Altered reactivity of isolated segmental lumbar arteries of dogs following exposure to ethanol and phenol

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Abstract

Celiac plexus neurolysis is a useful analgesic technique in patients with upper abdominal cancer. Although complications are infrequent, occasionally celiac neurolysis results in paraplegia. It is hypothesized that paraplegia after celiac neurolysis results from neurolytic drug-induced spasm of lumbar segmental arteries that perfuse the spinal cord, although no data are available to support or refute the idea. Whether drugs used for celiac plexus neurolysis alter the reactivity of dogs' lumbar segmental arteries was studied in vitro. Rings of lumbar segmental arteries, suspended in Krebs-Ringer solution in organ baths, were passively stretched to the optimal point on their length-tension curve. After a 45-min rest the responsiveness of each ring was established by adding an ED50 concentration of norepinephrine to the bath. Subsequently, Krebs-Ringer solution containing a single concentration of phenol or ethanol was added. Concentrations studied included 1%, 3%, 6%, 7%, 8%, 9%, and 12% phenol; and 3%, 6%, 10%, 25%, 50%, 75%, and 90% ethanol. The magnitude of the phenol-induced contractile response was directly related to concentration, with 8%, 9% and 12% phenol, producing sustained contractile responses compared to norepinephrine-induced control contractile responses. The ethanol-induced contractile response was inversely related to concentration. Ethanol (3% and 6%) produced sustained contractile responses compared to norepinephrine-induced control contractile responses. Studies were then done to further elucidate the agonist properties of phenol and ethanol. The contractions caused by ethanol or phenol did not appear to be mediated through adrenergic, opioid, muscarinic, or serotonin receptors or sodium channels. Addition of procaine eliminated the sustained response to ethanol-induced contraction, while it did not with phenol-induced contractions. It is possible that a concentration of phenol or alcohol of the magnitude found to cause contraction of these vessels could be achieved clinically. Nevertheless, it is important to emphasize that this study provides no direct evidence that alcohol or phenol will lead to ischemia of the magnitude to cause paraplegia in the clinical setting.

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