vasoactive intestinal peptide/infarction

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

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

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

VIP, SS and PP which exist in gastrointestinal tract and CNS might be to play an important role in nervous system as neurotransmitters of neuromediaters. There have been a few of reports about their changes in plasma and CSF in ICVD. The effects of acupuncture, which was used in treatment of ICVD

BACKGROUND 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

Cardiac sympathetic neurons stimulate heart rate and the force of contraction through release of norepinephrine. Nerve growth factor modulates sympathetic transmission through activation of TrkA and p75NTR. Nerve growth factor plays an important role in post-infarct sympathetic remodeling. We used

Regional cerebral blood flow (rCBF) during controlled hemorrhagic hypotension (140-20 mm Hg) was assessed 10-14 days after chronic unilateral sectioning of parasympathetic and/or sensory fibers innervating pial vessels in spontaneously hypertensive rats (SHR). rCBF was measured in the cortical

OBJECTIVE To explore the neuroprotective effect of vasoactive intestinal peptide (VIP) in rat ischemic brain injury. METHODS VIP was administered via intracerebroventricular injection in SD rats prior to focal cerebral ischemia by intraluminal occlusion of the middle cerebral artery. The infarct

OBJECTIVE To explore the neuroprotective action of vasoactive intestinal peptide (VIP) on ischemia and reperfusion in the rat. METHODS VIP was given via intracerebroventriclar injection after a 2 hour transient middle cerebral artery occlusion using filament model. The infarct volume was

The aim of this study was to investigate the effects of vasoactive intestinal peptide (VIP) on neurogenesis and neurological function after cerebral ischemia. Rats were intracerebroventricular administered with VIP after a 2h middle cerebral artery occlusion (MCAO) and sacrificed at 7, 14 and 28

Vasoactive intestinal peptide (VIP) exerts neuroprotective effects under various neurotoxic conditions in vitro. In the present study, we investigated the effects of VIP on transient ischemic brain damage. Focal cerebral ischemia was induced using middle cerebral artery occlusion (MCAO) for 120 min

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

BACKGROUND Several neurohumoral mechanisms involved in cardiovascular regulation are activated in the failing heart, but only limited information is available regarding the influence of long-term nitrate therapy. METHODS This was a double-blind, randomized comparison of isosorbide-5-mononitrate

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