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)

The thrombolytic and hemodynamic properties of intracoronary streptokinase (SK) application were studied in an in-vivo canine model with left circumflex coronary artery thrombosis, initiated by electrical stimulation (150 microA, DC for 6 h) of the artery's intima via an implanted silver wire. In pentobarbital-anesthetized, open-chest dogs acute myocardial ischemia was determined by a dehydrogenase-dependent staining of the coronary artery perfusion area. Thrombus weight was determined post-mortem. Saline-treated control animals developed coronary thrombosis after 3.1 +/- 0.4 h of stimulation. Thrombus weight was 64 +/- 3.1 mg. Acute infarct volume was 32 +/- 3.1% of total left ventricle, and 53 +/- 6.2% of the coronary artery risk region for infarction. At occlusive thrombosis, blood pressure, ventricular pressure and the LV dP/dtmax fell significantly, whereas heart rate and the end-diastolic filling pressure increased. Severe ST-segment elevation and loss of R wave voltage indicated myocardial ischemia. At 20 min into thrombotic vessel occlusion, 2,000 IU/min SK were infused by way of a Sones-catheter advanced to the thrombus. Coronary thrombosis consistently lysed after 12 +/- 0.7 min of SK infusion, and coronary blood flow as well as hemodynamics were restored. Only minor acute infarction was found indicating viability of ischemic jeopardized myocardium. In another group, the continuous SK-infusion (20 IU/kg/min) concomitant with electrical vessel stimulation prevented coronary thrombosis and acute ischemia, and no significant hemodynamic alterations were noted. These results indicate that intracoronary SK-infusion can lyse acute thrombosis as sequel of electrical stimulation. This prevents development of acute myocardial infarction. Continuous SK-infusion can completely prevent coronary thrombosis in response to intimal injury.
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PMID:Thrombolytic effects of intracoronary streptokinase on canine coronary artery thrombosis. 673 17

Thrombotic occlusion of the abdominal aorta secondary to umbilical artery cannulation in two critically ill neonates with severe ischemia is presented. Emergency surgical treatment by abdominal aortotomy and thrombectomy resulted in survival of both patients. Details of the operative technique are reviewed. Etiologic factors predisposing to this disastrous complication are discussed. Recommendations for prevention and a logical approach to diagnosis and management are outlined.
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PMID:Neonatal aortic thrombosis: complication of umbilical artery cannulation. 683 45

A total of 231 patients with atheromatous ulcerations of the carotid artery and obstructions due to critically stenotic plaques or kinks underwent reconstructive surgery mainly of the internal carotid artery, under general anesthesia, normocarbia, and without increasing the systemic blood pressure. Continuous electroencephalography and phot pulses from the cutaneous territories of the internal and the external carotid arteries were used to monitor 250 carotid operations. An intraoperative test, clamping of the common carotid artery and its two branches for 3 min, was performed on each patient. An internal shunt was routinely used in 18 patients. In the remaining 232 operations, an internal shunt was selectively used in only 13 of the 15 patients in whom there was focal showing on the EEG and/or a reduction in the amplitude of the ipsilateral supraorbital pulses to less than 25% of their preclamping values. In the group in which no shunt was used, the duration of the carotid clamping varied from 6 to 59 min, with a mean of 26 min. Seven patients died, but death was related to brain ischemia during surgery in only two. There were no ischemic neurological complications, except in the patients who died. This results in a mortality and morbidity rate of 0.8%. In those patients in whom a shunt was used, CCPPG recordings clearly indicated obstruction of the shunt during surgery. Thrombotic occlusions of the distal end of the shunt in one case and of the repaired vessel in another two were diagnosed. Electroencephalographic and CCPPG monitoring provided useful information of the state of cerebral function, the level of anesthesia, and the occurrence of cardiac dysrhythmia or hypotension and its effect on brain circulation. It is believed that this monitoring technique greatly contributed to the decreased mortality and morbidity in our series.
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PMID:EEG and carotid cutaneous plethysmographic monitoring during carotid reconstructive surgery. 730 8

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1/2 hours, disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK therapy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual coronary thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.
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PMID:Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase. 731 18

Volvulus of the ascending colon (ACV) in the horse results in microvascular injury and necrosis of the intestinal mucosa. This study investigated the site and type of microvascular injury which occurs within the mucosa and submucosa following ACV. Histopathology of volvulus treated ponies demonstrated mucosal necrosis with microvascular hemorrhage and thrombosis. Thrombi occurred within the subepithelial capillaries and edema and hemorrhage developed throughout the mucosa and submucosa. Vascular casts allowed 3-D viewing of samples obtained from the entire pelvic flexure and demonstrated two distinct microvascular changes: 1) disruption of the colonic glandular capillary network occurred concomitantly with the mucosal injury, and 2) extensive endothelial leakage from the submucosal microvasculature contributes to edema formation. Thus, microcorrosion casting of the equine pelvic flexure provided an effective means to characterize the location and severity of vascular leakage and visualize the extent and severity of injury to the capillary network not easily depicted by histopathology. Microvascular casting in conjunction with routine histopathology provided additional information on the pathomorphologic changes in this model of ischemia/reperfusion injury.
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PMID:Ischemia/reperfusion injury of the ascending colon in ponies: a correlative study utilizing microvascular histopathology and corrosion casting. 802 96

Thrombotic coronary artery occlusion dominates pathophysiology of coronary artery disease. Thrombolysis, therefore, is the decisive approach for the treatment of coronary artery obstruction. Development and size of myocardial infarction as a consequence of coronary occlusion, however, is also dependent on certain myocardial factors, among which the size of the myocardial area supplied by the occluded vessel duration of coronary occlusion myocardial oxygen consumption the extent of collateral blood flow ischemic tolerance and ischemic preconditioning are the most important. In unfavorable circumstances, the duration of ischemia is the dominating factor. Therefore, the highest priority must be given to initiate treatment as early as possible.
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PMID:[Vascular occlusion and myocardial infarct]. 832 86

We developed a fibrin-rich thrombotic focal cerebral ischemic model with reproducible and predictable infarct volume in rats. In male Wistar rats (n = 77), a thrombus was induced at the origin of the middle cerebral artery (MCA) by injection of thrombin via an intraluminal catheter placed in the intracranial segment of the internal carotid artery (ICA). Thrombus induction and consequent ischemic cell damage were examined by histopathological analysis and neurological deficit scoring, and by measuring changes in cerebral blood flow (CBF) using laser-Doppler flowmetery (LDF), perfusion-weighted imaging (PWI), and by diffusion weighted imaging (DWI). Histopathology revealed that a fibrin-rich thrombus localized to the origin of the right MCA. Regional cerebral blood flow (rCBF) in the right parietal cortex was reduced by 34-58% of preinjection levels after injection of thrombin in rats administered 30 U of thrombin (n = 10). Magnetic resonance imaging (MRI) showed a reduction in CBF and a hyperintensity DWI encompassing the territory supplied by the right MCA. The infarct volume in rats administered 80 U of thrombin was 31.29 +/- 12.9% of the contralateral hemisphere at 24 h (n = 13), and 34.7 +/- 16.4% of the contralateral hemisphere at 168 h (n = 6). Rats administered 30 U of thrombin exhibited a hemispheric infarct volume of 34.0 +/- 14.5% (n = 9) at 24 h and 29.7 +/- 13.9% (n = 8) at 168 h. In addition, thrombotic rats (n = 3) treated with recombinant tissue plasminogen activator (rt-PA) (10 mg/kg) 2 h after thrombosis showed that CBF rapidly returned towards preischemic values as measured by PWI. This model of thrombotic ischemia is relevant to thromboembolic stroke in humans and may be useful in documenting the safety and efficacy of thrombolytic intervention as well as for investigating therapies complementary to antithrombotic therapy.
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PMID:A new rat model of thrombotic focal cerebral ischemia. 904 Apr 91

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

A 58-year old lady, involved in a head-on motor vehicle crash suffered a severe intestinal injury associated with an intimal flap lesion of the distal abdominal aorta. Thrombotic occlusion of the aortic bifurcation with clinical evidence of lower extremity ischemia was noted. The management of blunt injury to the abdominal aorta is discussed with special regard to placing prosthetic material in a potentially infected field.
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PMID:[Blunt abdominal trauma with lesion of the abdominal aorta--a case report]. 934 Jan 35

We undertook a prospective evaluation to prove a new mechanical thrombectomy device, the shredding embolectomy thrombectomy catheter (S.E.T. catheter), for the treatment of patients with acute lower-limb ischemia. The study evaluated the success, patency, mortality, limb salvage, and complication rates for 51 patients treated from January 1994 through June 1996, with this device, which was an 8-F three-lumen catheter. The onset of symptoms was 8.6 +/- 9 days. Thrombus length was 18 +/- 9 cm situated in 44 native vessels and in 7 bypasses, 42 limbs were graded as threatened. Hydromechanical thrombectomy with the S.E.T. catheter proved to be a quick and safe adjunct for therapy of acute femoropopliteal thromboembolic occlusions with a high initial success rate and an acceptable mid-term patency rate.
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PMID:Shredding embolectomy thrombectomy catheter for treatment of acute lower-limb ischemia. 1039 40


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