vasoactive-intestinal-peptide and Arterial-Occlusive-Diseases

In anesthesized white rabbits blood was extracorporeally circulated from the left carotid artery into the penile corporeal bodies with a constant flow rate. Corpus cavernosum pressure (CCP) responses to intracavernous injections of drugs were recorded in animals with aortic nonocclusion and aortic occlusion, respectively. Vasoactive intestinal polypeptide (VIP, 1 microgram, 5 micrograms, and 20 micrograms), dissolved in 0.5 mL volumes, induced no significant increases in CCP compared with equivalent volumes of solvent, but the peptide increased the time interval until return of CCP to steady state level. Peptide histidine methionine induced a significant increase in the maximal CCP obtained in nonocclusion, and the time interval until return of CCP to steady state levels was increased in both aortic nonocclusion and occlusion. Neuropeptide Y produced an increase in the maximal CCP in animals with aortic occlusion, and a minor increase in the time interval until return of CCP values to steady state levels in both aortic nonocclusion and occlusion. Thus, all the peptides tested were capable of influencing the smooth muscle tissues involved in penile outflow regulation.

Topics: Animals; Aortic Diseases; Arterial Occlusive Diseases; Male; Neuropeptide Y; Penis; Peptide PHI; Pressure; Rabbits; Vasoactive Intestinal Peptide

The concentrations of substance P (SP) and vasoactive intestinal polypeptide (VIP) were determined in plasma in normal volunteers during acute occlusive ischaemia (n=5) and in patients with chronic ischaemia (n=5) due to obliterative arterial disease in the lower limbs. Venous SP, but not VIP, increased significantly in the early post-occlusive period in normal volunteers (P less than 0.02). In the patients no significant veno-arterial difference in plasma concentration of SP or VIP could be detected across normal or chronic ischaemic areas. The results may suggest a role for SP in the acute post-occlusive vasodilation and/or in the post-occlusive heat-pain sensation. A role for SP in chronic ischaemia could not be defined. Plasma VIP was unchanged in both acute and chronic ischaemia.

Topics: Aged; Arterial Occlusive Diseases; Humans; Ischemia; Leg; Middle Aged; Substance P; Vasoactive Intestinal Peptide

1. The cutaneous vasodilatation following arterial occlusion ("reactive hyperemia") was studied in the rat hind paw. A peak increase in venous outflow of 200-250% was observed within 1 min after a 3 min occlusion period. 2. Chronic denervation as well as capsaicin pretreatment reduced the postocclusive cutaneous vasodilatation by more than 60% (P less than 0.01). This demonstrates that the reactive vasodilatation is of neurogenic origin and mediated by small diameter afferent fibres. 3. Reduction of the postocclusive cutaneous vasodilatation after histamine depletion by compound 48/80 indicates the involvement of histamine. 4. Among all neuropeptides known to occur in primary sensory neurones only substance P and vasoactive intestinal polypeptide cause vasodilatation when infused i.a. into the rat paw. In contrast to antidromic sensory nerve stimulation or i.a. substance P infusion, vasoactive intestinal polypeptide does not cause plasma extravasation. The vasodilator potency of vasoactive intestinal polypeptide is about 1/500 of substance P in the rat paw. Therefore only substance P is able to mimic the reactive vasodilatation. 5. It is concluded that the postocclusive cutaneous vasodilatation is caused mainly by the release of substance P from peripheral endings of small diameter nerve fibres. The "axon reflex", also involving neurogenic vasodilatation, is assumed to be exerted by the same mechanism.

Topics: Animals; Arterial Occlusive Diseases; Axons; Histamine Release; Male; Neurotransmitter Agents; Peripheral Nerves; Rats; Reflex; Skin; Substance P; Vasoactive Intestinal Peptide; Vasodilation