Laryngeal cancer, aryl hydrocarbon hydroxylase inducibility and smoking. A follow-up study.

In 58 cases with laryngeal cancer (10 supraglottic and 48 glottic), aryl hydrocarbon hydroxylase (AHH) inducibility and smoking habits were studied. All but 2 were smokers and most of them heavy tobacco consumers. The AHH levels were divided into high, intermediate and low groups and were compared to a large healthy control material also divided into the aforementioned groups. A highly significant overrepresentation of patients with a high AHH level (p less than 0.0005) as well as a significant underrepresentation of low AHH levels (p less than 0.025) were found. Smokers with a high AHH level run a fourfold risk of developing laryngeal cancer as compared to non-smokers with low AHH levels. They also develop cancer earlier in life and get recurrences and secondary malignancies more frequently. As in oral and oropharyngeal cancer a high AHH inducibility seems to be of pathogenetic as well as of prognostic importance even in laryngeal cancer.

Localization and effects of neuropeptide Y, vasoactive intestinal polypeptide, substance P, and calcitonin gene-related peptide in human temporal arteries.

Nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) were seen in the adventitia or at the adventitia-media border of the human temporal artery. Pharmacological experiments on isolated temporal artery segments revealed that NPY potentiated the vasoconstrictor responses to noradrenaline, but had no vasoconstrictor ability or only a small vasoconstrictor ability per se. VIP, peptide histidine methionine 27 (PHM-27), SP, neurokinin A (NKA), and CGRP potently relaxed vessels precontracted by prostaglandin F2 alpha, the relative potency being CGRP greater than SP greater than NKA = VIP = PHM-27. The amount of relaxation varied between 67 and 91% of the prostaglandin F2 alpha-induced contraction. The peptide effects were not antagonized by classic adrenergic or cholinergic blockers, suggesting interactions via separate receptor sites.