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)

This experiment was designed to determine if intraventricular administration of basic fibroblast growth factor (bFGF) could promote cerebral angiogenesis in a model of mild chronic forebrain ischemia. Wistar rats underwent bilateral carotid artery ligation. Animals received intraventricular injections of bFGF every 4 days for 28 days. Basic fibroblast growth factor caused a significant dose-dependent increase in capillary density compared to ischemic controls in all regions examined. These results support the hypothesis that chronic intraventricular administration of bFGF induces in vivo cerebral angiogenesis.
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PMID:Basic fibroblast growth factor promotes in vivo cerebral angiogenesis in chronic forebrain ischemia. 172 39

The effects of the vasoactive perivascular neuropeptides calcitonin gene-related peptide (CGRP), neurokinin A (NKA), neuropeptide Y (NPY), and vasoactive intestinal polypeptide (VIP) on proliferation of cultured human umbilical vein endothelial cells (HUVECs) were investigated. CGRP was shown to increase both cell number and DNA synthesis, whereas NKA, NPY, and VIP were ineffective. 125I-labeled CGRP was shown to bind to HUVECs and this binding was displaced by addition of unlabeled CGRP, suggesting the existence of specific CGRP receptors. The effect of CGRP on formation of adenosine 3',5'-cyclic monophosphate (cAMP) and inositol phosphates (InsP), two intracellular messengers known to be involved in regulation of cell proliferation, was investigated. CGRP stimulated cAMP formation but was without effect on the formation of InsP. Proliferation, as well as cAMP formation, was also stimulated by cholera toxin. Basic fibroblast growth factor stimulated growth without affecting cAMP or InsP formation, whereas thrombin, which increased InsP formation, did not stimulate proliferation. We thus suggest that CGRP may act as a local factor stimulating proliferation of endothelial cells; that the mechanism of action is associated with cAMP formation; and that this effect of CGRP may be important for formation of new vessels during physiological and pathophysiological events such as ischemia, inflammation, and wound healing.
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PMID:Calcitonin gene-related peptide stimulates proliferation of human endothelial cells. 215 44

The objective of this study was to determine whether basic fibroblast growth factor (bFGF), a known angiogenic factor, can promote new vessel growth when infused within the pericardial space in a model of chronic myocardial ischemia. Intravenous angiotensin II (AII) was infused to induce left ventricular hypertrophy and concomitant ischemia in New Zealand white rabbits. Basic FGF was infused into the intrapericardial space with an osmotic pump. Animals were assigned to one of four groups: group 1 received intrapericardial bFGF and intravenous AII, group 2 received intrapericardial bFGF and intravenous saline solution, group 3 received intrapericardial albumin and intravenous AII, and group 4 received intravenous AII only. Epicardial angiogenesis was graded histologically on a scale of 0 to 2. Animals receiving intravenous administration of AII displayed left ventricular hypertrophy that disproportionately affected the interventricular septum with a wall thickness of 5.62 +/- 1.00 mm versus 3.98 +/- 0.61 mm in the AII group and the saline solution control group, respectively (p < 0.005). A highly localized angiogenic effect of bFGF was observed. The mean angiogenesis scores were 1.9, 1.4, 1.3, and 0.2 (p < 0.001) with an angiogenesis score of 2 (marked increase in vascularity) noted in 86%, 40%, 43%, and 0% of hearts in groups 1 through 4, respectively. We conclude that intrapericardial bFGF enhances new epicardial small-vessel growth in a rabbit model; furthermore this effect is enhanced in the presence of left ventricular hypertrophy.
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PMID:Intrapericardial basic fibroblast growth factor induces myocardial angiogenesis in a rabbit model of chronic ischemia. 753 43

Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad-spectrum mitogenic and non-mitogenic activities of FGFs inspired us to study its protecting effects on tissue injuries in ischemia reperfusion condition. We found that systemic administration of aFGF after reperfusion onset prevented severe skeletal muscle injuries. In rats treated with aFGF, the tissue edema was reduced significantly, the tissue viability was increased, and the muscle fibers contained more succinate dehydrogenase (SDH) and adenosine triphosphatase (ATPase). The pathological results supported the concept of improved prevention with aFGF treatment. The possible tissue protection by aFGF may come from its ability to regulate the concentration of extra- and intracellular calcium ion. Besides, it may moderate other Ca2+ dependent enzyme conversion processes. Also, it may take part in the vascular tone regulation under ischemia and reperfusion conditions. These results suggest further study of tissue ischemia prevention with FGF and its possible mechanisms in the future.
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PMID:Acidic fibroblast growth factor reduces rat skeletal muscle damage caused by ischemia and reperfusion. 754 Sep 68

Basic fibroblast growth factor (bFGF) is a potent mitogen for many cell lineages including fetal cardiomyocytes. Furthermore, bFGF has been shown to modify gene expression, in vitro, in adult nonproliferative ventricular myocytes. This effect is suspected to be partly responsible for the genetic modifications that occur in vivo under pathophysiological conditions such as ischemia or pressure overload and that lead to myocardial hypertrophy. However, little is known about the first steps of the molecular mechanisms that take place soon after cell activation by bFGF. In this study, using biochemical and electrophysiological approaches, we have established, on cardiomyocytes cultured from neonatal rat ventricles, that (i) differentiated beating cells express at least two classes of bFGF-receptors having high and low affinity (Kd = 10 +/- 2 pM and 1 +/- 0.5 nM); (ii) the stimulation of these bFGF receptors promotes an increase in the beating frequencies of cultured cardiomyocytes (40 +/- 10%); (iii) bFGF provokes the activation of poorly specific and voltage-independent calcium channels (12pS); (iv) inositol 1,4,5-trisphosphate enhances similar bFGF-induced Ca2+ currents and is therefore suspected to be a second messenger triggering this activation. These results support the presence, in cultured cardiomyocytes, of new calcium channels whose activation after bFGF binding may be partly responsible for the cell response to this growth factor.
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PMID:Basic fibroblast growth factor activates calcium channels in neonatal rat cardiomyocytes. 761 40

Basic fibroblast growth factor (bFGF) is a morphogenic, chemotactic, mitogenic, and angiogenic peptide found within the central nervous system (CNS) with potent neurotrophic effects. A potential role in ischemia-induced vascular growth has been suggested for bFGF. In this study, we show that single, topical administration of human recombinant basic fibroblast growth factor (rbFGF) in the rat cerebral cortex promotes capillary overgrowth and might mimic the angiogenic response observed after brain ischemia. The implication of this finding for the therapeutic use of basic FGF in angiogenic therapy is discussed.
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PMID:Single topical application of human recombinant basic fibroblast growth factor (rbFGF) promotes neovascularization in rat cerebral cortex. 768 66

Platelet factor 4, which has a potent affinity for heparin, has been shown to inhibit the binding of basic fibroblast growth factor to the cell surface receptor and to counteract the biological activities of basic fibroblast growth factor in certain peripheral tissues. In the present in vitro [125I]basic fibroblast growth factor binding experiments, platelet factor 4 consistently inhibited the binding of iodinated basic fibroblast growth factor to cell membranes of the gerbil hippocampus. To investigate the in vivo function of endogenous basic fibroblast growth factor and/or basic fibroblast growth factor receptor possibly activated in the ischemic gerbil brain, we infused platelet factor 4 continuously into the left lateral ventricle with an osmotic minipump. When platelet factor 4 infusion was started within three days after a 3-min ischemic insult, it significantly enhanced ischemia-induced learning disability and ischemic neuronal loss in the CA1 region of the hippocampus, as demonstrated by the results of the step-down passive avoidance task and by subsequent histological examinations. Infusion of platelet factor 4 into the cerebral ventricle of intact gerbils did not affect learning ability or CA1 neuron number. Basic fibroblast growth factor-neutralizing antibody, when infused continuously in the cerebral ventricle, also exhibited a neurotoxic effect in ischemic but not intact gerbils. Basic fibroblast growth factor co-infused with heparin, but not basic fibroblast growth factor alone, rescued a significant number of ischemic neurons which were destined to degenerate without the infusion of heparinized basic fibroblast growth factor, and it prevented ischemia-induced learning disability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of basic fibroblast growth factor-heparin and neurotoxic effect of platelet factor 4 on ischemic neuronal loss and learning disability in gerbils. 777 64

Basic fibroblast growth factor (bFGF) is a polypeptide growth factor that promotes neuronal survival. We recently found that systemic administration of bFGF protects against both excitotoxicity and hypoxia-ischemia in neonatal animals. In the present study, we examined whether systemically administered bFGF could prevent neuronal death induced by intrastriatal injection of N-methyl-D-aspartate (NMDA) or chemical hypoxia induced by intrastriatal injection of malonate in adult rats and 1-methyl-4-phenylpyridinium (MPP+) in neonatal rats. Systemic administration of bFGF (100 micrograms/kg) for three doses both before and after intrastriatal injection of either NMDA or malonate in adult rats produced a significant neuroprotective effect. In neonatal rats, bFGF produced dose-dependent significant neuroprotective effects against MPP+ neurotoxicity, with a maximal protection of approximately 50% seen with either a single dose of bFGF of 300 micrograms/kg or three doses of 100 micrograms/kg. These results show that systemic administration of bFGF is effective in preventing neuronal injury under circumstances in which the blood-brain barrier may be compromised, raising the possibility that this strategy could be effective in stroke.
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PMID:Basic fibroblast growth factor protects against excitotoxicity and chemical hypoxia in both neonatal and adult rats. 779 Apr 10

We examined the effect of interleukin-6 (human recombinant) on glutamate-induced neuronal death of cultured 20-day fetal rat hippocampal neurons. After 7 days in culture, the hippocampal neurons were markedly degenerated by the addition of L-glutamate and also N-methyl-D-aspartate. The neuronal death was prevented by the addition of MK801, a potent N-methyl-D-aspartate antagonist. Interleukin-6 at the concentration of 50 ng/ml has a significant preventive effect on the glutamate-induced neuronal death. Basic fibroblast growth factor at the concentration of 100 ng/ml gave also significant protective effect on hippocampal neurons, but nerve growth factor was ineffective in preventing the toxicity. It has been postulated that glutamate plays an important role in the pathogenesis of neuronal death such as ischemia and the various neurological diseases. Interleukin-6 might have somewhat physiological or pathological role in these events.
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PMID:Interleukin-6 protects cultured rat hippocampal neurons against glutamate-induced cell death. 791 97

Although fibroblast growth factor has been identified in normal and ischemic myocardium, temporal changes in mitogenic activity due to fibroblast growth factors in ischemic tissue have not been well established, nor has correlation been made with the known early increases in coronary collateral flow. This study sought to measure fibroblast growth factor activity in myocardium after coronary ligation. Accordingly the left anterior descending coronary artery of dogs was ligated and coronary collateral flow measured with radioactive microspheres. The heart was arrested after 2 h (four dogs), 1 week (four dogs), 2 weeks (three dogs), or 8 weeks (four dogs). Just before arrest collateral flow was again measured with radioactive microspheres, and the perfusion territory of the ligated vessel was demarcated with an intracoronary injection of Evans blue. The stained ischemic region was separated into central and peripheral portions. A transmural sample was removed from each portion for quantitation of tissue radioactivity and the rest was used for isolation of fibroblast growth factor and the measurement of mitogenic activity with vascular endothelial cells. To determine which fibroblast growth factor (FGF-1 or FGF-2) was being produced by the myocardium, aliquots of the isolated protein were first treated with specific antibodies to FGF-1 or FGF-2 before being assayed for mitogenicity. Coronary collateral flow did not change between 5 min and 2 h following coronary ligation, but was significantly increased at later time points. The ischemic/normal myocardial basic fibroblast growth factor mitogenic activity ratio in the peripheral ischemic tissue was increased after 2 h of ischemia (1.41 +/- 0.34), but the increase was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal changes in myocardial basic fibroblast growth factor (FGF-2) activity following coronary artery ligation in the dog. 807 23


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