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)

Surgical treatment of varicose veins occasionally can be followed by severe limb ischemia either after surgery or sclerotherapy. We report here two cases with the clinical features and the therapeutic strategy. The first case concerned a woman operated by venous stripping. A post-operative acute ischemia occurred and was treated by femoro-femoral bypass and lumbar sympathectomy. However this procedure did not avoid persistent chronic ischemia, sciatica paralysis and equinus ankle blockage. A secondary arterial procedure associated with intensive physiotherapy and ankle arthrodesis led to a poor functional result, partly because of an irreversible algodystrophia. The second case concerned a woman treated by sclerotherapy. An injection of the drug in the retro-malleolar area was immediately followed by an acute foot ischemia. Heparin, xylocaine and sodium nitroprusside perfusion avoided a foot amputation, however osteoporosis and algodystrophia occurred. A sympathectomy was necessary two years later. These dramatic complications although unusual, may occur even with experienced physicians. Therefore a great attention is always necessary during these simple procedures. In case of acute ischemia, early diagnosis and aggressive treatment are necessary, but prevention remains more secure.
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PMID:[Arterial complications following surgery or sclerotherapy of varices]. 394 17

It is not unusual to find ischemia of limbs in drug addicts and two new cases are reported, together with a literature review, allowing analysis of physiopathologic mechanisms and therapeutic modalities. The first case was a 20 year old man who presented with sensory-motor ischemia of the right hand after injection of heroin into the radial artery. Arteriography showed partial occlusion of the deep palmar arch and all collateral arteries of fingers. Regression of ischemia followed administration of thrombolytics, heparin and vasodilators, arteriography showing restoration of palmar arch and digital arteries flow apart from that of the 4th finger. The latter developed distal necrosis which required, in spite of thoracic sympathectomy, amputation of the 3rd phalanx. Histology of amputation piece showed presence of intra-arterial foreign bodies. The second case was a 30 year old man who presented with an acute sensory-motor ischemia of left calf and foot after injection of heroin into the retromalleolar groove. Arteriography showed absence of opacification of vascular axes in the middle third of leg and an atheromatous plaque in left main iliac artery. Heparin therapy plus lumbar sympathectomy resulted in reheating of the foot, but ischemia recurred one month later. A repeat arteriography with oblique images demonstrated that the plaque in the main iliac artery was larger than it appeared in frontal images and that an embolus had developed in the deep femoral artery. Final treatment in this patient involved an inter-femoral saphenous vein bypass and amputation of 4th toe. Histology of amputation piece showed only a banal arterial thrombosis without foreign body.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute ischemia of the extremities and drug addiction]. 394 20

Bovine testicular hyaluronidase (BTH) reduces experimental myocardial infarct size and ameliorates electrocardiographic signs of ischemia. This study was done to determine if heparin, an in vitro inhibitor of hyaluronidase activity, blocks the action of BTH in the myocardium of dogs after coronary artery occlusion. BTH was administered intravenously as 5,000 NF units/kg at 0.5 and 2.5 hours after coronary occlusion. Heparin was administered intravenously as a 150-unit/kg loading dose, followed by 10 units/kg per hour i.v., beginning 15 minutes before coronary occlusion. The area of myocardial ischemia at risk was assessed by a radiolabeled microsphere technique; the area that developed necrosis was assessed by a histochemical technique. In vivo activity of BTH was assessed by a colorimetric analysis of the BTH substrate, i.e., hyaluronic acid (HA), extracted from myocardial tissue. For biochemical analysis of HA, the heart was divided into anterior myocardium, which included ischemic tissue and posterior nonischemic myocardium. The myocardial HA content of dogs treated with BTH plus heparin (anterior, 3.44 +/- 0.40 micrograms HA/mg protein; posterior, 3.69 +/- 0.33 micrograms HA/mg protein) was not significantly different from control (anterior, 3.61 +/- 0.29 micrograms HA/mg protein; posterior, 3.55 +/- 0.23 micrograms HA/mg protein). In contrast, BTH lowered myocardial HA content (anterior, 2.16 +/- 0.21 micrograms HA/mg protein; posterior, 2.08 +/- 0.14 micrograms HA/mg protein) compared with either BTH plus heparin or control groups in both anterior myocardium (p = 0.006) and posterior myocardium (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin inhibits bovine testicular hyaluronidase activity in myocardium of dogs with coronary artery occlusion. 670 49

The no-reflow phenomenon is a dreaded complication in free tissue transplantations. After a critical period of warm ischemia, insufficient reflow is observed after vessel anastomosis and opening of the artery. In an experimental study in 72 rats, groin flaps were harvested with the nutrient superficial epigastric vessels and transplanted to the neck using a microvascular technique with anastomoses to the carotid artery and jugular vein. Before transplantation, the isolated flaps were perfused either with saline solution, with Iloprost, with and without heparin, or the nutrient vessels were simply flushed with heparin solution. After saline perfusion, there was no venous reflow, after pure Iloprost perfusion, there was venous return in 26% of the flaps, after Heparin-Iloprost perfusion in 88% and after flushing with heparin alone in 93%. The addition of heparin to Iloprost seems to improve the reflow rate. The most effective protection against a no-reflow phenomenon, however, is flushing the nutrient vessels with a heparin solution.
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PMID:[Experimental studies of the no-reflow phenomenon with prostacyclin]. 750 60

Percutaneous cardiopulmonary support (PCPS) was used in 5 patients (4 males and 1 female); 70.2 +/- 10.8 years old) who underwent open heart surgery and failed to wean from the extracorporeal circuit because of profound heart failure unresponsive to maximal doses of catecholamines and intra-aortic balloon pump support. Duration of PCPS was 6975 +/- 5516 min, and the average flow was 1.51 +/- 0.26 l/min/m2. Heparin-coated circuit including the oxygenator was used to minimize the necessary dose of heparin, and activated clotting time (Celite ACT) was maintained between the range of 130 and 200 seconds. Despite this low-dose heparinization, mediastinal hematoma formation and subsequent cardiac tamponade occurred in 4 patients. Weaning from PCPS was successful in 3 patients for whom reexploration to remove hematoma was performed, and 2 of these 3 achieved long-term survival. During the use of PCPS, ipsilateral femoral artery, through which part of the pump flow was actively perfused. Owing to this maneuvering, limb ischemia did not occur in any case. From these findings, we could conclude that reexploration for mediastinal hematoma should be performed in weaning from PCPS for postoperative patients, even when low-dose heparinization was employed, and that active perfusion through the 18g catheter downstream to the ipsilateral lower limb is effective in preventing limb ischemia during relatively long time PCPS.
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PMID:[Relatively long time use of percutaneous cardiopulmonary support after unsuccessful weaning from intra-operative extracorporeal circulation--clinical considerations from an experience of 5 patients]. 759 40

Vasospastic reactions are known to be a complication of thromboembolic prophylaxis with Heparin-dihydroergotamine. We describe a rare case after successful replantation of an amputated thumb. On the third day after surgery, Heparin-dihydroergotamine was administered once. Within three hours, the thumb turned pale and cold. At revision, a spasm of the artery proved to be the cause of ischemia. Therapeutic efforts were unsuccessful, even intraarterial injection of Prostaglandin E1 and the interposition of a vein graft. Amputation became necessary. Because of the possible complication with ergotism and the consequence of a failed replantation, we suggest not to use Heparin-dihydroergotamine for thromboembolic prophylaxis in microsurgery.
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PMID:[Loss of the replanted thumb by drug-induced ergotism]. 762 27

Intracoronary thrombosis is fundamental in the pathogenesis of acute coronary syndromes, although the causes of thrombosis are still unclear. As thrombin generation is crucial for thrombus formation, the inhibition of thrombin is a primary aim to prevent the evolution of an initial repair process into a pathological thrombus. Thrombin inhibition can be achieved by several drugs. Heparin is the principal antithrombin drug currently used in acute syndromes; it acts mainly by binding to antithrombin III and increasing its inhibitory effect on thrombin and other coagulation factors. The heparin-antithrombin III complex, however, does not inhibit thrombus-bound thrombin; moreover, iv heparin requires frequent laboratory monitoring and dose adjustments. Despite these limitations, continuous infusion of i.v. heparin has been found to be effective in unstable angina and in myocardial infarction, especially when treated with accelerated rt-PA. New antithrombin drugs that selectively and directly inhibit thrombin are hirudin, its synthetic derivate hirulog, and argatroban. These drugs have several theoretical advantages over heparin: greater stability of the aPTT--with the need for less laboratory monitoring--and greater efficacy--associated mainly with its capacity to inhibit clot-bound thrombin. Clinical pilot studies seem to indicate a greater antithrombotic efficacy compared with heparin, but a greater number of hemorrhagic events in patients with acute myocardial infarction receiving thrombolysis. In conclusion, the use of heparin is certainly indicated in patients with unstable angina and persistent ischemia and in acute myocardial infarction treated with accelerated rt-PA. The use of new antithrombin drugs, although promising, requires further clinical evaluation.
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PMID:[Antithrombin therapy in acute coronary syndromes]. 763 17

Adjunctive therapy for acute myocardial infarction should include aspirin, beta-adrenergic blocking agents, and, in most patients, consideration of the use of angiotensin-converting enzyme inhibitors, especially if left ventricular function is reduced. Heparin has an important adjunctive role in enhancing early vessel patency in patients who receive tissue-type plasminogen activator and in decreasing the frequency of reocclusion of an infarct-related artery during any thrombolytic therapy. Heparin must also be administered to all patients who undergo primary angioplasty. Intravenously administered nitroglycerin and orally administered nitrates are probably most effective in patients with symptomatic ischemia. Calcium channel blockers and prophylactic antiarrhythmic agents are not indicated for most patients with acute myocardial infarction. Currently, insufficient evidence is available to recommend the widespread use of intravenously administered magnesium sulfate in the setting of acute myocardial infarction. In patients with ischemic pain, judicious intravenous administration of morphine can provide relief. Use of warfarin sodium should be reserved for patients at risk for left ventricular mural thrombus. Although the use of lipid-lowering agents after myocardial infarction has been controversial, recent studies have demonstrated the importance of such therapy for secondary prevention of death and morbidity.
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PMID:Adjunctive therapy in the management of patients with acute myocardial infarction. 773 Dec 56

The effects of low molecular weight heparin derivatives with a low anticoagulant activity on transplant arteriosclerosis (TA) in a rat aortic transplant model were investigated. TA was induced by ischemia in the syngeneic transplants and primarily by immunological mechanisms in the allogeneic transplants. Treatment with the heparin derivatives, OAM 71262 or LA-heparin, was administered in a dosage of 250 micrograms/kg/hr by mini-osmotic pumps during 8 weeks. No immunosuppressive regimen was given to the recipient rats in either model. All rats were killed 8 weeks after aortic grafting. The grafts were examined for intimal and medial changes using an image analysis system. Heparin derivatives had a beneficial effect on both the intimal thickening and the medial injury in the syngeneic transplants, but not in the allogeneic grafts. In the syngeneic LA-heparin treated grafts, the thickness of the intima was less than that in the syngeneic control grafts (P < 0.05). In the syngeneic transplants, a significant increase was observed in the media after treatment with OAM 71262 (P < 0.01) as well as those with LA-heparin (P < 0.001). In the syngeneic grafts treated with both heparin derivatives, a significant reduction in the antigen expression of alpha-actin-containing smooth muscle cells in the intima, transforming growth factor-beta 1 both in the media and adventitia, and platelet-derived growth factor-beta receptors in the adventitia was observed immunohistochemically. In summary, low molecular weight heparin derivatives with low anticoagulant activity partially inhibited ischemia-induced syngeneic TA, whereas no such effect could be demonstrated in nonimmunosuppressed recipients with allogeneic grafts.
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PMID:Inhibition of transplant arteriosclerosis in rat aortic grafts by low molecular weight heparin derivatives. 777 66

Heparin has been found to decrease ischemia/reperfusion injury in skeletal muscle and other tissue/organ systems. The timing of heparin administration to the muscle vasculature has not been explored. We investigated the use of heparinized blood as a washout solution during ischemia to reduce ischemia/reperfusion injury. A rat cutaneous maximus muscle free flap was subjected to a 10-hr period of room temperature ischemia, then was heterotopically transplanted to the groin via microsurgical revascularization to the femoral vessels. In three experimental groups, flaps were subjected to brief ex vivo perfusion with autologous heparinized blood, at 2, 5, or 8 hr into the 10-hr ischemic interval. In the two other groups, the flaps were not perfused, and the animals were systemically heparinized either before ischemia or before transplantation, respectively. A control group underwent no flap perfusion or systemic heparinization. After transplantation, flaps were given a 48-hr period of in vivo reperfusion, then were harvested for evaluation. Flaps undergoing ex vivo perfusion or preischemic heparinization had no significant differences in weight gain (edema) compared with flaps receiving posttransplant heparinization or no heparinization (controls). The dehydrogenase staining of muscle biopsies was significantly faster (indicative of viable tissue) for perfused flaps and the flaps for which the animals received preischemic heparinization, when compared with flaps for which the animals received posttransplant heparinization or no heparinization. From these results, we conclude that heparin offers protection from ischemia/reperfusion injury when it can be introduced into the vascular network either prior to or during the ischemia period. These findings suggest the possibility of using heparinized washout solutions to enhance survival in amputated extremities.
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PMID:Intravascular heparin protects muscle flaps from ischemia/reperfusion injury. 778 11


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