vasoactive-intestinal-peptide and Ischemia

Vasoactive intestinal peptide (VIP) is a pleiotropic neuropeptide, acting as a neuromodulator and neuroprotective peptide in the CNS after injuries. We have previously described that pituitary adenylate cyclase-activating polypeptide (PACAP), another member of the same peptide family, is retinoprotective in ischemic lesions. The aim of this study was to investigate the protective potential of VIP in bilateral common carotid artery occlusion (BCCAO)-induced ischemic retinal lesion. Two-month-old rats were subjected to BCCAO and treated with intravitreal VIP injection. Their retinas were processed for histology after 2 weeks of survival. We measured the number of the cells/100 μm of the ganglion cell layer and the thickness of each layer such as the outer nuclear, outer plexiform, inner nuclear, and inner plexiform layers as well as that of the whole retina. We found that treatment with 1,000 pmol VIP, but not 100 pmol VIP, had significant protective effects in BCCAO-injured retina, as shown by the morphometric analysis. Comparing the neuroprotective effects of VIP and PACAP in BCCAO-operated retinas, PACAP was more effective, already protective at 100-pmol doses. Similar to other studies, we found that VIP must be given at least in 10 times more concentration than PACAP to achieve a similar degree of neuroprotection in the retina.

Topics: Animals; Apoptosis; Carotid Artery, Common; Carotid Stenosis; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Intravitreal Injections; Ischemia; Male; Models, Neurological; Neuroprotective Agents; Pituitary Adenylate Cyclase-Activating Polypeptide; Rats; Rats, Wistar; Retinal Degeneration; Retinal Neurons; Retinal Vessels; Retinitis; Time Factors; Vasoactive Intestinal Peptide

The influence of carotid artery occlusion (10, 30 and 60 min) on regulatory mechanisms implicated in the vasorelaxant responses of isolated glandular branch of rabbit facial artery to acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) was examined.. In organ bath studies with arterial rings precontracted with phenylephrine (1 microM), before and after carotid artery occlusion, changes in isometric tension were recorded.. Endothelium-dependent vasorelaxation by ACh and endothelium-independent vasorelaxation by VIP were significantly reduced, started from 30 and 10 min of carotid occlusion, respectively. Inhibitory effect of indomethacin on ACh vasorelaxation was enhanced whilst effect of N(G)-nitro-L-arginine reduced, started from 30 min of carotid occlusion. Sodium nitroprusside-induced vasorelaxation was not changed after carotid occlusion. Inhibition of VIP vasorelaxation by L-N(omega)-nitroarginine-2,4-L-diaminobutyric-amide, was reduced, started from 30 min of carotid occlusion. Forskolin enhanced VIP-induced vasorelaxation in control rings but this effect was reduced started from 30 min of occlusion. In the presence of VIP, vasorelaxant effect of ACh was increased; the increase was reduced, started from 10 min of carotid occlusion.. The present investigation provides evidence for the decreased responsiveness to both, ACh-endothelium-dependent and VIP-endothelium-independent vasorelaxation in rabbit facial artery after carotid occlusion. In addition, the data suggest that ischaemia alters contribution of endothelial nitric oxide (eNO) and prostaglandin to ACh, and vascular smooth muscle's cAMP and neuronal NO to VIP vasorelaxant effects.

Topics: Acetylcholine; Animals; Arteries; Bradykinin; Carotid Artery Diseases; Carotid Artery, Common; Colforsin; Cyclic AMP; Endothelium, Vascular; Epoprostenol; Female; Indomethacin; Ischemia; Male; Muscle, Smooth, Vascular; Nitric Oxide; Nitroarginine; Nitroprusside; Phenylephrine; Rabbits; Sialadenitis; Signal Transduction; Submandibular Gland; Vasoactive Intestinal Peptide; Vasoconstrictor Agents; Vasodilation; Vasodilator Agents

Intestinal ischemia impairs gastrointestinal motility. The aims of this study were to investigate the effect of intestinal ischemia on gastrointestinal transit and on the expression of enteric transmitters in the rat, and whether the glutamate N-methyl-d-aspartate receptors influence these effects. Ischemia (1 h), induced by occluding the superior mesenteric artery, was followed by 0 or 24 h of reperfusion. Normal and sham-operated rats served as controls. Serosal blood flow was measured with laser Doppler flow meter. Gastrointestinal transit was measured as time of appearance of a marker in fecal pellets. Immunohistochemistry was used to evaluate the number of neurons immunoreactive for neuronal nitric oxide synthase (NOS) or vasoactive intestinal polypeptide and the density of substance P immunoreactive fibers in the myenteric plexus. The N-methyl-d-aspartate receptors antagonist, (+)-5-methyl-10,11-dihydro-5HT-[a,b] cyclohepten-5,10-imine (MK-801) (1 mg/kg i.v.) or the NOS inhibitor, N-nitro-l-arginine (10 mg/kg i.v.) was administered prior to ischemia. Serosal blood flow was decreased by 70% during ischemia, but it was not altered in sham-operated rats. Gastrointestinal transit was significantly prolonged in ischemic/reperfused rats compared with controls. There was a significant increase in the number of vasoactive intestinal polypeptide and neuronal nitric oxide synthase immunoreactive neurons, and a marked decrease of substance P immunoreactive fibers in ischemia followed by 24 h of reperfusion animals compared with controls. These alterations were not observed in ischemia without reperfusion. A significant delay of gastrointestinal transit and increase of vasoactive intestinal polypeptide neurons were also observed in sham-operated rats. The changes in transmitter expression and gastrointestinal transit in ischemic/reperfused rats were prevented by pre-treatment with the NOS inhibitor, N-nitro-l-arginine or the N-methyl-d-aspartate receptors antagonist, MK-801. This study suggests an involvement of the glutamatergic system and its interaction with nitric oxide in intestinal ischemia/reperfusion. Ischemia/reperfusion might induce local release of glutamate that activates N-methyl-d-aspartate receptors leading to increased production of nitric oxide and adaptive changes in enteric transmitters that might contribute to gastrointestinal dysmotility.

Topics: Analysis of Variance; Animals; Arginine; Dizocilpine Maleate; Drug Interactions; Enzyme Inhibitors; Excitatory Amino Acid Antagonists; Gastrointestinal Motility; Gastrointestinal Transit; Immunohistochemistry; Ischemia; Laser-Doppler Flowmetry; Male; Neural Inhibition; Neuronal Plasticity; NG-Nitroarginine Methyl Ester; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Regional Blood Flow; Reperfusion Injury; Time Factors; Vasoactive Intestinal Peptide

Vasoactive intestinal polypeptide is one of the body's most potent vasodilators and has been shown to increase blood flow in a number of tissues. Its effects on postburn skin perfusion and progressive ischemia was investigated in rats exposed to partial- and full-thickness experimental skin burns. Systemic administration of VIP elicited a significant drop in mean arterial blood pressure versus saline (p<0.001) and VIP antiserum (p<0.001) both in burned and nonburned animals. VIP also decreased heart rate versus saline (p<0.05) and anti-VIP (p<0.001) in nonburned and burned animals. In contrast, VIP antiserum significantly increased blood pressure (p<0. 001) and heart rate (p<0.001) versus saline in all the groups. Skin perfusion in normal skin was significantly impaired by VIP infusions as compared to saline (p<0.01) while VIP-antiserum did not differ significantly from saline. Similarly, VIP significantly reduced blood flow versus saline-treatment in partial-thickness (p<0.01) and full-thickness burns (p<0.05) while VIP-antiserum had no significant effect on skin perfusion in any of the burned groups as compared to saline treatment. The present results show that VIP is directly involved in general cardiovascular control but plays a minor role in the maintenance of skin perfusion following a thermal injury as suggested by the lack of effect of VIP-antiserum. In contrast, exogenous administration of VIP significantly and dramatically impaired skin perfusion in normal and burned skin probably by increasing blood flow in organs of higher priority such as the brain and heart and concomitantly inducing a pronounced vasoconstriction in the skin, probably as a result of increased sympathetic effect on peripheral organs in order to maintain blood pressure.

Topics: Analysis of Variance; Animals; Blood Pressure; Burns; Cardiovascular Physiological Phenomena; Confidence Intervals; Heart Rate; Immune Sera; Ischemia; Laser-Doppler Flowmetry; Male; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Skin; Sodium Chloride; Sympathetic Nervous System; Vasoactive Intestinal Peptide; Vasodilator Agents

Topics: Animals; Blood Transfusion; Hemorrhage; Histamine Release; Ischemia; Kidney; Male; Malondialdehyde; Mast Cells; Necrosis; NG-Nitroarginine Methyl Ester; Nitric Oxide; Rats; Rats, Sprague-Dawley; Vasoactive Intestinal Peptide

The effect of vasoactive intestinal peptide (VIP) on the nerve-stimulated contraction, tissue oxygenation, lipid peroxidation and antioxidant enzymes activities-superoxide dismutase and catalase was investigated in the rat gastrocnemius muscle exposed to 4 h ischemia-4hr reperfusion. Ischemia caused significant decrease in muscle contractile force, oxygenation and superoxide dismutase enzyme activity. Reperfusion of ischemic muscle increased the muscle contractile force and restored the tissue oxygenation to the baseline level. Superoxide dismutase and catalase activities of reperfused muscle increased significantly. However neither ischemia nor reperfusion affected gastrocnemius muscle malondialdehide (MDA) levels. VIP administration at the onset of reperfusion significantly increased skeletal muscle contractile force and tissue oxygenation even higher than baseline and reperfusion values. VIP also normalized the increased superoxide dismutase and catalase activities of reperfused skeletal muscle. In conclusion, VIP, acting as a powerful antioxidant and preserving contractile machinery seems to be a promising endogenous peptide that can salvage the skeletal muscle from severe ischemia-reperfusion injury.

Topics: Analysis of Variance; Animals; Catalase; Ischemia; Male; Malondialdehyde; Muscle Contraction; Muscle, Skeletal; Oxygen Consumption; Rats; Rats, Wistar; Reperfusion; Superoxide Dismutase; Time Factors; Vasoactive Intestinal Peptide

Transplantation of small intestine is a neural model that permits studies of expression of the neuropeptide, vasoactive intestinal peptide, following extrinsic denervation, transection of intrinsic neural pathways, and an ischemic interval. Tissue levels of vasoactive intestinal peptide were examined at 3 months in ileum from a sham operation, in ileum after resection of proximal small intestine, in ileum after resection of proximal small intestine and extrinsic denervation, in ileum after resection of proximal small intestine and 30 min of ischemia, and in ileum obtained 3 months after ileal isografting in Lewis-to-Lewis combinations. Vasoactive intestinal peptide levels were increased in transplanted rat ileum, resection controls, denervation controls, and ischemic controls compared to sham-operated ileum (pANOVA < 0.01). The increased levels of this peptide were highest in denervation controls and lowest in ischemic controls. Northern blot analysis using rat vasoactive intestinal peptide cDNA identified a single 1.7-kb transcript in normal and transplanted rat ileum. The density of vasoactive intestinal peptide transcripts was increased in transplanted ileum (8450 +/- 540) compared to normal ileum (5790 +/- 620) (P < 0.01), and the ratio of this transcript to glyceraldehyde-3-phosphate dehydrogenase density units was also increased in transplanted ileum (0.81 +/- 0.08) compared to normal ileum (0.40 +/- 0.07; P < 0.01). Enhanced transcriptional regulation was the likely mechanism for increased tissue vasoactive intestinal peptide. The increased tissue levels appeared to be a response to extrinsic denervation and transection of intrinsic neural pathways, while an ischemic interval appeared to decrease tissue levels of the peptide.

Topics: Animals; Denervation; Gene Expression Regulation; Intestine, Small; Ischemia; Radioimmunoassay; Rats; Rats, Inbred Lew; RNA, Messenger; Transplantation, Isogeneic; Up-Regulation; Vasoactive Intestinal Peptide

To measure colonic arterial (CA) and colonic venous (CV) plasma neuropeptide concentrations during low-flow ischemia and reperfusion of the large colon in horses.. 10 adult horses.. CA and CV plasma samples collected from anesthetized horses during experimentally induced low-flow colonic ischemia and reperfusion were assayed for vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), using radioimmunoassays. In 6 anesthetized horses, colonic ischemia (20% of baseline (BL]) was maintained for 3 hours, then blood flow was restored and monitored for 3 hours. Hemodynamic variables were monitored continuously and recorded at 30-minute intervals. CA resistance was calculated from colonic blood flow (Q(colon)) and mean CA pressure values at each time. Blood was obtained from CA and CV catheters at 0, 1, 2, 3, 3.25, 3.5, 4, 5, and 6 hours; plasma VIP, CGRP, and SP concentrations were quantified, using radioimmunoassays. In 4 additional horses, VIP and CGRP were measured in CA and CV blood at 0, 0.25, 0.5, 0.75, and 1 hour.. Heart rate was significantly increased at 5.5 and 6 hours; other alterations in systemic hemodynamic variables were not significant. Decrease in Q(colon) during ischemia was significant; Q(colon) rebounded to a value significantly greater than BL value within 5 minutes of reperfusion and was maintained above the BL value during 3 hours of reperfusion. Mean CA pressure was significantly decreased during ischemia, but returned to a value not different from the BL value by 3.25 hours. Mean CV pressure remained unchanged from the BL value during ischemia, but increased to a value significantly greater than the BL value by 3.25 hours and remained increased through 6 hours. CA resistance began to decrease during early ischemia and was significantly less than the BL value by 3.25 hours; it remained less than the BL value through 4 hours. Increase in CV VIP concentration was significant by 0.25 hour of ischemia, but decreased to a value not different from BL value by 3.25 hours. Increase in CV CGRP was significant at 3.25 hours, but this variable returned to a value not different from BL value by 3.5 hours.. CV VIP concentration increases during low-flow colonic ischemia, and CV and CA CGRP and CA SP concentrations increase during early reperfusion.

Topics: Animals; Arteries; Blood Pressure; Calcitonin Gene-Related Peptide; Cardiac Output; Colon; Heart Rate; Hemodynamics; Horses; Ischemia; Muscle, Smooth; Neuropeptides; Radioimmunoassay; Regional Blood Flow; Reperfusion; Substance P; Time Factors; Vasoactive Intestinal Peptide; Veins

Infrarenal aortic cross-clamping is associated with remote vascular events, including myocardial infarction and renal insufficiency. The purpose of this study was to determine whether hindlimb ischaemia and reperfusion associated with infrarenal aortic cross-clamping results in the production of vasoactive regulatory neuropeptides. A canine model of infrarenal aortic cross-clamping was used for the study. Serial blood samples were drawn, prior to, at the time of, and serially following placement of the clamp and subsequent release of the clamp and reperfusion. Ischaemia resulted in increased mean(s.e.m.) plasma levels of neuropeptide Y (NPY) (initial 10.0(1.8) pmol/l versus ischaemia 24.7(2.3) pmol/l, P < 0.001) and vasoactive intestinal polypeptide (VIP) (initial 2.53(0.5) pmol/l versus ischaemia, 7.3(1.3) pmol/l, P < 0.05). Reperfusion produced three-fold elevation of VIP (initial 2.5(0.5) pmol/l versus reperfusion 9.6(1.5) pmol/l, P < 0.001), two-fold elevation in the plasma levels of endothelin-1 (initial 1.3(0.1) pmol/l versus reperfusion maximum 2.5(0.3) pmol/l, P < 0.01) and NPY (initial 10.0(0.8) pmol/l versus reperfusion maximum 23.9(2.3) pmol/l, P < 0.001). Ischaemia and reperfusion did not alter calcitonin gene-related peptide (CGRP) (a potent vasodilator) levels. Endothelin-1 (ET-1) plasma levels were also increased following haemorrhagic shock (initial 1.3(0.1) pmol/l versus exsanguination 3.4(0.4) pmol/l, P < 0.001), but not during ischaemia (initial 1.3(0.1) pmol/l versus ischaemia maximum 1.7(0.2) pmol/l, P = 0.7). It was concluded that vasoactive regulatory peptides are released following ischaemia, reperfusion and shock in the canine infrarenal aortic revascularization model and, therefore could contribute to remote vascular events observed with infrarenal aortic cross-clamping.

Topics: Animals; Aorta, Abdominal; Calcitonin Gene-Related Peptide; Dogs; Endothelin-1; Female; Ischemia; Leg; Male; Neuropeptide Y; Radioimmunoassay; Reference Values; Reperfusion Injury; Vasoactive Intestinal Peptide

Topics: Animals; Catalase; Choroid; Female; Ischemia; Lipid Peroxidation; Male; Malondialdehyde; Rats; Reperfusion Injury; Retina; Retinal Vessels; Superoxide Dismutase; Vasoactive Intestinal Peptide

The effect of vasoactive intestinal peptide (VIP) on the activities of superoxide dismutase and catalase was investigated in renal tissues of rats exposed to 30% hemorrhage followed by reperfusion. In addition to enzyme activities, renal tissues were also histologically evaluated. Thirty percent hemorrhage had no significant effect on the activity of either enzyme. Reperfusion altered the activity of renal catalase but not of superoxide dismutase. On the other hand, administration of VIP (25 ng.kg-1) together with shed blood retransfusion protected the renal tissue from hemorrhagic ischemia-reperfusion injury without increasing superoxide dismutase and catalase activity. These results seem to be related either to the inhibitory effect of VIP on production or quenching activity of some reactive oxygen species. In conclusion, VIP may be a novel promising therapeutic approach toward defenses against hemorrhagic ischemia-reperfusion injury as an antioxidant.

Topics: Analysis of Variance; Animals; Catalase; Female; Hemorrhage; Ischemia; Kidney; Male; Rats; Reperfusion; Superoxide Dismutase; Vasoactive Intestinal Peptide

Reperfusion of ischaemic intestine is characterised by an initial hyperaemia with ensuing mucosal repair. This study investigated possible roles for gut vasoactive neuropeptides and trophic peptides in these phenomena. Groups of rats were monitored during superior mesenteric artery occlusion for five or 20 minutes, with or without subsequent reperfusion for five minutes. Peptide concentrations (fmol/ml) in arterial blood, were measured using specific radioimmunoassays. Intestinal ischaemia alone did not cause haemodynamic disturbance or peptide release. Reperfusion, after five minutes of ischaemia, resulted in arterial hypotension and a rise in plasma vasoactive intestinal polypeptide (mean (SEM)) (37 (3), control 11 (4), p < 0.001). After 20 minutes of ischaemia, reperfusion resulted in greater hypotension (p < 0.05) and release of both vasoactive intestinal polypeptide (31 (3), p < 0.05 v control) and the more potent vasodilator beta-calcitonin gene related peptide (49 (3), control 23 (1), p < 0.001). By contrast, the vasodilators alpha-calcitonin gene related peptide and substance P and the vasoconstrictors neuropeptide Y, peptide YY, and somatostatin were not released. Bombesin, a stimulatory neuropeptide, was released after 20 minutes of ischaemia/reperfusion (13 (2), control 7 (3), p < 0.05). Plasma enteroglucagon rose from control (51 (4)) to 110 (16) (p < 0.001) and to 158 (27) (p < 0.005) after five and 20 minutes of ischaemia/reperfusion. The potent enteric vasodilators vasoactive intestinal polypeptide and beta-calcitonin gene related peptide, unopposed by vasoconstrictors, may promote post-ischaemic intestinal hyperaemia. The rise in plasma enteroglucagon may point to diffuse mucosal injury and is consistent with the putative trophic role of this peptide.

Topics: Animals; Blood Pressure; Bombesin; Calcitonin Gene-Related Peptide; Glucagon-Like Peptides; Heart Rate; Intestines; Ischemia; Male; Rats; Rats, Wistar; Reperfusion; Vasoactive Intestinal Peptide

1. The number (but not the affinity) of vasoactive intestinal peptide (VIP) receptors in small intestinal epithelial cells decreased following intestinal ischaemia in rats as compared to sham-operated animals. 2. There was a parallel decrease of the efficiency (but not the potency) of the neuropeptide upon cyclic AMP formation at the same level after intestinal ischaemia. 3. The surgical manipulation did not modify the level of VIP immunoreactivity in the gut segment studied. 4. These results suggest that the VIPergic system is not directly involved in the high loss of water and electrolytes that appears following intestinal ischaemia.

Topics: Animals; Cyclic AMP; Intestinal Mucosa; Intestine, Small; Ischemia; Male; Radioimmunoassay; Rats; Rats, Inbred Strains; Receptors, Gastrointestinal Hormone; Receptors, Vasoactive Intestinal Peptide; Vasoactive Intestinal Peptide

Plasma levels of catecholamines and neuropeptides (met-enkephalin, ME; neurotensin, NT; neuropeptide Y, NPY; peptide YY, PYY; vasoactive intestinal polypeptide, VIP; cholecystokinin, CCK; bombesin, BMB) were examined in the femoral artery (FA), adrenal vein (AD), and portal vein (PV), in eight cats under halothane anesthesia at baseline (S1), at the end of a 2-hr ligation period of the major splanchnic arteries (celiac trunk, superior and inferior mesenteric arteries) (S2), immediately (S3) and 30 min (S4) after splanchnic reperfusion, and after the administration of naloxone (1 mg/kg, i.v.) (S5). During S2, there was a significant increase in portal vein VIP levels, while the other variables (hemodynamics, hormone levels) remained unchanged. During early shock (S3), significant (10- to 30-fold) increases in adrenal secretion of all catecholamines, ME, NT, NPY, and PYY occurred, while VIP and PYY were significantly released into the PV, and two- to tenfold increases in femoral artery catecholamine and ME levels were observed. Later shock (S4) led to a further fivefold increase, compared to S3, in adrenal release of norepinephrine (NE), dopamine (DA), and ME. Following naloxone administration (S5), the adrenal medullary release of NE, epinephrine (EPI), DA, NT, and NPY was significantly (twofold) increased; however, the animals' hemodynamic situation did not improve.

Topics: Adrenal Glands; Animals; Bombesin; Catecholamines; Cats; Cholecystokinin; Enkephalin, Methionine; Hemodynamics; Intestinal Mucosa; Ischemia; Ligation; Mesenteric Arteries; Naloxone; Neuropeptide Y; Neuropeptides; Neurotensin; Peptide YY; Peptides; Shock, Septic; 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

Intestinal ischemia shock is obtained in fasted rats by 40-minute splanchnic arterial occlusion (SAO) or by 35-minute portal vein occlusion (PVO). Survival is prolonged by plasma treatment; further prolongation is obtained by additional administration of glucose. After SAO early hyperglycemia is marked. Plasma adrenaline rises steeply after opening of the arteries and remains high, while plasma insulin remains unaltered. The hyperglycemia is abolished by adrenalectomy and section of the major splanchnic nerves (MSN) proximal to the adrenals but not by section of the MSN distal from the adrenals or by vagotomy. It is concluded that the sympathetic nervous system is stimulated by a substance, possibly related to VIP, released from the intestines. After PVO hyperglycemia is less marked. Plasma adrenaline as well as insulin are increased. During late and fatal hypoglycemia after PVO plus plasma treatment, the liver still appears to be functionally intact. It is assumed that gluconeogenesis is reversibly inhibited by as yet unknown factors. The hypoglycemia cannot be abolished by injection of common substrates of gluconeogenesis but the combination fructose plus glucagon plus NAD is highly effective.

Topics: Adrenal Medulla; Adrenalectomy; Animals; Blood Glucose; Epinephrine; Female; Gluconeogenesis; Hyperglycemia; Hypoglycemia; Intestines; Ischemia; Kidney; Liver; Portal Vein; Rats; Shock; Vasoactive Intestinal Peptide

In a series of 17 dogs of which 6 were controls experiments were undertaken to measure arterial and portal vasoactive intestinal peptide (VIP) levels during reduced cephalic mesenteric artery flow states and following reperfusion of the ischaemic mid gut. The flow states examined were basal flow, 50 per cent of basal flow and 25 per cent of basal flow. Zero flow was examined for 20 min and reperfusion of the ischaemic mid gut for 20 min. Peripheral and portal VIP levels were found to be massively elevated during all the flow states studied but particularly during reperfusion of the ischaemic mid gut.

Topics: Anesthesia; Animals; Dogs; Gastrointestinal Hormones; Intestines; Ischemia; Mesenteric Arteries; Perfusion; Portal Vein; Regional Blood Flow; Splenectomy; Vasoactive Intestinal Peptide

Vasoactive intestinal polypeptide (VIP) is released into the portal circulation in large quantities by ischaemic bowel. In view of its known high concentration in the gut and potent vasoactive properties it may well be implicated in the pathogenesis of the serious haemodynamic changes produced by gut ischaemia.

Topics: Animals; Gastrointestinal Hormones; Intestines; Ischemia; Liver Circulation; Swine; Vasoactive Intestinal Peptide