Spinal Cord Stimulation, Physiology    1 2 3 4

Reis DJ. Granata AR. Joh TH. Ross CA. Ruggiero DA. Park DH.

Brain stem catecholamine mechanisms in tonic and reflex control of bloodpressure. [Review] [70 refs]

Hypertension. 6(5 Pt 2):II7-15, 1984 Sep-Oct.

Abstract:

Neurons of the lower brain stem maintain resting levels of arterial pressure (AP), mediate reflex responses from cardiopulmonary receptors, and are an important site of the hypotensive actions of alpha 2-adrenergic agonists. Details of the pathways and transmitters that mediate tonic and reflex control of AP are emerging. Afferent fibers of cardiopulmonary receptors in the ninth and tenth nerves terminate bilaterally in the nucleus of the tractus solitarius (NTS). Although some neurons contain substance P, the primary neuro-transmitter appears to be the excitatory amino acid L-glutamate (L-glu). Neurons in rostral ventrolateral medulla, which most probably comprise the C1 group of epinephrine neurons, are also critical in AP control. C1 neurons project to innervate cholinergic preganglionic sympathetic neurons in the spinal cord. Stimulation of the C1 area electrically or with L-glu increases AP, while lesions or local injection of the inhibitory amino acid gamma- aminobutyric acid (GABA) lowers AP to levels comparable to spinal cord transection. Lesions of C1 neurons or their pathways abolish vasodepressor reflexes from baroreceptors and vagal afferents. In contrast, noradrenergic neurons of the caudal ventrolateral medulla, the A1 group, project rostrally to innervate, in part, vasopressin neurons of the hypothalamus. Stimulation of A1 neurons lowers AP, while lesions or GABA elevates it. We propose that C1 neurons comprise the so-called tonic vasomotor center of the brain stem and also mediate, via a projection from the NTS, the vasodepressor limb of baroreflexes. The NTS-C1 projection may be GABAergic.

[References: 70]

Norrsell H. Eliasson T. Albertsson P. Augustinsson LE. Emanuelsson H. Eriksson P. Mannheimer C.

Department of Medicine, Sahlgren's University Hospital/Ostra. Sweden. henrik.norsell@invmed.gu.se

Effects of spinal cord stimulation on coronary blood flow velocity.

Coronary Artery Disease. 9(5):273-8, 1998.

Abstract:

BACKGROUND: Spinal cord stimulation (SCS) has been used in the treatment of severe angina pectoris since the 1980s. Several studies have shown both an antianginal and an anti-ischaemic effect. There are several theories about the mechanism behind the anti-ischaemic effect of SCS, including the possibility that it is dependent on an increase in coronary flow velocity.

OBJECTIVE: To determine if there were effects of SCS on coronary flow velocity during cardiac stress. METHOD: Eight patients with severe anginal pain secondary to coronary artery disease who had been implanted with an SCS device were included in the study. In addition, four patients with syndrome X were examined. If possible, a Doppler guidewire was placed in the vessel corresponding to the ischaemic area revealed on a prior myocardial scintigram. A temporary pacemaker electrode was placed in the right atrium. Atrial pacing started at 80 beats/min and increased by 10 beats/min every 2 min until the patient experienced moderate angina; the pacing frequency was then maintained at the same level. After 2 min of pacing at this frequency, SCS treatment commenced; after a further 5 min, pacing was stopped.

Throughout the procedure, coronary flow velocity, assessed as average peak velocity (APV), was monitored continually.

RESULTS: APV increased during pacing in all the patients with coronary artery disease (mean increase 53%; P< 0.02). There were no significant changes in APV during maximum pacing frequency when stimulation was introduced.

CONCLUSIONS: Theresults of this study do not support the theory that the anti- ischaemic effect of SCS is dependent on an increase in coronary flow velocity.