Postocclusive cerebral hyperemia is markedly attenuated by chronic trigeminal ganglionectomy

Abstract

Marked hyperemia may develop in brain following temporary cessation of blood flow and is associated with the morbidity following cardiac arrest, stroke, and head injury. Regional cerebral blood flow was measured using radiolabeled microspheres and compared in 10 symmetrical regions after chronic unilateral trigeminal ganglionectomy (n = 8), trigeminal rhizotomy (n = 4), or sham operation (n = 4) following 10 min of combined brachiocephalic-left subclavian occlusion and hypotension (mean arterial blood pressure less than 50 mmHg) in cats. Blood flow was symmetrical at rest in the three groups and was undetectable during the ischemic period. Within 30 min after re-establishing flow, values in cortical gray matter increased symmetrically to approximately 250 ml.100 g-1.min-1 in the rhizotomy and the sham groups. Increases of similar magnitude were measured on the intact side following trigeminal ganglionectomy but flow was attenuated by greater than 50% ipsilateral to the ganglionectomy. Marked hyperemia developed during reperfusion in thalamus, caudate, deep cortical white matter, midbrain, and pons, but no asymmetries were present in the three groups. These data suggest that cortical hyperemia is mediated by trigeminal neurogenic mechanisms via axonal reflexlike mechanisms and suggest the importance of therapeutic strategies based on blockade of this nerve or its constituent neuropeptides.

Postischemic Cerebral Blood Flow and Neuroeffector Mechanisms

“…For exam ple, the hyperemic response to acute severe hypertension beyond the limits of autoregu lation, or to acute generalized seizures, is reduced following trigeminal ganglionecto my, but not following trigeminal rhizotomy [6,7]. Because section of the nerve root pre vents central transmission but does not cause wallerian degeneration of peripheral axons, the increases in CBF are mediated by axon-reflex-like mechanisms.…”

“…of either sex and weighing 2.2-5.2 kg, were used for all experiments. Chronic left trigeminal ganglionectomy was per formed in 8 animals [5][6][7],…”

“…St. Louis, Mo., USA) together with controlled hemor rhage into a reservoir. At the conclusion of the study, regional CBF was calculated as described previously [6,7],…”

“…The generation of vasoactive metabolites during ischemia, such as lactic acid, adeno sine and free oxygen radicals, contribute to postocclusive hyperemia [3,4], Recent re ports from our laboratory have demon strated the importance of axon-reflex-like mechanisms to a number of hyperperfusion states [5][6][7]. Sensory axons are largely unmy elinated C Fibers which form a plexus within the adventitia.…”

Effect of adrenergic drugs on cerebral blood flow, metabolism, and evoked potentials after delayed cardiopulmonary resuscitation in dogs.

“…However, Moskowitz et al 19 suggest that nerves, albeit nonsympathetic nerves, are capable of modifying postischemic hyperemia. We found that epinephrine infusion increased plasma levels approximately 10-fold over that in the control group with aortic balloon inflation, but that CBF was similar over an equivalent range of cerebral perfusion pressure.…”