Mechanisms of pain-induced local cerebral blood flow changes in the rat sensory cortex and thalamus.

Abstract

It is a well-known phenomenon that cerebral blood flow is coupled to neural activation induced by non-noxious somatosensory stimulation. However, basic questions related to pain-induced cerebral blood flow changes remain unanswered. In the present study, the sciatic nerve of anesthetized rats was subjected to electric stimulation with noxious and non-noxious parameters. Changes in local cerebral blood flow and neuronal activity were determined simultaneously in the sensory cortex and in the thalamus by laser-Doppler flowmetry and c-fos immunohistochemistry, respectively. The role of different vasoregulatory mechanisms and the pain-induced increase in mean arterial blood pressure (MABP) were examined with specific blocking agents and by means of rapid intra-arterial transfusion. Noxious stimulation resulted in significant enhancement of neuronal activity both in the thalamus and in the somatosensory cortex indicated by marked c-fos expression in these areas. Cortical and thalamic blood flow (cBF and tBF) increased by 47+/-4 and 44+/-3% during the stimulation while the MABP elevated by 35+/-2%. Similar changes in MABP induced by intra-arterial transfusion had no effect on tBF, while cBF increased only by 18+/-5%. Blockade of ATP sensitive potassium channels (K(+)(ATP)) and sympathetic beta-receptors significantly attenuated the pain-induced blood flow increases in both investigated areas, while inhibition of nitric oxide synthase was effective only in the thalamus. The blockade of the sympathetic alpha-receptors, opiate receptors, and the cyclooxygenase enzyme had no effect on the pain-induced cerebral blood flow elevations. These findings demonstrate that during noxious stimulation, cerebral blood flow is adjusted to the increased neural activity by the interaction of vasoconstrictor autoregulatory and specific vasodilator mechanisms, involving the activation of sympathetic beta-receptors, K(+)(ATP)-channels and the release of nitric oxide.

• Authors: Benedek Erdos, Zsombor Lacza, Ida E Tóth, Emese Szelke, Tamás Mersich, Katalin Komjáti, Miklós Palkovits, Péter Sándor
• Journal: Brain research (Brain Res) Vol. 960 Issue 1-2 Pg. 219-27 (Jan 17 2003) ISSN: 0006-8993 [Print] Netherlands
• PMID: 12505675 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• ATP-Binding Cassette Transporters
• Endorphins
• Enzyme Inhibitors
• KATP Channels
• Narcotic Antagonists
• Potassium Channel Blockers
• Potassium Channels
• Potassium Channels, Inwardly Rectifying
• Receptors, Adrenergic, alpha
• Receptors, Adrenergic, beta
• uK-ATP-1 potassium channel
• Nitric Oxide
• Naloxone
• Nitric Oxide Synthase
• Nitric Oxide Synthase Type I
• Nos1 protein, rat
• Prostaglandin-Endoperoxide Synthases

Topics

• ATP-Binding Cassette Transporters
• Animals
• Blood Gas Analysis
• Blood Pressure (drug effects, physiology)
• Cerebrovascular Circulation (drug effects, physiology)
• Endorphins (physiology)
• Enzyme Inhibitors (pharmacology)
• Genes, fos (genetics)
• Immunohistochemistry
• KATP Channels
• Male
• Naloxone (pharmacology)
• Narcotic Antagonists (pharmacology)
• Nitric Oxide (physiology)
• Nitric Oxide Synthase (antagonists & inhibitors)
• Nitric Oxide Synthase Type I
• Pain (physiopathology)
• Physical Stimulation
• Potassium Channel Blockers (pharmacology)
• Potassium Channels (physiology)
• Potassium Channels, Inwardly Rectifying
• Prostaglandin-Endoperoxide Synthases (physiology)
• Rats
• Rats, Wistar
• Receptors, Adrenergic, alpha (physiology)
• Receptors, Adrenergic, beta (physiology)
• Sciatic Nerve (physiology)
• Somatosensory Cortex (blood supply, physiopathology)
• Stereotaxic Techniques
• Thalamus (blood supply, physiopathology)