Extravasation of macromolecules and vascular reactivity of microvessels in response to nicotine in the hamster.

The effects of nicotine on the microvasculature were assessed in the hamster cheek pouch and in fetal tissue grafted into the cheek pouch. Transvascular exchange of FITC-dextran (70-150 K) was measured in the cheek pouch of normal hamsters challenged with either intravenous or suffused nicotine, and in streptozotocin-induced, diabetic hamsters challenged for one week with nicotine delivered by a mini-osmotic pump. The effects of nicotine on microvascular diameter were measured in cheek pouch vessels and in grafts 9-12 days after transplantation. Suffused nicotine did not cause leaky site formation or alter dextran clearance from the pouch. Intravenous nicotine had no effect on either of these parameters but potentiated histamine-induced leaky site formation (40%) and clearance (20%); clearance but not leaky site formation was normalized after cessation of nicotine infusion. Chronic nicotine treatment of diabetic hamsters had no effect on either basal or histamine-induced extravasation as monitored by leaky site or clearance measurements. Suffused nicotine had no effect on arteriolar diameter in the cheek pouch, or in renal, pulmonary or atrial allografts. These results indicate that nicotine can modulate histamine-induced extravasation of macromolecules but has no effect on diameter of arterioles in the non-adrenergically innervated vascular beds studied.