vasoactive-intestinal-peptide and Cerebral-Infarction

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 with good efficiency, on VIP, SS and PP have not been known. For researching their changes in ICVD and effects of electro-acupuncture on them, and finding the mechanism of acupuncture in treatment of ICVD, the study was performed. The levels of VIP, SS and PP in 64 patients with acute cerebral infarction were determined. The points of acupuncture were Quchi (LI 12), Waiguan (SJ 5), Huantiao (BG 30), and Zusanli (ST 36). The routine treatment included dextran, nicotinic acid, aspirin, dipyridamole and radix salviae miltiorrhizae composita. The CSF and blood were taken before the begining of treatments and after a course of treatment. The level of VIP, SS and PP were measured by radiommunoassay. Results showed the level of CSF VIP in the patients was significantly lower as compared with controls. The level of plasma SS in the patients was lower, but the difference was not significant as compared with controls, and level of plasma PP in the patients was significantly increased when it was compared with controls. After electro-acupuncture treatment, in patients with good efficiency, CSF VIP recovered to normal level and the levels of plasma and CSF SS were significantly increased, while the level of plasma PP had no significant change. The results suggest that acupuncture might regulate the disturbances of metabolism of VIP and SS in CNS.

Topics: Acupuncture Points; Adult; Aged; Cerebral Infarction; Electroacupuncture; Female; Humans; Male; Middle Aged; Pancreatic Polypeptide; Somatostatin; Vasoactive Intestinal Peptide

To explore the neuroprotective effect of vasoactive intestinal peptide (VIP) in rat ischemic brain injury.. VIP was administered via intracerebroventricular injection in SD rats prior to focal cerebral ischemia by intraluminal occlusion of the middle cerebral artery. The infarct volume was assessed with TTC staining, and immunohistochemistry was performed to analyze the S100beta expression in the cerebral tissue, with the serum concentrations of S100beta detected by double-antibody sandwich enzyme-linked immunosorbent assay.. After VIP injection, the relative infarct volume in the rats with cerebral ischemia was significantly reduced by 32.3% as compared with the volume in the control group on day 1 (P<0.05), and the number of S100beta-positive cells was significantly decreased in the cerebral tissue (P<0.05). The injection also resulted in significantly decreased serum S100beta concentrations in the rats (P<0.05).. VIP injection can reduce the infarct volume in rats with focal cerebral ischemia, suggesting the neuroprotective effect of VIP in brain ischemia possibly by reducing S100beta overexpression.

Topics: Animals; Brain Ischemia; Cerebral Infarction; Nerve Growth Factors; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; S100 Calcium Binding Protein beta Subunit; S100 Proteins; Vasoactive Intestinal Peptide

The effect of acute cerebral occlusion on the distribution of cerebral perivascular nerves containing catecholamine, neuropeptide Y, and vasoactive intestinal peptide was studied in the three commonly used rat models of cerebral ischemia: Unilateral permanent middle cerebral artery (MCA) occlusion induced with an intraluminal thread technique; unilateral MCA occlusion produced by extraluminal electrocoagulation of the MCA; and transient arterial occlusion of the whole brain induced extracranially by the four-vessel clasp occlusion method for 30 minutes. Animals were sacrificed 3 days after occlusion and the distribution of the perivascular nerves of the MCA studied. Intraluminally occluded MCAs showed a similar distribution of perivascular nerves to those of contralateral and sham-operated MCAs. Extraluminally occluded MCAs demonstrated a marked decrease in perivascular nerves containing catecholamine and peptides while the contralateral MCAs showed normal distribution of the nerves. Extracranial occlusion caused no discernible change in the distribution of perivascular nerves in occluded and sham-operated animals. This study indicates that the different methods of cerebral arterial occlusion have variable effects on the perivascular innervation. Arterial occlusion induced by intraluminal or transient extracranial procedures does not impair cerebral perivascular innervation at least up to 3 days post-occlusion. In contrast, cerebral arterial occlusion by extraluminal electrocoagulation diminishes the perivascular nerves around the occluded cerebral artery.

Topics: Animals; Catecholamines; Cerebral Arteries; Cerebral Infarction; Ischemic Attack, Transient; Male; Microscopy, Fluorescence; Nerve Fibers; Neuropeptide Y; Rats; Rats, Sprague-Dawley; Vasoactive Intestinal Peptide

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 barrel fields bilaterally by laser Doppler blood flowmetry. Immunohistochemistry of middle cerebral artery (MCA) whole mount preparations was used to verify the surgical lesion. During hemorrhagic hypotension, rCBF was equivalent on the two sides in shams, after selective sensory denervation, or in parasympathetically sectioned animals exhibiting small decreases (less than or equal to 30%) in immunoreactive vasoactive intestinal peptide (VIP)-containing fibers. After chronic parasympathetic denervation, decreases in perfusion pressure were accompanied by greater reductions in rCBF on the lesioned side; changes in vascular resistance were also attenuated on that side. The rCBF response to hypercapnia (PaCO2 50 mm Hg), however, was symmetrical and robust. To examine the effects of impaired neurogenic vasodilation on the pathophysiology of cerebral ischemia, infarct size was measured 24 h following tandem MCA occlusion in denervated animals. Infarction volume was larger after selective parasympathetic sectioning (sham, 156 +/- 27 vs. 196 +/- 32 mm3, respectively) but only in those denervated animals demonstrating greater than or equal to 40% decrease in immunoreactive VIP-containing fibers within the ipsilateral MCA. Lower than expected blood flow/perfusion pressure in the cortex distal to an occluded blood vessel may relate the observed blood flow responses to the occurrence of larger cortical infarcts in parasympathetically denervated animals. If true, the findings suggest a novel role for neurogenic vasodilation in the pathophysiology of cerebral ischemia and in rCBF regulation within the periinfarction zone.

Topics: Animals; Blood Pressure; Brain; Brain Chemistry; Brain Ischemia; Cerebral Arteries; Cerebral Hemorrhage; Cerebral Infarction; Cerebrovascular Circulation; Hypercapnia; Hypotension; Immunohistochemistry; Male; Parasympathetic Nervous System; Rats; Rats, Inbred SHR; Vasoactive Intestinal Peptide

Studies were undertaken in Long Evans rats to examine the hypothesis that chronic unilateral sectioning of vasodilating nerve fibers (parasympathetic and/or sensory) innervating the circle of Willis increases infarction volume following unilateral branch occlusion of the middle cerebral artery (MCA) combined with temporary (45 min) bilateral common carotid occlusion. Infarct size was measured 24 h after surgical occlusion from seven coronal slices. Infarction volume (mean +/- SD) in sham animals (group A) and surgically naive animals (group B) measured 153 +/- 43 and 131 +/- 38 mm3, respectively. After lesions of both sensory (nasociliary nerve) and parasympathetic efferents at the ethmoidal foramen (group C, combined lesion) or selective lesions of parasympathetic efferents (group D), infarction volume increased [214 +/- 47 mm3 (p less than 0.01) and 209 +/- 46 mm3 (p less than 0.05), respectively]. No increases were detected after cutting the nasociliary nerve alone (group E) or occluding the external ethmoidal artery (group F) [145 +/- 39 mm3 (p greater than 0.05) and 124 +/- 63 mm3 (p greater than 0.05), respectively]. The infarct was predominantly located within cortical gray matter and became enlarged on its superior and inferior aspects after parasympathectomy. Large infarcts were noted whether animals breathed spontaneously (all of the above) or were artificially respired or whether animals were anesthetized with xylazine and ketamine or chloral hydrate. Taken together, these studies suggest a previously unrecognized protective role for autonomic parasympathetic fibers in the pathophysiology of focal cerebral ischemia that is not shared by sensory fibers. The importance of autonomic vasodilating fibers to blood flow in ischemic brain merits further study.

Topics: Animals; Blood Vessels; Calcitonin Gene-Related Peptide; Cerebral Arteries; Cerebral Cortex; Cerebral Infarction; Denervation; Immunoenzyme Techniques; Ligation; Male; Nerve Fibers; Parasympathetic Nervous System; Pia Mater; Rats; Vasoactive Intestinal Peptide