Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A forty-two years old male underwent an aortic arch replacement for an emergency treatment of dissecting aortic aneurysm (DeBakey type I). Separate cardiopulmonary bypass was used with main arterial inflow cannula inserted to right femoral artery. After the operation, ischemia of the right lower extremity led to acute renal failure due to myonephropathic-metabolic syndrome. Peritoneal dialysis, hemodialysis, and continuous arterio-venous hemofiltration were performed. Renal failure improved gradually. At the diuretic phase serum calcium concentration began to rise. Inspite of large amount of fluid and furosemide injection it became higher and finally reached to 20 mg/dl level. Calcitonin injection (320 mu/day) was very effective. In 2 months after surgery serum creatinine and calcium concentrations went down to normal range. Abnormalities in calcium metabolism are frequent in rhabdomyolysis-induced acute renal failure. However, it is rare to encounter such a remarkable hypercalcemia as seen in this patient. When treating MNMS we should pay attention to the changes of serum calcium concentration.
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PMID:[Dissecting aortic aneurysm associated with myonephropathic-metabolic syndrome and hypercalcemia]. 202 21

Calcitonin gene-related peptide (CGRP) is a bioactive neuropeptide with potent vasodilatory properties. The effect of CGRP on the no-reflow phenomenon was studied in rats. Island flaps based on the epigastric vessels were exposed to 11 hours of warm ischemia. CGRP was given as single doses before, before and after, or after the ischemic insults. Pre-ischemic treatment with CGRP increased flap survival at concentrations ranging from 10(-9) mol/L to 10(-7) mol/L. The survival rate of saline and untreated control flaps was 18.4%, calculated on the basis of tissue survival areas. The optimum survival rate after preischemic CGRP treatment was 60.3%, and after both preischemic and postischemic CGRP treatment, 66.3% (p less than 0.005 as compared with controls). Given as a single dose after the ischemic period, CGRP increased flap survival to 45.5% at 10(-7) mol/L (p less than 0.05), but no effect was found at lower concentrations. Apart from free radical scavengers, CGRP is the only agent known to delay the no-reflow phenomenon after a single postischemic dose.
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PMID:Calcitonin gene-related peptide delays the no-reflow phenomenon in the rat island flap. 297 83

Calcitonin gene-related peptide (CGRP) was shown to increase the survival area of ischaemic tissue from 45% in control animals to about 90% in treated animals. This effect was demonstrated in a musculocutaneous flap model in the rat. The concentrations used were 2 X 10(5) times lower than those known to cause an increase in skin blood flow under normal conditions. Treatment with one single dose up to 36 h postoperatively was found to increase the flap survival area. It is suggested that the mechanism/s by which CGRP increases survival of ischaemic tissue may be different from vasodilation or that the sensitivity is altered during ischaemic conditions and that CGRP may be a powerful tool to reduce ischemia in various clinical conditions.
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PMID:Calcitonin gene-related peptide increases survival of a musculocutaneous critical flap in the rat. 350 77

Nineteen patients with surgical or traumatic flaps and one patient with a congenital vein vault deficiency were treated with the vasodilatory compound calcitonin gene-related peptide (CGRP) intravenously. The patients showed compromised circulation due to ischemia and/or venous stasis. In all but three patients, the treatment resulted in an improved tissue circulation, as measured by laser Doppler flowmetry. Thirteen of the flaps survived completely, and in three flaps a partial necrosis was encountered (< or = 25 percent). The three flaps that did not respond at all to calcitonin gene-related peptide treatment did not survive. Calcitonin gene-related peptide was shown to be much more effective than transcutaneous electrical nerve stimulation (TENS). Thus calcitonin gene-related peptide provides a pharmacologic tool to improve blood flow in surgical and traumatic flaps with compromised circulation in humans.
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PMID:Calcitonin gene-related peptide treatment of flaps with compromised circulation in humans. 843 Jan 38

Ischemia resulting from flap harvesting and vascular manipulation during microsurgery may be responsible for flap ischemic sufferance and, ultimately, necrosis. Recently, the regulatory role of the sensory nervous system in ischemia has attracted much interest. Calcitonin gene-related peptide (CGRP), a neuropeptide, is a naturally occurring vasodilator with no constrictive effects. In the present study, we developed a model of partial, chronic ischemia in the rat epigastric flap and investigated the effects of ischemia on concentrations of CGRP-like immunoreactivity (-LI) in ischemic skin and in different regions of the rat brain (striatum, hippocampus, pituitary, hypothalamus, and frontal and occipital cortex). A neurovascular island flap based on the superficial epigastric vessels was raised in 10 animals. Ischemia of the flap was obtained by ligating the feeding artery so that the blood flow was reduced to 25% of the normal circulation. An electromagnetic Doppler positioned on the artery was used to monitor the blood flow reduction. Ten nonoperated animals were used as controls. Ten days after the operation, CGRP-LI was significantly increased in five of six brain regions analyzed (striatum excepted). Significantly decreased concentrations of CGRP-LI were found in seven ischemic flaps, as opposed to the control group. In the remaining three flaps, no significant changes in CGRP concentration were observed. The highest blood flux values (detected using a laser Doppler) in the flaps correlated positively with the highest concentrations of CGRP-LI in the flap tissue. The results of the present study suggest that endogenous CGRP may be involved in the adaptive response to ischemia.
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PMID:Calcitonin gene-related peptide in experimental ischemia. Implication of an endogenous anti-ischemic effect. 879 71

We evaluated the nerve blood flow (NBF), light and electron microscopy, and adrenergic innervation of rat sciatic nerve at 2-45 days after the application of four loose ligatures. Ischemia developed at the lesion edge, creating an endoneurial dam. Calcitonin gene-related peptide, norepinephrine and NBF were increased within the lesion. Morphologic alterations consisted of early endoneurial edema, followed by myelinated fiber degeneration, with relative sparing of small myelinated and unmyelinated nerve fibers, and leukocyte adhesion to microvessels. Axonal degeneration predominated over demyelination. At 45 days, profuse regeneration of small myelinated fibers was seen. The mechanism of lesional sensitization is discussed.
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PMID:Chronic constriction model of rat sciatic nerve: nerve blood flow, morphologic and biochemical alterations. 900 58

Calcitonin gene-related peptide is a potent intrinsic vasodilator, can induce prostacyclin release, and may inhibit membrane lipid peroxidation. This study examines the effect of calcitonin gene-related peptide on vessel diameters, capillary perfusion, and contractile function of skeletal muscle after 4 or 5 hours of ischemia and during immediate reperfusion using the rat cremaster muscle model. Forty-two male rats were used; half of these received 0.2 ml of 10(-7) M calcitonin gene-related peptide after 0, 15, and 30 minutes of reperfusion, while the other half received normal saline as a control. By means of intravital videomicroscopy, the diameters of 10 vessels per muscle were measured prior to ischemia and during reperfusion. The fluorescein filling area was determined at 15, 30, and 60 minutes of reperfusion. After 1 hour of reperfusion, muscle function was examined in vitro by quantifying the contractile response to electric field stimulation of the muscles in an organ bath system. There was a significant increase in the diameter of the arterioles, but not the small arteries, at every time point from 10 to 60 minutes of reperfusion. The fluorescein filling area was increased in treated muscles at every time point. Contractile function was not significantly preserved. In light of the ability of calcitonin gene-related peptide to relieve vasospasm and improve capillary perfusion, it may be useful in reducing reperfusion injury in the future.
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PMID:Calcitonin gene-related peptide and reperfusion injury. 916 27

Calcitonin gene-related peptide (CGRP) is a potent vasodilator and immune cell modulator. In two studies within the hippocampal formation (HF), CGRP-like immunoreactivity (CGRP-LI) was increased in the inner molecular layer of the dentate gyrus after adrenalectomy and in mossy cells after colchicine-induced destruction of granule neurons. Given the increase in CGRP-LI following damage to the granule cell region of the HF, we investigated another trauma model, ischemia, that targeted different areas of the HF, CA1 region, and subiculum to ascertain the regional expression of this peptide after insult. Following ischemia, light microscopic evaluation showed CGRP-LI in basket cell-like neuronal perikarya within the dorsal subiculum and CA1 region of the hippocampus and in varicose fibers within the CA2 region of the hippocampus. Control rats rarely expressed CGRP-LI within neurons in these regions. In ischemic brains, double-labeled immunocytochemistry with antibodies to various neural markers demonstrated co-localization of CGRP-LI primarily within surviving subicular and CA1 cells resembling interneurons containing parvalbumin-LI or calbindin-LI. Electron microscopic analysis of the CA1 region from ischemic brains showed that CGRP-LI was contained in terminals with numerous small synaptic vesicles that formed symmetric synapses with perikarya and large dendrites of pyramidal cells, some of which were degenerating. Collectively, the data from this study and our previous study indicate that damage induces CGRP-LI expression in interneurons and nonprincipal cells in the area of damage, and we hypothesize that CGRP expression in surviving neurons within damage-related regions of the hippocampus is likely to be an important, and possibly a protective, component of the response of the nervous system to injury.
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PMID:Induction of calcitonin gene-related peptide-like immunoreactivity in hippocampal neurons following ischemia: a putative regional modulator of the CNS injury/immune response. 952 88

Calcitonin gene-related peptide [CGRP]--a powerful vasodilator, is a 37 amino acid peptide that is find primarily in the central and peripheral nervous system. It affects the regulation of local blood flow, smooth muscle tone and glandular secretion. It is an endocrine regulator and in the lungs it also exerts a bronchoconstricting effect. CGRP has a proliferative effect on human endothelial cells. Therefore, it is important for the formation of new vessels, example, in ischemia, inflammations, and in the healing of wounds. Plasma levels of CGRP are increase in patients with chronic cardiac failure and sepsis, indicating that CGRP may be another important peptide in chronic illness. We have therefore measured the release of this peptide and another sensory peptide [Substance P (SP)]; a vasoconstrictor peptide [Endothelin (ET)]; and a perivascular peptide [Neuropeptide Y (NPY)], within 24 hours of injury, in the plasma of patients with soft tissue injury. Neuropeptides were measure by enzyme immunoassay technique. Median: (lower quartile-upper quartile) in pmol/L CGRP level was elevated in patients [50.37: (12.4-110.9)] compared to controls [13.9: (10.9-36.96)] p<0.05; Endothelin and NPY did not vary much between groups p=NS; ET: patients [8.7: (1.7-87.1), controls 8.8: (1.7-32.9)]; NPY: Patients [11.7: (10.5-14.99), controls 11: (10.3-12.8)]. SP was increase in patients [302.3: (79.9-707.3)], than controls [5.6: (3.2-36.6)] p<0.05. Furthermore, Elastase (a decisive marker for inflammation and infectious complications), was measure (ng/L), and found to be slightly higher in patients (102: 25.5-223), than controls (91.8: 45.9-127). In summary, plasma levels of sensory peptides increased significantly, in patients with soft tissue injury, in contrast to vasocostrictor peptides that remained unchanged. These sensory peptides may yet be another group of neuromodulators playing a significant role in immune, pain, inflammatory and wound healing in soft tissue injury patients.
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PMID:Calcitonin gene-related peptide and other neuropeptides in the plasma of patients with soft tissue injury. 1050 54

Calcitonin gene-related peptide (CGRP) and substance P co-exist in capsaicin-sensitive primary sensory neurons and are released from the myocardium after activation of sensory nerve fibres as well as by ischemia in animals. This study was undertaken to try to clarify the potential involvement of immunoreactive (ir) CGRP in anginal pain and myocardial ischemia in humans. One clinical group (n = 87) and one experimental group (n = 14) were studied. The clinical group was admitted to a coronary care unit with suspected or definite acute myocardial infarction (AMI). The experimental group consisted of patients with severe angina pectoris (NYHA III-IV). This group was subjected to atrial pacing up to the appearance of angina pectoris. Mean irCGRP levels at admission for the clinical group with and without AMI showed no significant difference. Neither were any significant differences found in irCGRP concentrations between patients with pain as compared to those without pain or in the group who had had chest pain >30 min before hospital admission as compared to those with chest pain <30 min. Extraction ratios for lactate and irCGRP was calculated in the experimental group. No statistically significant covariance was found between irCGRP extraction ratio and lactate extraction ratio (r(xy) = -0.006) at the time of appearance of angina during atrial pacing. Despite the facts that CGRP may be liberated by a variety of physiological stimuli and may act as a potent vasodilator in the human vasculature, no evidence has been found in this study that CGRP release is increased as a consequence of ischemia or ischemic pain.
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PMID:Acute ischemic chest pain is not associated with increased calcitonin gene-related peptide (CGRP) levels in peripheral plasma nor in the coronary circulation. 1054 Sep 19


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