vasoactive-intestinal-peptide and Myocardial-Infarction

Cardiac ischemia-reperfusion alters sympathetic neurotransmission in the heart, but little is known about its effect on neuropeptide expression in sympathetic neurons. Ischemia followed by reperfusion induces the production of inflammatory cytokines in the heart, including interleukin-6 and cardiotrophin-1. These cytokines and related molecules inhibit the expression of neuropeptide Y (NPY), and stimulate the expression of vasoactive intestinal peptide (VIP), substance P (SubP), and galanin (GAL) in cultured sympathetic neurons. Therefore, we quantified NPY, VIP, SubP, and GAL mRNA in neurons of the stellate ganglia 1 week after ischemia-reperfusion to determine if neuropeptide expression was altered in cardiac sympathetic neurons. NPY, VIP, and SubP mRNAs were unchanged compared to unoperated control animals, but GAL mRNA was increased significantly. The increased GAL mRNA was not accompanied by elevated GAL peptide content in the stellate ganglia. Galanin content was increased significantly in the heart, however, indicating that elevated GAL mRNA led to increased peptide production. GAL content was increased in the left ventricle below the coronary artery ligation, but was not increased significantly in the atria or the base of the heart above the ligation. The buildup of GAL specifically in the damaged left ventricle is consistent with previous reports that GAL is transported to regenerating nerve endings after axon damage.

Topics: Animals; Coronary Vessels; Galanin; Gene Expression; Heart; Ligation; Male; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion; Neurons; Neuropeptide Y; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; RNA, Messenger; Substance P; Sympathetic Nervous System; Vasoactive Intestinal Peptide

Using the method of indirect immunofluorescence the distribution of vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide (CGRP) was investigated in autopsy specimens of human stellate ganglia following acute myocardial infarction (AMI). The dramatic increase of both VIP- and CGRP-immunoreactivities in principal ganglionic neurons as well as of calcitonin gene-related peptide in perineuronal nets was revealed. It was concluded that hypoxia and myocardial ischaemia following AMI are the main inducing factors for activation of both vasoactive regulatory neuropeptide synthesis. The upregulation of VIP and CGRP expression in sympathetic ganglionic neurons may provide regulatory and trophic support to the ischaemic heart.

Topics: Autopsy; Calcitonin Gene-Related Peptide; Humans; Middle Aged; Myocardial Infarction; Nerve Fibers; Neurons; Reference Values; Stellate Ganglion; Vasoactive Intestinal Peptide

Vasoactive intestinal peptide (VIP) acts as a vasodilator on coronary and gastrointestinal arteries. During coronary occlusion, the locally released VIP may exert a protective effect on the heart, but it may aggravate the shock state through its vasodilatory effect in the gastrointestinal tract.. After left thoracotomy, the left circumflex coronary artery (LCx) was prepared, and a pneumatic occluder was introduced around it. After 60 min of coronary occlusion, the LCx was reperfused in six dogs (reperfusion group), while in another six the occlusion was maintained for 6 h (occlusion group). Five dogs served as sham-operated controls. The plasma concentration of VIP was determined at baseline, after the 60 min occlusion and 10 min, 3 h and 6 h after reperfusion, or 3 h and 6 h after continuous occlusion in the coronary sinus and in the femoral and portal veins.. The plasma VIP concentrations in all three vessels were increased after 60 min of LCx occlusion. During the 6 h constant coronary occlusion, concentrations remained increased in both the coronary sinus and the portal vein, but not in the femoral vein. In the reperfusion group, 10 min after reperfusion, the plasma concentrations of VIP in all three vessels had decreased.. Coronary artery occlusion causes a long-term increase in plasma VIP concentrations that decreases after reperfusion, when measured in the portal vein and coronary sinus, but not in the femoral veins.

Topics: Animals; Biomarkers; Blood Pressure; Coronary Vessels; Digestive System; Disease Models, Animal; Dogs; Heart Rate; Myocardial Infarction; Myocardial Reperfusion; Myocardium; Radioimmunoassay; Vasoactive Intestinal Peptide; Vasodilation

Plasma levels of vasoactive intestinal peptide increase early after acute myocardial infarction (AMI) and are significantly higher during the first 2 weeks of AMI in survivors and younger patients (<60 years) than in those who died and in older (>60 years) patients. Data suggest that vasoactive intestinal peptide is involved in neuroendocrine activation occurring in AMI and could be regarded as a marker of the course of AMI.

Topics: Adult; Age Factors; Aged; Aged, 80 and over; Female; Humans; Male; Middle Aged; Myocardial Infarction; Time Factors; Vasoactive Intestinal Peptide

Topics: Adult; Aged; Aged, 80 and over; Analysis of Variance; Case-Control Studies; Female; Humans; Male; Middle Aged; Myocardial Infarction; Reproducibility of Results; Vasoactive Intestinal Peptide

The plasma levels of vasoactive intestinal peptide in peripheral vein were measured in human acute myocardial infarction. The plasma vasoactive intestinal peptide level was increased within 1 h after the onset of the symptoms of acute myocardial infarction (Group 1, n = 9), compared with normal values (6.3 +/- 0.7 vs. 2.8 +/- 0.9 pg/ml, P < 0.05). Two or more hours after the onset of acute myocardial infarction there was no subsequent increase in peripheral plasma vasoactive intestinal peptide levels (n = 26). Ten days after the onset of acute myocardial infarction, the elevated plasma vasoactive intestinal peptide levels in Group 1 had normalized (3.5 +/- 0.5 pg/ml).

Topics: Aged; Blood Pressure; Echocardiography; Electrocardiography; Female; Follow-Up Studies; Heart Rate; Humans; Male; Myocardial Infarction; Time Factors; Vasoactive Intestinal Peptide; Veins

Acute myocardial infarction (AMI) is known to be associated with a complex neuroendocrine activation, especially concerning sympathetic and renin-angiotensin systems, cortisol, atrial natriuretic peptide and endothelin. Results of our study show that the vasoactive intestinal peptide (VIP), also, is early involved in the neuroendocrine activation occurring in AMI. Plasma concentration of VIP, significantly increased in AMI patients within 6 hours after the onset of chest pain, soon decreased and remained below than normal along the first week. At the 14th day of the AMI, plasma levels of VIP returned into the normal range. A significant increase of VIP plasma concentration is detectable in the first hours of AMI in survived as compared with died patients. The phenomenon seems to be a suitable process to provide an endogenous support to the ischemic heart and to counteract the negative effects of other neuroendocrine activated factors.

Topics: Adult; Aged; Aged, 80 and over; Female; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Time Factors; Vasoactive Intestinal Peptide

Aim of our study was to investigate the pathophysiological role of vasoactive intestinal peptide (VIP) in the neuroendocrine activation occurring in acute myocardial infarction (AMI). Plasma VIP concentration has been assayed in 30 patients with AMI, 22 males and 8 females, aged 41-82 years, without other important diseases. VIP plasma values, assayed on admission to the Coronary Care Unit, within 4-6 hours after the onset of chest pain, everyday for the first week and on day 14, were significantly higher in survivors and in patients aged < 60 years. VIP plasma concentration was not statistically correlated with CPK and CPK-MB. VIP seems to play a pathophysiological role in the neuroendocrine activation occurring in AMI. Low VIP plasma levels are associated with an unfavorable short-term prognosis. Moreover, it appears that VIP secretion is negatively influenced by aging.

Topics: Adult; Aged; Aged, 80 and over; Analysis of Variance; Female; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Radioimmunoassay; Survivors; Time Factors; Vasoactive Intestinal Peptide