Spinal cord lactate concentration during chemical stimulation of the nucleus tractus solitarii in anesthetized rats.
This study was conducted to determine the mechanism of spinal cord blood flow (SCBF) decrease following the nucleus tractus solitarii (NTS) activation. In urethane-anesthetized, paralyzed and artificially ventilated rats, neurons in the NTS were chemically stimulated by microinjection of L-glutamate (1.7 nmol; 50 nl) and the lactate concentration, one of indicators of local neuronal metabolism, in the spinal cord was monitored in real time using an enzyme electrode. Before the chemical stimulation study, the responses of the enzyme electrode and its specificity were tested in vitro and in vivo. The electrode responded to step changes in lactate concentration and a calibration plot and regression line were obtained in vitro. The lactate concentration was significantly (P < 0.01) increased during induced apnea in vivo (n = 8). The lactate concentration in the spinal cord was not significantly changed by chemical stimulation of the NTS when arterial blood pressure (ABP) remained above the lower limit of spinal cord autoregulation (n = 21). When chemical stimulation of the NTS decreased ABP to below the lower limit of autoregulation (n = 18), the lactate concentration in the spinal cord was significantly (P < 0.01) increased. This may only be due to hypotensive effects because the lactate concentration was also significantly (P < 0.01) increased when the ABP was passively decreased below the lower limit of autoregulation by controlled hemorrhage in intact (n = 11) and sinoaortic denervated rats (n = 10). Intravenous lactate injection produced no significant increase in the current from the enzyme electrode in the spinal cord (n = 4). Using the electrode with inactivated enzyme solution, the current from the electrode did not change with the increase in lactate in the spinal cord. These findings indicate that the enzyme electrode can detect rapid changes of lactate, a product of anaerobic metabolism. These results also indicate that the spinal cord vasoconstrictor response elicited by chemical stimulation of the NTS, which was performed above the lower limit of spinal cord autoregulation in our previous study, may be due to neurogenic regulatory mechanism, but not to the secondary effects of changes in metabolism.
Ikegami
Y
Y
Department of Systems Physiology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Kitakyushu, Japan.
Maeda
M
M
Yokota
A
A
Nakai
M
M
Sapru
H N
HN
Hayashida
Y
Y
D000758:Anesthesia; D000818:Animals; D001011:Aorta / Q000294:innervation; D001049:Apnea / Q000378:metabolism / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D003714:Denervation; D018698:Glutamic Acid / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D006470:Hemorrhage / Q000150:complications / Q000503:physiopathology; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology; D007275:Injections, Intravenous; D007773:Lactates / Q000032:analysis* / Q000494:pharmacology; D008297:Male; D017551:Microdialysis; D008839:Microelectrodes; D008845:Microinjections; D051381:Rats; D017208:Rats, Wistar; D017552:Solitary Nucleus / Q000737:chemistry / Q000187:drug effects* / Q000201:enzymology; D013116:Spinal Cord / Q000737:chemistry* / Q000201:enzymology; D013268:Stimulation, Chemical
D007773:Lactates; D018698:Glutamic Acid