The authors describe a patient with dopa-responsive dystonia who developed neuroleptic malignant syndrome with prolonged catatonia following treatment with neuroleptic agents. Use of these agents probably expanded the patient's neuronal dysfunction beyond the nigrostriatal system to involve multiple dopaminergic systems. Electroconvulsive treatment alleviated the prolonged catatonia.
reported that the relaxation of isolated rabbit aorta and other arteries induced by acetylcholine and other agonists for muscarinic receptors was dependent on the presence of endothelial cells within the preparations [2]. After removal of these cells, acetylcholine could no longer induce relaxation. Endothelium-dependent relaxation by acetylcholine results from the release of a diffusable relaxing substance, which was later termed endothelium-dependent relaxing factor (EDRF) [3,4]. It has been shown that this EDRF is nitric oxide (NO) [5][6][7]. Moreover, NO is involved in numerous physiological functions [8][9][10][11][12][13][14][15][16][17][18][19][20]. It inhibits platelet aggregation and adhesion and leukocyte adhesion, and modulates smooth muscle cell proliferation [8]. In the peripheral nervous system, NO is a mediator released by a widespread network of nerves [9][10][11]. It contributes to cytotoxicity against tumor cells, bacteria, viruses and microorganisms in activated macrophages [12][13][14]. In the brain, it has been shown that NO plays a physiological role in synaptic transmission by elevating the cyclic GMP (cGMP)
The present study was undertaken to examine the effects of microinjection of sodium nitroprusside (SNP), which releases nitric oxide (NO) spontaneously, into the nucleus tractus solitarii (NTS) on cerebral circulation. Cerebral blood flow (CBF) was measured in urethane-anesthetized (1.5 g middle dotkg-1, i.p.), paralysed and artificially ventilated rats using labeled microspheres or laser Doppler flowmetry. The CBF was significantly decreased by microinjection of SNP (5 nmol, n=10, microsphere technique; 0.5 nmol, n=6, laser Doppler flowmetry) into the unilateral NTS. Microinjection of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of the formation of NO, prevented cerebral vasoconstrictor responses induced by microinjection of L-glutamate into the NTS (n=10). Microinjection of NG-monomethyl-D-arginine (D-NMMA) had no effect on the cerebral vasoconstrictor responses induced by L-glutamate (n=11). Unilateral microinjections of L-NMMA into the NTS (n=9), of SNP into the area adjacent to the NTS (n=9), of vehicle solution into the NTS (n=10), and of light-inactivated SNP into the NTS (n=6) had no effect on cerebral circulation. Cerebral autoregulation was well maintained in our protocols (n=9). These results indicate that microinjection of SNP, an NO donor, into the NTS decreases CBF.
The cerebral blood flow (CBF) was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. Microinjection of L-glutamate (1.7 nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- S.E.M.) to 48 +/- 9 ml.min-1.(100g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side but not in other structures such as brain stem and cerebellum (n = 9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n = 10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase following chemical stimulation of the VLDA (n = 11). Microinjection of the vehicle solution into the VLDA had no effects on systemic and cerebral circulation (n = 7). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.
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