ABSTRACT
BACKGROUND: While the effects of excitatory amino acids have been characterized in the central nervous system, relatively little is known about their possible modulation of elements responsible for hyperalgesia within peripheral tissue. The purpose of this study was to investigate the role of excitatory amino acid receptors in mechanical hyperalgesia induced by a subcutaneous injection of Freund's complete adjuvant (FCA) into the rat hind paw. METHODS: Inflammations were induced by injecting FCA on the dorsal surface of the right hind paw of rats. Effects of excitatory aminoacid agonists or antagonists on mechanical hyperalgesia were investigated by a subcutaneous injection of a drug to the inflamed paw. Mechanical hyperalgesia was expressed as percent change in paw withdrawal threshold compared to baseline value that was measured before drug injection after inflammation was induced with FCA. RESULTS: In normal rats, an intraplantar (i.pl.) injection of L-glutamate, but not of D-glutamate (3 pmol/0.1 ml each) produced a mechanical hyperalgesia in the hind paw with a lowered paw paw-withdrawal threshold to pressure. In rats that developed the mechanical hyperalgesia associated with inflammation in the hind paw following an i.pl. injection of FCA (0.15 ml), the injection of a N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (1 pmol/0.1 ml) into the inflamed paw increased the paw pressure threshold (24.24.6% increase from baseline, P < 0.05). On the other hand, the injection of a non-NMDA receptor antagonist, 6-cyano-7-nitroqiunoxaline-2,3-dione (CNQX, 10 pmol/0.1 ml) into the inflamed paw had no effect on the FCA-induced lowering of the paw pressure threshold. CONCLUSIONS: The results suggest that NMDA, but not non-NMDA receptors play a substantial role in mediating the development of mechanical hyperalgesia induced in the inflamed paw following an i.pl. FCA injection.
Subject(s)
Animals , Rats , 6-Cyano-7-nitroquinoxaline-2,3-dione , Central Nervous System , Dizocilpine Maleate , Excitatory Amino Acids , Glutamic Acid , Hand , Hyperalgesia , Inflammation , Injections, Subcutaneous , N-Methylaspartate , Negotiating , Receptors, GlutamateABSTRACT
BACKGOUND: When ischemia reduces blood supply, hypothermia remains the sine qua non for reducing demand. An alternative to whole body deep hypothermia is an isolated cerebral hypothermia via perfusion of cooled blood through one internal carotid artery. The goal of this study was to evaluate the effect of isolated cold hemisphere perfusion during the cerebral ischemia on the formation of brain edema. METHODS: The studies were designed to perfuse a saline solution into both carotid arteries with a different temperature (left 15degreesC, right 38degreesC) in the same animal. Cerebral ischemia was produced by a combination of the both carotid artery saline perfusion and systemic hypotension to a mean arterial blood pressure of 40 mmHg for 10 minutes. Ninety minutes after reperfusion, brain water contents were measured using the kerosene/bromobenzene density gradient and compared with warm saline perfusion and normal control group. RESULTS: Brain water content of cold saline perfusion hemisphere measured at 90 minutes after ischemia showed decreased water content compared to warm saline perfusion hemisphere (p<0.05). CONCLUSIONS: Cerebral cold saline perfusion during the ischemia decreased the formation of brain edema. These results showed hypothemia is one of the most effective ways to protect brain from the ischemia.