Trigeminal Nerve and Brainstem Catecholamine Systems in Cerebral Vasospasm

Abstract

Cisternal blood injection in the rat and squirrel monkey produces a biphasic cerebral vasospasm, a decrease in cerebral blood flow (CBF) and an increase in glucose uptake (CMRglu) due to an anaerobic glucolysis actually representing a decrease in metabolism. Lesioning of the A2-nucleus, its ascending cathecolamine pathways or their projection site, the median eminence in the hypothalamus, prevents the occurrence of spasm. A unilateral postganglionic trigeminal lesion causes an ipsilateral constriction of the cerebral arteries while a preganglionic lesion does not affect the baseline arterial diameter. Both kinds of trigeminal lesions induce a global increase in glucose uptake of about 50% without influencing CBF. Following subarachnoid hemorrhage (SAH) the decrease in CBF in both groups of lesioned animals is similar to that seen in controls. After SAH there is no further change in CMRglu in the animals with a preganglionic lesion, while in the postganglionically lesioned animals there is an additional increase in CMRglu of about 50% as compared to controls or animals with a preganglionic lesion. Treatment with the peptidergic substance P (SP) antagonist, spantide, or gammaglobulin against SP prevents or significantly reduces the degree of spasm and the changes in flow and metabolism normally seen post-SAH. The non-peptidergic neurokinins NK1 and NK3 antagonists do not influence flow and metabolism in SAH animals. The NK2 seems to change both flow and metabolism post-SAH in rats.

Subarachnoid Hemorrhage Induces Dynamic Changes in Regional Cerebral Metabolism in Rats

“…Another study, however, showed that glucose uptake increased by as much as 250% when measured 48 h after cisternal injection (Delgado et al, 1986a). This SAH-induced increase in glucose utilization was confirmed in a report by Svendgaard et al (1998) in which both rats and monkeys were studied. However, when investigators addressed mitochondrial oxidative capacity using cytochrome oxidase histochemistry, they reported that some regions of the brain exhibited an acute decrease followed by a late (72 h) increase in reactivity (Marzatico et al, 1988(Marzatico et al, , 1990.…”

Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage

“…For example, animal models of SAH have demonstrated the importance of pontine adrenergic pathways projecting to the median eminence as well as trigeminal nerve afferents innervating intracranial blood vessels in producing vasospasm [12,[21][22][23][24][25]. However, in a cat model of SAH, it was demonstrated that the sympathetic overactivity was triggered by elevated ICP [26].…”

Trigeminal ganglion neuron density and regulation of anterior choroid artery vasospasm: In a rabbit model of subarachnoid hemorrhage

“…[71617] It is widely believed that blood, or its degradation products, causes vasospasm by directly affecting the walls of the cerebral arteries. [29] The pathogenesis of the arterial narrowing that occurs following a SAH is not fully understood.…”

“…[91128] Unilateral postganglionic trigeminal lesions result in ipsilateral constriction of the cerebral arteries and consequent decrease of the CBF; however, pre-ganglionic lesions do not affect the baseline diameter of cerebral arteries. [2629]…”

“…[562229] The goal of this study was to determine the relationship between the number of neurons in the ophthalmic root of the TGG and changes in the diameter of the AChA, associated with SAH-induced vasospasm.…”