Hasil untuk "physics.flu-dyn"

Bryan M. Grabias, K. Konstantopoulos

Sarah E. Matt, L. Johnson, J. Shupp et al.

Daniel E. Conway, Sungmun Lee, S. Eskin et al.

Hui-rong Liu, Li Qi, Luyi Wu et al.

AIM To observe the analgesic effects of moxibustion in rats with chronic visceral hyperalgesia and its influence on the concentration of dynorphin (Dyn) and endomorphin (EM) in spinal cord. METHODS The rat model of chronic visceral hyperalgesia was established by colorectal distention (CRD). In moxibustion (MX) group, moxibustion was applied once daily for 7 d; in sham moxibustion (SM) group, moxibustion was given to the same acupoints but with the non-smoldered end of the moxa stick. Model control (MC) group and normal control group were also studied. The scoring system of abdominal withdrawal reflex was used to evaluate visceral pain for behavioral assessment. Enzyme linked immunosorbent assay was performed to determine the concentrations of Dyn and EM in spinal cord. RESULTS Moxibustion significantly decreased visceral pain to CRD in this rat model, and no significant difference was detected between the SM group and the MC group. In MX group, moxibustion also increased the concentrations of Dyn and EM in spinal cord, and no significant difference was found between the SM group and the MC group. CONCLUSION Moxibustion therapy can significantly enhance the pain threshold of rats with chronic visceral hyperalgesia, and the effect may be closely related to the increased concentration of Dyn and EM in spinal cord.

A. Cohen, N. Dyn, Basarab Matei

A. M. Kawasaki, R. Knapp, A. Walton et al.

W. Fang, Yanjun Cui, T. F. Murray et al.

L. Treloar

K. O. Lim, D. Boughner

T. Wilson

R. Day, H. Akil

D. Bronstein, H. Ye, K. Pennypacker et al.

R. Bakshi, A. Newman, A. Faden

The endogenous opioid dynorphin A-(1-17) (Dyn A) has been implicated as a mediator of tissue damage after traumatic spinal cord injury (TSCI) and causes hindlimb paralysis when administered intrathecally. Motor impairment following intrathecal Dyn A is attenuated by antagonists of excitatory amino acids (EAAs); whether opioid receptors mediate such injury has been questioned. TSCI causes various biochemical changes associated with secondary tissue damage, including alterations in tissue amio acids, phospholipids, and fatty acids. Such changes reflect injury severity and correlate with motor dysfunction. The present studies examined whether dynorphin administration causes similar biochemical alterations and whether effects of Dyn A can be modified by treatment with opioid-receptor antagonists. At 24 hr after intrathecal Dyn A, there were significant declines in tissue levels of glutamate, aspartate, and glycine. Increases in total free fatty acids were found at 2 and 24 hr, reflecting changes in both saturated and unsaturated components, which were associated with significant decreases in tissue cholesterol and phospholipid phosphorus at the earlier time point. Each of these neurochemical changes, as well as corresponding motor deficits, were limited by pretreatment with the opioid antagonist nalmefene. In separate experiments, both nalmefene and the selective kappa-opioid antagonist nor-binaltorphimine (nor-BNI) limited dynorphin- induced motor dysfunction; effects of nor-BNI were dose related, and those of nalmefene were stereospecific. Therefore, behavioral and neurochemical consequences of Dyn A administration are mediated in part through opiate receptors, most likely kappa-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

J. Jasperse, M. Laughlin

L. Lucas, P. Pompei, J. Ono et al.

D. Kunz, W. Kunz, C. S. Scott et al.

S. Lakshminarayanan, Thomas W. Gardner, J. Tarbell

S. Yan, B. Kayser, M. Tobiasz et al.

S. Kudo, R. Morigaki, J. Saito et al.