This study was performed to examine the mean arterial pressure and nociceptive jaw opening reflex after microinjection of glutamate into the amygdala in freely moving rats, and to investigate the mechanisms of antinociceptive action of amygdala. Animals were anesthetized with pentobarbital sodium (40 mg/kg, ip). A stainless steel guide cannula (26 gauge) was implanted in the amygdala and lateral ventricle. Stimulating and recording electrodes were implanted into each of the incisor pulp and anterior digastric muscle. Electrodes were led subcutaneously to the miniature cranial connector sealed on the top of the skull with acrylic resin. After 48 hours of recovery from surgery, mean arterial pressure and digastric electromyogram (dEMG) were monitored in freely moving rats. Electrical shocks (200 ${\mu}sec$ duration, $0.5{\sim}2$ mA intensity) were delivered at 0.5 Hz to the dental pulp every 2 minutes. After injection of 0.35 M glutamate into the amygdala, mean arterial pressure was increased by $8{\pm}2$ mmHg and dEMG was suppressed to $71{\pm}5%$ of the control. Injection of 0.7 M glutamate elevated mean arterial pressure by $25{\pm}5$ mmHg and suppressed dEMG to $20{\pm}7%$ of the control. The suppression of dEMG were maintained for 30 minutes. Naloxone, an opioid receptor antagonist, inhibited the suppression of dEMG elicited by amygdaloid injection of glutamate from $28{\pm}4\;to\;68{\pm}5%$ of the control. Methysergide, a serotonin receptor antagonist, also inhibited the suppression of dEMG from $33{\pm}5\;to\;79{\pm}4%$ of the control. However, phentolamine, an ${\alpha}-adrenergic$ receptor antagonist, did not affect the suppression of dEMG. These results suggest that the amygdala can modulate both cardiovascular and nociceptive responses and that the antinociception of amygdala seems to be attributed to an augmentation of descending inhibitory influences on nociceptive pathways via serotonergic and opioid pathways.
Purpose: The purpose of this study was to examine the effect of DHEA (Dehydroepiandrosterone) on muscle weight and Type I and II fiber cross-sectional area of affected and unaffected hindlimb muscles in rats with neuropathic pain induced by unilateral peripheral nerve injury. Methods: Neuropathic pain was induced by ligation and cutting of the left L5 spinal nerve. Adult male Sprague-Dawley rats were randomly assigned to one of two groups: The DHEA group (n=10) had DHEA injections daily for 14 days, and the Vehicle group (n=10) had vehicle injections daily for 14 days. Withdrawal threshold, body weight, food intake and activity were measured every day. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected from the both hindlimbs. Body weight, food intake, activity, muscle weight and Type I, II fiber cross-sectional area of the dissected muscles were measured. Results: The DHEA group showed significant increases (p<.05), as compared to the vehicle group for muscle weight of the unaffected plantaris, and in Type II fiber cross-sectional area of the gastrocnemius muscle. The DHEA group demonstrated a higher pain threshold than the vehicle group whereas total diet intake and activity score were not significantly different between the two groups. Conclusion: DHEA administration for 14 days attenuates unaffected plantaris and gastrocnemius muscle atrophy.
The purpose of this study was to determine the effects of high voltage pulsed current (HVPC) stimulation on wound healing. Thirty-four Sprague-Dawley adult female rats were assigned to experimental and control groups. Each rats were anesthetized with pentotal sodium, and a 10 mm full-thickness incision was made on the back. From 24 hours after surgery, the rats of experimental groups were stimulated with HVPC, $140{\mu}s$, 120 pps, 30-40 V for 30 minutes, daily. The rats were sacrified 2 days, 4 days and 6 days after stimulation, respectively. The skin was removed, and processed for light microscopic examination. The length of incisional wounds were measured by microcaliper, and nucleolar organizer regions were counted under light microscope. For the histological observations the specimens were stained with Hematoxylin and Eosin, Masson Trichrome, Gomori Reticulum and Ag-NOR. There was a significant decrease in the length of incisional wound in experimental group compared with control group at 6 days HVPC stimuation (p<0.05). In experimental group, wound were significant difference (p<0.01) between the duration of post surgery. The mean numbers of nucleolar organizer regions per nucleus were significantly increased in the experimental group at 6 days HVPC stimulation (p<0.05), and were significantly difference (p<0.01) between the duration of post surgery in experimental group. Histological examination of the wound site suggested a more rapid of epithelialization and collagen formation between experimental groups compared with control groups. The result may indicated that the HVPC with $140{\mu}s$, 120 pps, 30-40 V for 30 minutes promoted surgical wound healing in the rat.
The interaction between a calcium channel blocker nifedipine and atrial natriuretic peptide (ANP) was examined in normotensive and renal hypertensive rats. The infusion of either ANP or nifedipine produced a significant decrease in mean arterial pressure (MAP). The combined infusion of ANP with nifedipine resulted in a greater fall of MAP than did the infusion of each drug alone. ANP significantly increased urinary volume and excretion of sodium, while nifedipine was without effects. The diuretic/natriuretic effects of ANP were potentiated by the combined infusion with nifedipine. The vasodepressor and renal effects of ANP or nifedipine were qualitatively similar between the normotensive and hypertensive rats. Nifedipine caused an upward and leftward shift of the ANP dose-relaxation curve of the phenylephrine-precontracted thoracic aortic rings isolated from the normotensive rats , suggesting that the vasodilation sensitivity to ANP is increased in the presence of nifedipine. These results indicate that nifedipine enhances the vasodepressor effect of ANP, the likely mechanisms being attributable to a contraction of effective intravascular volume as a consequence of potentiated renal excretion and a greater peripheral vasodilation.
Purpose: The purpose of this study was to investigate the effect of Ulmus root-bark dressing in fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) of induced pressure ulcers in rats. Methods: 54 male Sprague-Dawley rats were used and randomly divided into 2 groups. The rats were anesthetized and pressure ulcers were induced at 140 mmHg for three hours, using a personally-designed pressing apparatus. Ulmus dressing was applied in the experimental group (n=27) and saline gauze dressing in the control group (n=27). Each of the dressings was changed every other day, and after a month, the wounds were examined by microscopy biweekly for 20 weeks. Results: After 4 weeks, the epidermis of the wounds was recovered, but inflammatory infiltration of the dermis was remained. After 6 weeks, inflammatory cells were diminished and the number of capillaries was decreased. Examined by immunofluorescence staining, the FGF positive cells in the experimental group changed negatively after 18 weeks, but the control group still existed even after 20 weeks. VEGF positive cells in the experimental group also changed negatively after 20 weeks, but the control group still existed. Conclusion: The findings of this study demonstrate that Ulmus dressing is effective in minimizing scar formation and inflammatory reaction by decreasing FGF and VEGF in the terminal phase of wound healing.
Purpose: The purpose of this study was to examine the effects of the ulmus root-bark dressing on tissue regeneration in experimentally-induced pressure ulcers in rats. Method: A randomized pretest/post-test control group time-series study design was used. Thirty-three male Sprague-Dawley rats were used in this study. The rats were anesthetized with 100mg/kg of ketamine. Pressure ulcers were induced at 140mmHg for three hours using a personally-designed pressing apparatus. For four weeks, the ulmus root-bark dressing was applied every other day in the experimental group (n=18) and a wet gauze dressing in the control group (n=15). For data analysis, the statistical program SPSS WIN 12 was used. The wounds were examined by light microscopy andelectron microscopy. Result: There were significant statistical differences in the size of the pressure ulcers as time went by(p=0.006). It should be noted that there were no significant statistical differences in the number of capillaries. Using light microscopy the inflammatory infiltration and neovascularization in the dermis in the experimental group emerged densely in the early stages, but recovered rapidly at the latter stages. In addition, the reepithelization of the epidermis occurred earlier than in the control group. By electron microscopy, the cell organelles of the capillary endothelial cells and the basal lamina of capillaries in the experimental group showed a more rapid maturation during the latter stages, compared with the control group. Conclusion: According to this study, it can be concluded that the ulmus root-bark dressing is effective regarding the healing of pressure ulcers.
Journal of Physiology & Pathology in Korean Medicine
/
v.29
no.5
/
pp.416-421
/
2015
This study was performed to comparative investigate the distribution of primary sensory and motor neurons associated with Daereung(PC7) acupoints by using neural tracing technique. A total 16 SD rats were used in the present study. After anesthesia, the rats received microinjection of 6 ㎕ of cholera toxin B subunit(CTB) into the corresponding sites of the acupoints Daereung(PC7), in the human body for observing the distribution of the related primary sensory neurons in dorsal root ganglia(DRGs) and motor neurons in the spinal cord(C3∼T4) and sympathetic ganglia. Three days after the microinjection, the rats were anesthetized and transcardially perfused saline and 4% paraformaldehyde, followed by routine section of the DRGs, sympathetic chain ganglia(SCGs) and spinal cord. Labeled neurons and nerve fibers were detected by immunohistochemical method and observed by light microscope equipped with a digital camera. The labeled neurons were recorded and counted. From this research, the distribution of primary sensory and motor neurons associated with Daereung(PC7) acupoints were concluded as follows. Muscle meridian related Daereung(PC7) controlled by spinal segments of C5∼T1, C6∼T4, respectively.
This study was performed to investigate the antioxidative effect of Ligusticum chuanxiong Hort extracts (LCE) against the hyperlipidemia of high-fat diet-fed obese rats. The rats were divided into the three groups (normal group, control group and sample group) to perform the experimental research. 1.5 ml/kg of LCE was intraperitoneally administered into the sample group for 21 days. The equal dose of 0.9% saline was intraperitoneally administered into the normal group and the control group. On day 22, they were anesthetized with ether and dissected. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) were examined in serum of rats. Superoxide dismutase (SOD) was measured in mitochondrial fraction. Malondialdehyde (MDA), catalase (CAT), and glutamate peroxidase (GPx) were determined in liver homogenate. High-fat diet markedly increased the levels of AST, ALT and MDA, significantly decreasing those of SOD, CAT and GPx. But Ligusticum chuanxiong Hort-pretreatment decreased the levels of AST, ALT, and MDA. increasing those of SOD, CAT and GPx. These results demonstrated the antioxidative effects, suggesting that LCE could be the candidate for the functional material.
Acute ischemic stroke results from sudden decrease or loss of blood supply to an area of the brain, resulting in a coinciding loss of neurological function. The antioxidant action of melatonin is an important mechanism among its known effects to protective activity during ischemic/reperfusion injury. The focus of this research, therapeutic efficacy of melatonin on recovery of neurological function following long term treatment in ischemic brain injured rats. Male Sprague-Dawley rats (n=40; 8 weeks old) were divided into the control group, and MCAo groups (Vehicle, MT7 : MCAo+ melatonin injection at 7:00, MT19 : MCAo+melatonin injection at 19:00, and MT7,19 : MCAo+melatonin injection at 7:00 and 19:00). Rat body weight and neurological function were measured every week for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of zoletil (40 mg/kg) and xylazine (10 mg/kg) and sacrificed for further analysis. Tissues were then collected for RNA isolation from brain tissue. Also, brain tissues were analyzed by histological procedures. We elucidated that melatonin was not toxic in vital organs. MT7,19 was the most rapidly got back to mild symptom on test of neurological parameter. Also, exogenous melatonin induces both the down-regulation of detrimental genes, such as NOSs and the up-regulation of beneficial gene, including BDNF during long term administration after focal cerebral ischemia. Melatonin treatment reduced the loss of primary motor cortex. Therefore, we suggest that melatonin could be act as prophylactic as well as therapeutic agent for neurorehabilitative intervention.
The present study was designed to assess the role of spinal adenosine $A_2$ receptor in the regulation of cardiovascular functions such as mean arterial pressure (MAP) and heart rate (HR) in male Sprague-Dawley rats. Rats (250~300 g) were anesthetized with urethane and paralyzed with d-tubocurarine and artificially ventilated. blood pressure and HR were continuously monitored via a femoral catheter connected to a pressure transducer and a polygraph. Drugs were administered intrathecally using injection cannula through guide cannula which was inserted inthrathecally at lower thoracic level through a puncture of an atlantooccipital mombrane. Intrathecal injection of an adenosine $A_2$ receptor agonist, 5'-(N-cyclopropyl)-carboxamaidoadenosine (CPCA; 1, 2 and 3 nmol, respectively), produced a dose-dependent decrease in MAP and HR. Pretreatment with $N^{G}$-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor or 10 nmol of MDL-12,330, an adenylate cyclase inhibitor blocked significantly the depressor and bradycardic effect of 2 nmol of CPCA. But, Pretreatment with 3 nmol of bicuculline, gamma-aminobutyric acid A (GAB $A_{A}$) receptor antagonist, or 50 nmol of 5-aminovaleric acid, GAB $A_{B}$ receptor antagonist did not inhibit the depressor and bradycardic effect of 2 nmol of CPCA. These results indicate that adenosine $A_2$ receptor in the spinal cord plays an inhibitory role in the regulation of cardiovascular function and that the depressor and bradycardic action of adonosine $A_2$ receptor are mediated via the synthesis of nitric oxide and the activation of adenylate cyclase in the spinal cord of rats.s.s.s.
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