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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to evaluate whether combined treatment with a cardiovascular exercise rehabilitation program and low doses of heparin can induce changes in ergometric parameters of ischemia in patients with coronary artery disease (CAD). Heparin may potentiate the development of new vessels promoted by ischemia and therefore may produce important clinical improvement. Thirty-six patients with stable CAD and evidence of myocardial ischemia on exercise testing were randomized into three groups: a control group (n = 11) received the usual medical treatment; another group (n = 11) underwent three exercise sessions per week during 12 weeks; and a third group (n = 14) undertook this exercise program and also received calcium heparin 12,500 IU subcutaneously 20 to 30 minutes before each exercise session. Pretreatment and posttreatment exercise tests were compared. Patients who underwent the rehabilitation program had an increase in exercise duration and workload at the onset of 1 mm ST-segment depression, but only patients who received calcium heparin showed a significant increase in rate-pressure product at the ST-segment ischemic threshold (p = 0.035). This result suggests that higher levels of myocardial oxygen consumption were now tolerated, a change that may be related to an improvement in myocardial perfusion.
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PMID:Exercise training and heparin pretreatment in patients with coronary artery disease. 889 65

Heparin, an anticoagulant that is widely used for cardiac patients, has been studied to determine its effects on wound healing. The role of heparin in wound healing has been demonstrated in both in vitro and in vivo studies. In cell culture studies, heparin and growth factors are associated with rapid and effective endothelial cell repair. In clinical studies, patients with burns and those with diabetic foot ulcers showed an increase in capillary circulation and decreased healing time. In contrast, heparin may not be beneficial in populations with ischemia, malnourishment, and vascular problems, although research in these populations is limited. Nevertheless, heparin continues to have therapeutic advantages for wound healing in carefully selected patients.
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PMID:Effects of heparin on wound healing. 890 Jun 76

Heparin has long been established as an anticoagulant. Although heparin has been demonstrated to reduce brain injury after ischemia and reperfusion, its mechanism of action remains unknown. Recent investigations reveal that it can modulate biological processes such as binding to adhesion receptors on endothelial cells and leukocytes. The authors hypothesized that heparin's protective effect is closely related to its antileukocyte adherence property. They evaluated the efficacy of sulfated polysaccharides (unfractionated heparin, low-molecular-weight heparin, heparan sulfate, chondroitin sulfate C, and dextran sulfate) on leukocyte accumulation, infarction size, and neurological outcome after transient focal cerebral ischemia in rats subjected to 1 hour of ischemia and 48 hours of reperfusion. Forty-nine animals were included in the study. The animals receiving unfractionated heparin or dextran sulfate showed a significant reduction in leukocyte accumulation, infarct size, and neurological dysfunction 48 hours after reperfusion (p < 0.05) when compared to untreated animals. The animals receiving unfractionated heparin also showed significantly better results than the animals receiving an equivalent anticoagulant dose of low-molecular-weight heparin. These data indicate that heparin's antileukocyte property plays a more important role than its anticoagulant ability in neuronal protection. The relative potency of the sulfated polysaccharides tested in leukocyte depletion was closely related to their degree of sulfation. Thus, in addition to demonstrating the potential efficacy of heparin as a therapeutic agent for ischemia and reperfusion injury by the prevention of leukocyte accumulation, the results also serve as a basis for studying important cellular and molecular events that contribute to tissue damage.
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PMID:Reduction of brain injury using heparin to inhibit leukocyte accumulation in a rat model of transient focal cerebral ischemia. I. Protective mechanism. 892 2

Thirty-one-year-old woman with Kawasaki disease wanted a child. She had a large coronary aneurysm on the left main coronary artery and complete obstruction of the right coronary artery, but there was no sign of ischemia. Heparin anticoagulant therapy was begun 8 weeks after the onset of pregnancy. The activated partial thromboplastin time (APTT) was successfully maintained at 1.5 to 2.0 times normal value during pregnancy and puerperium. There were no thromboembolic complications during pregnancy or after an uneventful cesarean delivery. The neonate was healthy.
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PMID:Anticoagulant therapy during successful pregnancy and delivery in a Kawasaki disease patient with coronary aneurysm--a case report. 907 Sep 77

We have recently reported that heparin-binding epidermal growth factor-like growth factor (HB-EGF) mRNA is induced in the rat kidney after acute ischemic injury. The present studies were designed to investigate whether bioactive HB-EGF protein is also produced in response to renal injury induced by either ischemia/reperfusion or aminoglycosides. Heparin-binding proteins were purified from kidney homogenates by heparin affinity column chromatography using elution with a 0.2-2.0 M gradient of NaCl. A single peak of proteins that eluted at 1.0-1.2 M NaCl was detected in the postischemic kidney within 6 h of injury. This eluate fraction stimulated DNA synthesis in quiescent Balb/c3T3, RIE, and NRK-52E cell lines, all of which are responsive to the epidermal growth factor family of mitogenic proteins. The EGF receptor of A431 cells was also tyrosine phosphorylated by this eluate peak. Furthermore, immunoblotting with a polyclonal antibody against rat HB-EGF indicated that the eluate peak contained immunoreactive proteins of 22 and 29 kD mol wt, consistent with the reported sizes of the secreted form and membrane anchored form of HB-EGF, respectively. Immunohistochemical studies revealed that HB-EGF was produced predominantly in distal tubules in kidneys injured either by ischemia/reperfusion or aminoglycoside administration. We also found that during metanephric development immunoreactive HB-EGF was detected in the ureteric bud as early as E14.5 and persisted in structures arising from the ureteric bud throughout embryogenesis. These results suggest that in response to acute injury, HB-EGF is produced predominantly in distal tubules and that endogenous HB-EGF may be an important growth factor involved in renal epithelial cell repair, proliferation, and regeneration in the early stages of recovery after acute renal injury, as well as in nephrogenesis.
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PMID:Production of heparin binding epidermal growth factor-like growth factor in the early phase of regeneration after acute renal injury. Isolation and localization of bioactive molecules. 915 85

A 54-year-old man with a left ventricular free wall rupture following acute anterior myocardial infarction underwent a repair surgery with percutaneous cardiopulmonary support (PCPS). During surgery and postoperatively, PCPS provided sufficient support flow. The patient was successfully weaned from PCPS on the 15th postoperative day and discharged subsequently. In the management of cardiac rupture patients, PCPS has the merit of preventing rupture progression and the advantage of recovery of pulmonary function. However, there are several problems to solve. The support effectiveness and recovery of the patient's heart should be carefully evaluated. Effective left heart decompression also needs to be established. Heparin-coated circuits still need proper anticoagulation treatment to prevent thrombus formation especially while support flow is low. A circuit construction that allows easier maintenance and safer exchange of oxygenators and pump heads is suggested. Ischemia of the cannulated leg should be prevented by femoral artery perfusion.
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PMID:Various problems during long-term percutaneous cardiopulmonary support. 921 55

Heparin has potential use as an antiinflammatory treatment in many lung diseases but its therapeutic use is limited by inherent anticoagulant activity. The anticoagulant nature of heparin can be eliminated by a number of chemical treatments, but often not without loss of other important pharmacological activities. Lyophilization of porcine mucosal heparin under extreme alkaline conditions (pH > or = 13) produces a nonanticoagulant heparin remarkable for the selective loss of only 2-O and 3-O sulfates, leaving 6-O and N-sulfates intact. In contrast to the commonly used nonanticoagulant analog N-desulfated, N-reacetylated heparin, selectively O-desulfated heparin retains potent activity as an inhibitor of the cationic neutrophil proteases human leukocyte elastase and cathepsin G, both in vitro and in vivo. Selectively O-desulfated heparin also inhibits complement lysis of erythrocytes, prevents ischemia-reperfusion injury of the lung, remains a potent antiproliferative treatment for cultured airway smooth muscle and normalizes altered neuronal M2 muscarinic receptor sensitivity and bronchial hyperreactivity after antigen challenge. These retained pharmacologic properties suggest possible use of this new nonanticoagulant heparin for the treatment of a variety of lung disorders.
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PMID:Selective O-desulfation produces nonanticoagulant heparin that retains pharmacological activity in the lung. 922 56

Thrombotic occlusion is responsible for most acute manifestations of coronary artery disease, including unstable angina and non-Q-wave myocardial infarction. Antiplatelet therapy plays a major role in reducing the risk of ischemic events in such patients. Since thrombin generation is vital to the pathogenesis of thrombosis, recent studies have focused on thrombin inhibition in the management of acute ischemia. Heparin is the most widely used anticoagulant for acute management of thrombosis and is the treatment of choice in preventing and treating venous thromboembolism. Given in therapeutic doses intravenously, it is more effective than aspirin in reducing the risk of death or myocardial infarction in patients with unstable angina. Low-molecular-weight (LMW) heparins have improved pharmacologic and pharmacokinetic properties over standard heparin that may result in greater efficacy and safety. LMW heparins may be given in a fixed dose subcutaneously without monitoring, resulting in greater clinical utility and cost-effectiveness compared with standard heparin. Given subcutaneously in fixed, weight-adjusted doses they are more effective and safer than intravenous heparin in treating deep-vein thrombosis. Several studies have evaluated LMW heparins in unstable angina. In a small open trial, LMW heparin (nadroparin) reduced the risk of acute myocardial infarction compared with aspirin alone or a combination of aspirin and standard heparin. In 2 large clinical trials, LMW heparin (dalteparin) has been shown to be effective in the management of unstable angina with a 63% reduction in risk of death or acute myocardial infarction over patients treated with aspirin alone (Fragmin during Instability in Coronary Artery Disease; FRISC) and to be as effective as intravenous heparin (Fragmin in Unstable Coronary Artery Disease; FRIC).
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PMID:New frontiers in the management of unstable coronary artery disease. 929 65

Heparin is a highly sulfated polysaccharide consisting of a repeating disaccharide structure as found in other glycosaminoglycanes. The intravenous and subcutaneous formulation of the drug is routinely used for its well-known, time-honored antithrombotic effect. However, available evidences linking heparin to angiogenesis raise the possibility of a therapeutically relevant antiischemic effect of the drug. Molecular biology data show that in a hypoxic milieu heparin could facilitate angiogenesis through interactions with a family of polypeptide growth factor mitogens that stimulate endothelial cell proliferation. Experimental data suggest that heparin can augment collateral circulation when combined with other potentially angiogenetic factors, such as repeated ischemia, coronary occlusion, or physical exercise. Clinical data, although very initial, encompassing a total of only 41 heparin-treated patients with coronary artery disease, suggest that heparin facilitates collateral development stimulated by exercise-induced myocardial ischemia in humans. According to the heparin-collateral hypothesis, the mechanism of action of heparin as an antiischemic medication would be independent of its anticoagulant action. The molecular targets of heparin are Factor Xa and IIa for antithrombotic action, heparin-binding growth factors (including fibroblast growth factor and vascular endothelial growth factor) for angiogenesis. The antithrombotic effect is not linked to a cellular target, whereas the angiogenetic effect directly stimulates endothelial cells. The molecular cofactor required for effect is antithrombin III for antithrombosis, and possibly endogenous adenosine for angiogenesis. The therapeutic effect is achieved within minutes or hours for antithrombosis, and within weeks or months for angiogenesis.
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PMID:The coronary angiogenetic effect of heparin: experimental basis and clinical evidence. 937 49

Carotid artery dissection is a major cause of cerebral infarction in the young. The extracranial portion of the internal carotid artery is much more frequently involved than the intracranial portion. In up to 20% of cases it is bilateral or associated with vertebral artery dissection. It is mainly characterised by local signs such as headache or facial pain, Horner's syndrome, lower cranial nerve palsies and pulsatile tinnitus, followed a few hours or days later by signs of cerebral or retinal ischemia. Ultrasound investigations show signs of distal stenosis or occlusion, highly suggestive of dissection, but the best diagnostic tool is presently the association of magnetic resonance imaging (MRI) and MR angiography which tend to replace intra-arterial angiography. The prognosis is highly variable: excellent in cases limited to local signs, but very poor leading to death or major sequelae in about 15% of cases. Various treatments have been suggested but no controlled trial has ever been performed in this condition. Heparin in the acute stage followed by warfarin or aspirin for 3 to 6 months is most commonly used.
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PMID:Internal carotid artery dissection: an update. 951 74


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