/kg) and Sprague-Dawley (0.52 +/- .06 L/h/kg) rat models. This data suggests the ability of lipids to significantly impair the intracellular transfer of cyclosporine and may impact on its clinical monitoring, efficacy and toxicity.

Animals↗
PubMed2000

Rat model of experimentally induced abacterial prostatitis.

BACKGROUND: An experimental model in rats was developed to investigate the significance of mucosal integrity in abacterial prostatitis. METHODS: Ethanol was instilled into the ventral prostates of male rats to reduce mucosal integrity; dinitrobenzenesulfonic acid (DNBS) was added as an irritant to induce inflammation. Controls received no treatment, ethanol only, DNBS only, or a suspension of bacteria. After various time points, rats were sacrificed, and their prostates were assayed for gross morphology, histological appearance, and cytokine levels. RESULTS: Prostates subjected to ethanol plus DNBS showed significant inflammation, most notably after 12, 24, and 48 hr. Inflammation judged by gross and histological observations and interleukin-1beta levels correlated well at these times. Rats given only ethanol, DNBS, or no treatment, acting as negative controls, displayed little or no inflammation; rats given a bacterial suspension, acting as positive controls, showed inflammation consistent with past studies. Cytokine assays revealed raised interleukin-1beta levels in this model, while tumor necrosis factor-alpha remained at a basal level. CONCLUSIONS: The loss of an intact mucosal surface in the prostate resulted in inflammation caused by an irritant. Interleukin-1beta appears to play a role in this inflammation, while tumor necrosis factor-alpha does not.

Animals↗
PubMed2003

[Experimental study on effect of the water extract of dogwood fruits on the liver and testis in rats model of kidney-yang deficiency].

OBJECTIVE: To explore the effect of Dogwood fruits on tonifying kidney-yang. METHOD: The effect of the water extract of Dogwood fruits on rats model of kidney-yang deficiency with the hydrocortisone was observed. RESULT: The water extract of Dogwood fruits could make normal the liver weight, and mitigate hepatocyte pathologic changes, increase the heptocellular levels of RNA and hepatin, and decrease the malondialdehyde (MDA) in rats model of kidney-yang deficiency. It could also make the viscera quotiety return to normal way and increase the levels of RNA in the interstitial cells of testicle in rats model of kidney-yang deficiency. CONCLUSION: Water extract of Dogwood fruits can protect and improve the functions of the liver and testicle in rats model of kidney-yang deficiency.

Animals↗
PubMed2005

The Fischer 344/NNiaHSd X Brown Norway/BiNia is a better model of sarcopenia than the Fischer 344/NNiaHSd: a comparative analysis of muscle mass and contractile properties in aging male rat models.

Sarcopenia, characterized by profound muscle atrophy and the loss of contractile function, contributes significantly to the development of frailty and functional impairment in older age. Although present in aging humans, rat models have failed to clearly demonstrate a similar degree of this age-associated loss of muscle mass and function. This investigation compared two models of rats raised specifically for aging studies, the Fischer 344/NNiaHSd (F344/N) and the Fischer 344/NNiaHSd X Brown Norway/BiNia (F344/NXBN), and sought to determine which model provides the most accurate representation of human sarcopenia. We found that aging had no effect on F344/N muscle mass or contractile function in the extensor digitorum longus (EDL) and soleus (SOL). Conversely, in the F344/NXBN model, aging was found to decrease EDL and SOL mass and contractile function. These changes were sufficient to satisfy the proposed criteria for the diagnosis of human sarcopenia based upon muscle mass and contractile function. Results indicate that the F344/NXBN provides a better model of the alterations seen in aging human muscle than the F344/N rat model.

Aging↗
PubMed1995

Effects of passive immunization against parathyroid hormone-related protein: PTHrP is the responsible factor in mediating hypercalcemia in the Walker carcinosarcoma 256 rat model.

The Walker carcinosarcoma (WCS) 256 is a well-characterized rat model of humoral hypercalcemia of malignancy (HHM). We addressed the question of whether parathyroid hormone-related protein (PTHrP) is the factor responsible for mediating HHM in this model. WCS 256 cells were subcutaneously implanted in female rats. We examined the plasma at days 0, 2, 4, 6, and 8. The midregional PTHrP measured by radioimmunoassay (RIA) and the plasma calcium increased significantly. Measuring PTHrP by a two-site immunoradiometric assay (IRMA) showed comparable results. There was a strong positive correlation between plasma calcium and midregional PTHrP (r = 0.85, p < 0.0001). A strong positive correlation between tumor weight and both midregional PTHrP (r = 0.83, p < 0.0001) and plasma calcium (r = 0.87, p < 0.0001) was also found. After surgical removal of the tumor at day 5, both plasma calcium and plasma PTHrP levels fell to within the normal range. Ip administration of native polyclonal antiserum against PTHrP(53-84) led to a significant decrease of plasma calcium. Extracted WCS 256 tumor showed 5-fold increased levels of midregional PTHrP compared with liver. Immunohistochemistry and Western blot were positive for PTHrP. RNA from the WCS 256 tumor was positive for PTHrP whereas liver tissue RNA was negative. WCS 256 cells grown in vitro also secreted PTHrP into the medium. We conclude that PTHrP is synthesized and secreted by WCS 256 and that PTHrP is the factor responsible for mediating hypercalcemia in the WCS 256 rat model.

Analysis of Variance↗
PubMed2006

Prostanoid receptor EP1 and Cox-2 in injured human nerves and a rat model of nerve injury: a time-course study.

BACKGROUND: Recent studies show that inflammatory processes may contribute to neuropathic pain. Cyclooxygenase-2 (Cox-2) is an inducible enzyme responsible for production of prostanoids, which may sensitise sensory neurones via the EP1 receptor. We have recently reported that while macrophages infiltrate injured nerves within days of injury, they express increased Cox-2-immunoreactivity (Cox-2-IR) from 2 to 3 weeks after injury. We have now investigated the time course of EP1 and Cox-2 changes in injured human nerves and dorsal root ganglia (DRG), and the chronic constriction nerve injury (CCI) model in the rat. METHODS: Tissue sections were immunostained with specific antibodies to EP1, Cox-2, CD68 (human macrophage marker) or OX42 (rat microglial marker), and neurofilaments (NF), prior to image analysis, from the following: human brachial plexus nerves (21 to 196 days post-injury), painful neuromas (9 days to 12 years post-injury), avulsion injured DRG, control nerves and DRG, and rat CCI model tissues. EP1 and NF-immunoreactive nerve fibres were quantified by image analysis. RESULTS: EP1:NF ratio was significantly increased in human brachial plexus nerve fibres, both proximal and distal to injury, in comparison with uninjured nerves. Sensory neurones in injured human DRG showed a significant acute increase of EP1-IR intensity. While there was a rapid increase in EP1-fibres and CD-68 positive macrophages, Cox-2 increase was apparent later, but was persistent in human painful neuromas for years. A similar time-course of changes was found in the rat CCI model with the above markers, both in the injured nerves and ipsilateral dorsal spinal cord. CONCLUSION: Different stages of infiltration and activation of macrophages may be observed in the peripheral and central nervous system following peripheral nerve injury. EP1 receptor level increase in sensory neurones, and macrophage infiltration, appears to precede increased Cox-2 expression by macrophages. However, other methods for detecting Cox-2 levels and activity are required. EP1 antagonists may show therapeutic effects in acute and chronic neuropathic pain, in addition to inflammatory pain.

Adult↗
PubMed2002

[Establishment of delayed encephalopathy rat model of carbon monoxide poisoning].

OBJECTIVE: To establish the delayed encephalopathy rat model of carbon monoxide (CO) poisoning. METHODS: 40 Wistar rats were randomly divided into 4 groups of 10 rats and were placed in the chambers of inside-built 10-chamber poisoning box. Mixed gas is ventilated with the volume fractions of 10.0 x 10(-4), 15.0 x 10(-4) and 16.5 x 10(-4) of CO in air into the chambers for group A, B and C respectively, and pure air was ventilated for group D. The gas flow rate was 800 L/h in the first 5 hours, 1,000 L/h in the middle 4 hours, and 1,200 L/h in the last 3 hours, with a whole ventilation time of 12 hours. Before and after CO poisoning maze test with radial eight-arm maze was conducted to assess the rats' intelligence. The appearance of coma or less than 3 correct arm-enterings in maze test between the 3rd and 28th day after poisoning was considered as the indications of delayed encephalopathy. TUNEL method, flow cytometry, and transmission electron microscopy were adopted to examine the cellular apoptosis in cerebral cortex and hippocampus area. RESULTS: There were 4 rats with delayed encephalopathy changes in groups B and C respectively, while no similar behavioral change appeared in groups A and D. TUNEL method showed an apoptotic rate of 45.0% to 65.0% in the rats with delayed encephalopathy of group B and an apoptotic rate of 55.0% to 80.0% in the rats with delayed encephalopathy of group C, most of the apoptotic cells being neurons. Flow cytometry showed an apoptotic rate of 50.5% +/- 4.2% in the rats with delayed encephalopathy of group B and an apoptotic rate of 55.9% +/- 7.8% in the rats with delayed encephalopathy of group C. By electron microscopy the percentage of typical apoptotic neurons was 5.0% approximately 15% in group B and 10.0% to 20.0% in group C, less than 5.0% in group A, and less than 1.6% in group D. CONCLUSION: A delayed encephalopathy rat model of CO poisoning has been successfully established based on the volume fraction of 15.0 x 10(-4) to 16.5 x 10(-4) of CO in air and a poisoning time of 12 hours. The pathological change is a mass neuron apoptosis in cerebral cortex and hippocampus.

Animals↗
PubMed1993

[The microcirculatory dynamics of prostaglandin E1 and/or nicardipine and their different reactions in the hyper- and hypodynamic state of septic shock in a rat model].

The reactions of the mesenteric microcirculation dynamics to prostaglandin E1(PGE1) and nicardipine were investigated under continuous biomicroscopy with a high speed video analyzer in septic shock models using rats. Both of the drugs induced similar reactions. In the hyperdynamic state, the vasodilation and increasing velocity of red blood cells (RBC) stimulated by both of these vasodilators were similar to those in normal control state. However, in the hypodynamic state the vasodilators especially PGE1 had little effect on increasing the velocity of RBC in spite of their vasodilating action. Therefore these vasodilators are useful in order to improve the microcirculatory blood flow in states such as early septic-shock state.

Alprostadil↗