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)

Thrombotic complications of heparin administration were observed in eight patients during a two year period. At sites of subcutaneous heparin injection, six patients developed areas of the skin and subcutaneous necrosis. Systemic thrombotic events and thrombocytopenia were observed in two of these patients when they received intravenous heparin and in two other patients who did not have primary skin necrosis. The complications included peripheral ischemia in three patients (two requiring amputation), myocardial infarction in two, and a cerebral infarction in one. All patients were receiving heparin for at least six days before complications occurred. Seven patients received heparin of bovine origin. Heparin-induced in vitro platelet aggregation was present in all six of the eight patients tested. (It was marked in four of these patients). It is theorized that skin necrosis and the other thrombotic complications observed are the result of heparin-induced in vivo platelet aggregation followed by intravascular thrombosis. Heparin-induced skin necrosis is a rare but serious hazard encountered with prophylactic heparin regimens. If heparin-induced thrombosis is present, the further use of heparin is contraindicated in most instances.
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PMID:Thrombotic complications of heparin therapy: including six cases of heparin--induced skin necrosis. 50 70

One unit (500 ml) of 10% Intralipid (an intravenous soy bean oil-egg yolk lecithin preparation) was infused into 20 normal subjects over 4 hr. Serum triglyceride concentration and plasma optic density (at 700 nm) increased to maximal levels of 339 +/- 102 mg/100 ml and 1.14 +/- 0.41, respectively, at the completion of the infusion, and returned to basal levels in most subjects within 4 hr. Pulmonary membrane diffusion was decreased in six subjects at rest and with exercise at 25 and 50% maximum oxygen uptake. Only one subject showed a minor change in PO2 and none showed clinical signs of ischemia. The changes in pulmonary diffusion reverted to basal levels when serum lipids were cleared. Heparin (60 IU/kg) prevented the marked increase in serum lipids and, as a consequence, the changes in pulmonary function. Changes in pulmonary function from Intralipid-induced lipemia are similar to those known to result from diet-induced lipemia. The findings suggest that in the presence of normal vasculature and pulmonary function, Intralipid-induced lipemia should cause no clinical consequences. However, patients with preexisting pulmonary or vascular disease may be at greater risk after Intralipid-induced lipemia.
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PMID:Relationship between Intralipid-induced hyperlipemia and pulmonary function. 81 3

Since ischemic anoxia in experimental animals has been reported to produce areas of cerebral postocclusive nonperfusion, the authors studied the effect of heparin on recovery from tourniquet-produced cerebrovascular injury in 41 barbiturate-anesthetized, ventilated cats (PaCO2 30 +/- 2.5 torr). Twenty-four control animals were subjected to 2-to-12-minute ischemic injuries without further treatment. Seven experimental animals were given heparin (1000 u/kg) 1 minute before 4-to-7-minute ischemic injuries, while 10 animals received heparin (1000 u/kg) immediately after 4-to-7-minute injuries. All animals were monitored with continuous arterial and intracranial pressure (ICP) recordings, EEG, and evoked cortical responses. Ischemia and evoked-response recovery times were linearly related in all groups (r = 0.998 control, r = 0.936 heparin preinjury, r = 0.951 heparin postinjury). Regression-line slope comparison indicated shorter evoked response and EEG recovery times in the heparin-treated groups than in the control group. Heparin administration did not effect elevations of ICP seen 6 and 12 hours postinjury in control versus experimental groups. In cats with injuries lasting 5 minutes or more, all control animals were decerebrate and apneic, while 5/12 heparin-treated animals had lesser neurologic deficits.
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PMID:The effects of heparin on recovery from ischemic brain injuries in cats. 98 24

Arterial emboli were extracted from 79 patients between 1955 and 1963 with polyethylene catheter suction systems and/or retrograde flushing and from 149 patients between 1963 and 1973 with Fogarty catheters. The Fogarty-era patients were older, had a greater incidence of ischemic heart disease, and presented with a greater degree of preoperative peripheral ischemia. The limb salvage rate of 87 percent after Fogarty catheter embolectomy was not statistically different from the salvage rate of 79 percent after suction catheter embolectomy, but the number of limbs with distal pulses postoperatively was significantly greater after Fogarty treatment, 64 vs. 42 percent. Delay in treatment and the presence of prior occlusive vascular disease adversely affected results in both eras. The in-hospital embolic recurrences occurred in 9 percent of the patients anticoagulated postoperatively and in 31 percent of those not anticoagulated. Heparin and warfarin were equally effective in preventing recurrences, but wound complications were seen in 33 percent of the heparinized patients, compared with 7 percent of those receiving warfarin and 4 percent of those not anticoagulated.
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PMID:Arterial embolectomy before and after the Fogarty catheter. 110 16

The use of a flexible polyvinyl tube bonded with tridodecylmethylammonium-heparin (Gott) as a temporary shunt during the resection of lesions of the descending thoracic aorta has proven a safe and simple means of providing adequate circulation to the abdominal viscera and spinal cord. This technique avoids the metabolic consequences of ischemia to the lower body, diminishes left ventricular afterload during aortic clamping, and obviates the requirement for systemic anticoagulation associated with pump bypass. Between September 1970 and October 1974, 24 patients have been operated using the TDMAC shunt. There were two deaths (9%) among the 22 patients undergoing elective resections. Two patients with acutely dissecting and ruptured aneurysms expired. Followup data has been obtained on all patients from one to 46 months postoperative. The ease with which the shunt is inserted and its adaptability to varied clinical and anatomic situations is stressed. We feel that TDMAC-Heparin shunt provides the best method of circulatory support for elective operative procedures on the descending thoracic aorta.
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PMID:The use of the TDMAC-heparin shunt in replacement of the descending thoracic aorta. 113 Aug 87

The authors present a series of 64 patients with arterial embolism in healthy arteries. 53 of these patients underwent one or several embolectomies, using a Fogarty catheter. Although arterial embolism has a poor prognosis owing to the constitutional background (15 p. 100 mortality and 12 p. 100 amputations), this is mainly due to the age of the patient. The severity of the initial attack and the delay between embolism and embolectomy seem to be the main factors in prognosis. Massive ischemia causes severe symptoms in these fragile patients and an early cure is necessary to compensate this disturbance. Heparin perfusion, whilst awaiting surgical treatment, is essential. Embolectomy by Fogarty's catheter may be carried out under local anesthesia; this remains the essential measure and has greatly improved the prognosis of this disease which used to be fatal in almost 60 p. 100 of cases, even in healthy arteries.
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PMID:[Embolism in healthy arteries]. 119 87

The functional significance of coronary collaterals in humans has been debated for many years. Correlations have now been made between the anatomic appearance of coronary collateral vessels visualized at the time of intracoronary thrombolytic therapy during the acute phase of myocardial infarction and the creatine kinase time--activity curve, infarct size, and aneurysm formation. These studies demonstrate a protective role of collaterals in hearts with coronary obstructive disease, showing smaller infarcts, less aneurysm formation, and improved ventricular function compared with patients in whom collaterals were not visualized. There is ample evidence that collaterals respond to myocardial ischemia by opening preexistent channels. When the cardiac myocyte is rendered ischemic, collaterals develop actively by growth with DNA replication and mitosis of endothelial and smooth muscle cells. Heparin-binding growth factors are present in the heart, but their biological activity is quiescent under normal physiological conditions. Once ischemia develops, these factors are activated and become available for receptor occupation, which may initiate angiogenesis after exposure to exogenous heparin. This characteristic of heparin to potentiate the mitogenic activity of acidic fibroblast growth factor has recently been used in the clinical setting as a possible therapeutic modality in patients with coronary artery disease. Patients performing 20 rounds of exercise serially after receiving intravenous injection of heparin showed significantly greater increases in exercise capacity and improvement of clinical symptoms compared with the control group who performed the same exercise without heparin. Further study of neovascularization may lead to a new therapeutic strategy for ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recent insights into coronary collateral circulation. 137 32

The efficacy of recombinant human extracellular-superoxide dismutase type C (EC-SOD C) on myocardial reperfusion injury was explored in hypothermically arrested rat hearts, as was its site of action. Forty isolated working rat hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The hearts were arrested by the administration of 10 mL of cold perfusate at the onset of ischemia. At the same time, they were randomly assigned to one of five groups; A: cold perfusate only; B: cold perfusate + EC-SOD C 10.4 mg/L (30,000 U/L); C: cold perfusate+bovine CuZn-SOD 7.5 mg/L (30,000 U/L); D: cold perfusate + EC-SOD C 10.4 mg/L + heparin 50,000U/L; E: cold perfusate + heparin 50,000 U/L. Heparin was given to prevent binding of EC-SOD C to endothelial cell surfaces. Left ventricular function was studied before ischemia and at the end of reperfusion. Percent recovery of maximal left ventricular dP/dt after reperfusion was more pronounced in group B (109 +/- 24%; p less than .05) than in groups A (42 +/- 40%), C (47 +/- 36%), D (44 +/- 33%) and E (58 +/- 25%). Likewise, percent recovery of the double product (heart rate x systolic left ventricular pressure) was better in group B (104 +/- 18%; p less than .05) than in the other groups (A: 47 +/- 37%, C: 49 +/- 36%, D: 50 +/- 35%, E: 69 +/- 31%). Compared to the preischemic level, creatine kinase increased significantly in the coronary effluent after reperfusion in groups A, C, D, and E, but not in group B. The results suggest that EC-SOD C, which attaches to the endothelial cell surfaces, might be particularly effective as protection against myocardial reperfusion injury when given together with cardioplegic solution.
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PMID:Effects of recombinant human extracellular-superoxide dismutase type C on myocardial reperfusion injury in isolated cold-arrested rat hearts. 151 40

The study of 44 patients treated with intra-arterial fibrinolysis is reported. All these patients had an impending subacute ischemia of the lower limbs, a major complication of atheromatous disease. The criteria for patient selection were clinical, hemodynamic and radiological. The procedure of the treatment associating Urokinase, Heparin and Naphthidrofluril are defined, as well as its follow-up. The results have been evaluated according to the clinical and radiological improvement. 2 patients died when the treatment ceased and 10 were amputated, ie 27% of failures. The fibrinolytic treatment allowed identifying the patients who might quickly receive an additional treatment. In our experience, this treatment seems to improve the prognosis of impending subacute ischemia.
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PMID:[Efficacy of intra-arterial fibrinolysis in subacute atheromatous ischemia of the lower limbs]. 205 82

The purpose of this study is to evaluate the effect of PGI2 analogue on the warm ischemic injury in the reimplantation model of the lung. Twenty-five mongrel dogs were subjected to this experiment in which the left thoracotomy and complete left hilar stripping were performed. The dogs were divided into 4 groups. The control group (8 dogs) did not have any medical treatment. I2 1 microgram group (7 dogs) received PGI2 analogue in the amount of 1 microgram/kg/min for 30 min during hilar dissection. I2 50 ng group (5 dogs) received PGI2 analogue in the amount of 50 ng/kg/min for 30 minutes. Heparin group (5 dogs) received 100 U/kg of heparin after hilar stripping. Then left, PA, PV, and Bronchus were clamped for 1 hour to make the left lung a warm ischemic state. To evaluate the function of the left lung subjected for a warm ischemia, right pulmonary artery was occluded for 10 minutes and PaO2, PaCO2, Qs/Qt, pulmonary artery pressure, pulmonary vascular resistance, thromboxane B2, and 6-keto-PGF1 alpha were measured. Two hours after reperfusion, pulmonary microangiography and histological investigation were performed. As a result of warm ischemia, PaO2 was 158 mmHg with 70% FiO2 1 hour after reperfusion in control group, whereas it was maintained at as high as 299 mmHg in I2 1 microgram group. PaCO2, Qs/Qt, pulmonary artery pressure, as well as the pulmonary vascular resistance were almost normal throughout the experiment in I2 1 microgram group, but they gradually elevated in control group during the experiments. In the other two groups these parameter are not so satisfactory as in I2 1 microgram group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of PGI2 analogue on the warm ischemic changes in canine lung]. 210 82


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