No abstract available.
Ductus Arteriosus* ; Indomethacin*

The peripheral nerves can restore their impaired function after injuries from trauma or surgery. The known factors affecting the recovery of damaged peripheral nerves include the severity of damage, nerve growth factor(NGF) from the damaged area and the concentrations of fibrinogen and thrombin. One of polypeptides, transforming growth factors beta(TGF-beta) has been known to be related to inflammation and healing process of various wound. The TGF-beta has to three subtypes, TGF-beta(1), TGF-beta(2) and TGF-beta(3). This study was performed to explore the effects of TGF-beta subtypes on the recovery phase of damaged nerve. Sciatic nerves of rat were compressed 200 dyne/mm2. The latencies were measured by stimulation of proximal and distal portion of compression injury site and expression of TGF-beta isoforms was studied in proximal and distal nerve of compression site and spinal cord by using avidin-biotin complex immunoperoxidase technique. The latencies were increased at one week after nerve injury and then recovered progressively following 4 weeks. The latencies were restored to almost normal values at 4 weeks after nerve injury. TGF-beta(1) and TGF-beta(3) were expressed weakly at the cytoplasm of Schwann cell in the distal portion after 12 hours of injury. The values of TGF-beta(1) and TGF-beta(3) were increased at 3rd day after injury and lasted till the 4th week which was the end point of nerve regeneration. The changes of proximal portion were different from those of distal portion. TGF-beta(1) and TGF-beta(3) of proximal portion showed stronger positive reaction than that of distal portion and the reaction was peaked at 3rd day after injury. TGF-beta subtypes were rarely present at neuronal cells and astrocytes in spinal cord from 12th hour to 3rd day after injury. The TGF-beta subtypes were weakly appeared at the 1st week after injury and successively increased to 4th week at which the latencies were restored to almost normal value. The patterns of revelation of TGF-beta subtypes showed that TGF-beta(1) was predominant at neuronal cell and TGF-beta(2) was at glial cells. We suggest that TGF-beta subtypes might be related to the regeneration process of nerve injuery.
Animals ; Astrocytes ; Cytoplasm ; Fibrinogen ; Immunoenzyme Techniques ; Inflammation ; Nerve Regeneration ; Neural Conduction* ; Neuroglia ; Neurons ; Peptides ; Peripheral Nerves ; Protein Isoforms ; Rats ; Reference Values ; Regeneration ; Sciatic Nerve* ; Spinal Cord ; Thrombin ; Transforming Growth Factor beta* ; Transforming Growth Factors ; Wounds and Injuries

The vanilloid receptor type-1 (VR1) is a nonselective cation channel activated by capsaicin and can be act as mediator of chemical and physical stimuli that elicit pain. The presence of VR1 in the dorsal root, trigeminal and nodose ganglia has been firmly established, but it unclear in the mouse intestinal wall. The distribution of VR1 receptors in mouse afferent neurons innervating the intestinal tract was investigated by immunohistochemistry. Also small and large intestines were dual-labelled with antibody for VR1 and marker for interstitial cells of Cajal (c-kit). VR1-immunopositive cells were localized on fine fibers in myenteric plexus and expressed weakly myenteric ganglia. The majority of VR1-immunopositive fibers are not colocalized with or apposed to c-kit positive interstitial cells of Cajal. Also electrophysiologically capsaicin had no effect on cultured interstitial cells of Cajal. It is concluded that VR1-immunoreactive intestinal nerves are mainly distributed in myenteric plexus of murine intestinal wall, and vanillod may be not directly related to interstitial cells of Cajal in regulation of intestinal motility.
Animals ; Capsaicin ; Ganglia ; Gastrointestinal Motility ; Immunohistochemistry ; Interstitial Cells of Cajal ; Intestines ; Mice* ; Myenteric Plexus* ; Neurons, Afferent ; Nodose Ganglion ; Spinal Nerve Roots

The vanilloid receptor type-1 (VR1) is a nonselective cation channel activated by capsaicin and can be act as mediator of chemical and physical stimuli that elicit pain. The presence of VR1 in the dorsal root, trigeminal and nodose ganglia has been firmly established, but it unclear in the mouse intestinal wall. The distribution of VR1 receptors in mouse afferent neurons innervating the intestinal tract was investigated by immunohistochemistry. Also small and large intestines were dual-labelled with antibody for VR1 and marker for interstitial cells of Cajal (c-kit). VR1-immunopositive cells were localized on fine fibers in myenteric plexus and expressed weakly myenteric ganglia. The majority of VR1-immunopositive fibers are not colocalized with or apposed to c-kit positive interstitial cells of Cajal. Also electrophysiologically capsaicin had no effect on cultured interstitial cells of Cajal. It is concluded that VR1-immunoreactive intestinal nerves are mainly distributed in myenteric plexus of murine intestinal wall, and vanillod may be not directly related to interstitial cells of Cajal in regulation of intestinal motility.
Animals ; Capsaicin ; Ganglia ; Gastrointestinal Motility ; Immunohistochemistry ; Interstitial Cells of Cajal ; Intestines ; Mice* ; Myenteric Plexus* ; Neurons, Afferent ; Nodose Ganglion ; Spinal Nerve Roots

In addition to the central and the peripheral nervous system, calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) has been identified throughout the enteric nervous system. Several functions of the CGRP in gastrointestinal (G-I) tract has been identified, but the effect of CGRP on G-I motility is unclear. The distribution of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) in the murine small bowel were studied by using immunohistochemistry, also analyzed functionally by using electrophysiological method. Immunohistochemical studies demonstrated that CGRP-LI is localized in both nerve fibers and myenteric ganglion cells in the whole-mount preparation of murine small intestine. Double labelling with CGRP and c-kit investigated by confocal microscope was shown that CGRP-LI enteric nerve fiber surrounded the c-kit positive interstitial cells of Cajal (ICC). Electrophysiological finding revealed that treatment of CGRP inhibited electrical activity on culture ICC. Our results suggest a CGRP innervation of murine small bowel ICC. The released CGRP from enteric nerve terminals may induce relaxation of small bowel through the inhibition of ICC.
Animals ; Calcitonin Gene-Related Peptide* ; Calcitonin* ; Enteric Nervous System ; Ganglion Cysts ; Immunohistochemistry ; Interstitial Cells of Cajal ; Intestine, Small* ; Mice ; Nerve Fibers ; Peripheral Nervous System ; Relaxation

Homeostasis of multicellular organism is controlled by proliferation and differentiation of cells as well as by cell death. The defects in programmed cell death contribute to the pathogenesis of rheumatoid arthritis (RA) and systemic lupus erythematous. RA is considered to be a proliferating disorder of synovial tissue which is accompanied by inflammatory cell infiltration and bone erosion. The aim of the study was to find whether potent inducers of apoptosis could be induced apoptosis in RA synovial cells. We examined the effects of drugs, such as dexamethasone, methotrexate, hydrogen peroxide, and ceramide on induction of apoptosis in cultured RA synovial cells. Used drugs did not induced apoptosis in RA synovial cells. Finally Fas antigen-mediated apoptosis of RA synovial cells was investigated by the addition of anti-Fas antibody. To examine the ICE (interleukin-1p-convertase; caspase-1) expression in synovial cells, RT-PCR of caspase-1 gene was performed. In synovial cells of RA, Fas induces that caspase-1 activation cause apoptosis.
Apoptosis* ; Arthritis, Rheumatoid* ; Cell Death ; Dexamethasone ; Homeostasis ; Humans ; Hydrogen Peroxide ; Ice ; Methotrexate

The indole alkaloid harmaline has been to cause tremor and ataxia, and produce cerebellar neurotoxicity in rat. Degeneration of Purkinje cell alligned in narrow parasagittal bands result from excitation of inferior olivary nucleus in harmaline-treated rats. The objective of this study was to investigate the hypothesis that excitation of climbing fiberinduced by harmaline mediates Purkinje cell injury or degeneration. For this purpose, the inferior olive of rats was chemically ablated by using 3-acetyl pyridine, a neurotoxic chemical, and cerebellar damage followed by administration of harmaline was analyzed using immunohistochemical markers for neurons, glial cells. The results demonstrated that a subset of Purkinje cell in the vermis and paravermis degenerated after harmaline treatment, but harmaline produced little or no Purkinje cell degeneration after inferior olivary ablation. These results suggested that harmalineinduced activation of inferior olivary neurons may lead to release of glutamate from climbing fiber synaptic terminal distributed over the Purkinje cells, and may lead to cytotoxic degeneration of Purkinje cells.
Animals ; Ataxia ; Cerebellum ; Glutamic Acid ; Harmaline* ; Neuroglia ; Neurons ; Olea ; Olivary Nucleus ; Presynaptic Terminals ; Purkinje Cells* ; Rats ; Tremor

We report a case of accidental intrathecal administration of Nucomyt(R)(acetylcysteine), a mucolytic agent used for intratracheal instillation. A 21-year-old healthy female with a complete syndactyly at the 4th and 5th toes was scheduled for a web release under spinal anesthesia. Immediately after accidental intrathecal administration of Nucomyt(R)2.4 ml instead of bupivacaine for spinal anesthesia, tonic extension developed at first in the lower extremities and then the upper extremities, too. Thiopental sodium 200 mg was injected intravenously twice. Endotracheal general anesthesia with N2O- enflurane-vecuronium was maintained for the operation for about two hours. For about 1 hour after emergence of general anesthesia, tonic extension intermittently developed in the lower extremities and was controlled with midazolam. Mild elevated blood pressure, tachycardia, tachypnea, high fever (up to 38.5degrees C) and respiratory acidosis occurred. Thirty minutes later, she became mentally clear with a normal neurologic examination. No delayed sequelae were detectable at a follow-up visit 1 month and 1 year after surgery.
Acetylcysteine* ; Acidosis, Respiratory ; Anesthesia, General ; Anesthesia, Spinal ; Blood Pressure ; Bupivacaine ; Female ; Fever ; Follow-Up Studies ; Humans ; Lower Extremity ; Midazolam ; Neurologic Examination ; Syndactyly ; Tachycardia ; Tachypnea ; Thiopental ; Toes ; Upper Extremity ; Young Adult

BACKGROUND: The sodium concentration in the central nervous system may play an important role in cardiovascular function and body fluid regulation. The purpose of this investigation was to examine the effects of intracerebroventricular (ICV) infusion of hypertonic NaCl solutions on the cardiovascular responses in normotensive and 2-kidney, 1 clip (2K1C) renal hypertensive rats. METHODS: 2K1C hypertension was made by clipping the left renal artery and were used 4 weeks later. Age-matched control rats received a sham treatment. Under thiopental (50 mg/kg, IP) anesthesia, both isotonic and hypertonic NaCl solutions (0.15 M, 0.6 M and 1.2 M) were ICV applied, while blood pressure and heart rate (HR) responses were continuously monitored. RESULTS: Central administration of hypertonic NaCl solution caused an elevation in mean arterial pressure (MAP) and HR in both normotensive and 2K1C hypertensive rats. The response magnitude in the blood pressure was positively correlated to the NaCl concentration in normotensive rats, while the pressor responses to hypertonic NaCl were comparable regardless of the concentration of NaCl in hypertensive rats. Despite of the HR responses were similar in between two groups, the magnitude of the MAP increases were more elevated in hypertensive than in normotensive control rats. Isotonic NaCl solution, when centrally applied, caused an elevation in blood pressure only in hypertensive rats. CONCLUSION: These results indicate that the central sensitivity to sodium chloride is altered in 2K1C renal hypertensive rats.
Anesthesia ; Animals ; Arterial Pressure ; Blood Pressure ; Body Fluids ; Central Nervous System ; Heart Rate ; Hypertension ; Hypertension, Renal ; Infusions, Intraventricular* ; Placebos ; Rats* ; Renal Artery ; Sodium ; Sodium Chloride ; Thiopental

Interstitial cells of Cajal (ICC) are the pacemalkers in gastrointestinal muscles, and these cells also mediate or transduce inputs from the enteric nervoius system. Immunolabelling of interstitial cells of ICC in intestinal wall is recently developed by using specific marker, anti-c-kit antibody. Immunohistochemistry was done for c-Kit-positive ICC network in attempt to provide a morphological basis for the mechanism regulating gastro-intestinal movement. Cryosection and whole-mount preparations of mouse ileum and colon were immunolabelled using the anti-c-Kit. Immunolabelled specimens were observed under a confocal laser scanning microscopy. According to three dimensional reconstruction study, it was found that the c-Kit-positive cells were widely distributed in the intestinal wall: (1) circular muscle layer, (2) myenteric plexus, (3) deep muscular plexus in ileum, (4) submucosal plexus and longitudinal muscle layer in colon. The characteristic profiles of ICC containing c-Kit-positive cells provide a morphological basis upon the mechanism regulating gastro-intestinal motility.
Animals ; Colon ; Ileum ; Immunohistochemistry ; Interstitial Cells of Cajal* ; Intestines* ; Mice* ; Microscopy, Confocal ; Muscles ; Myenteric Plexus ; Submucous Plexus