Spinal cord blood flow decreases following microinjection of sodium nitroprusside into the nucleus tractus solitarii of anesthetized rats.

This study was undertaken to examine whether or not nitric oxide (NO) is involved in synaptic transmission in the nucleus tractus solitarius (NTS) during control of the spinal cord circulation. Employing urethane-anesthetized, paralyzed and artificially ventilated rats, sodium nitroprusside (SNP), which produces NO, was microinjected unilaterally into the NTS and the spinal cord blood flow (SCBF) was determined using labeled microspheres. Arterial blood pressure (ABP) was decreased by unilateral microinjection of SNP into the NTS, but its value was kept within the normotensive range by blood transfusion, in order to measure SCBF at normotension. After microinjection of SNP into the NTS, the SCBFs of the cervical, thoracic and lumbar cords decreased significantly from 63 +/- 8 (mean +/- S.E.M.) to 49 +/- 7 (P < 0.05), from 54 +/- 7 to 37 +/- 7 (P < 0.05), and from 77 +/- 9 to 58 +/- 8 (P < 0.05) ml/min/(100 g), respectively (n = 10). Prior microinjection of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of the formation of NO from L-arginine, into the NTS blocked the spinal cord vasoconstrictor response produced by microinjection of L-glutamate into the NTS (n = 10). Prior microinjection of NG-monomethyl-D-arginine (D-NMMA), which does not inhibit the formation of NO from L-arginine, did not block the spinal cord vasoconstrictor response elicited by microinjection of L-glutamate (n = 11). Unilateral microinjection of L-NMMA into the NTS exerted no effect on the spinal cord circulation (n = 9). These findings suggest that NO may be involved in the control of the spinal cord circulation in the NTS.