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 purpose of this study was to determine whether normal fibrinogen contributes to the development of myocardial reperfusion injury by acting as a substrate in vivo for neutrophil adhesion. This was tested in a dog model of acute myocardial infarction that used pentobarbital anesthetized dogs subjected to 90 min regional myocardial ischemia and 5 h reperfusion. Dogs were treated with 1 unit/kg Ancrod (venom from the Malayan pit viper, Agkistrodon rhodostoma) or vehicle i.v. 60 min after left circumflex coronary artery occlusion. Therapeutic defibrination was verified in Ancrod-treated dogs by measurements of clottable fibrinogen, alpha-2 antiplasmin and plasminogen, by the activated partial thromboplastin time and by immunoelectrophoresis. Fibrinogen was depleted to below detectable limits of the assay (less than 0.05 mg/ml) after treatment with Ancrod. The defibrination effect was accomplished by the expected activation of the fibrinolytic system: alpha-2 antiplasmin was decreased by 10% and plasminogen activity was decreased by 30% with Ancrod treatment. There were no measureable differences between the two treatment groups in heart rate, mean arterial blood pressure, rate pressure product or circumflex coronary blood flow throughout the 90 min of regional ischemia or during the 5 h of reperfusion. The relative severity of ischemia between the two treatment groups was similar when assessed with radiolabeled microsphere measurement of myocardial blood flow. The accumulation of neutrophils (measured by myeloperoxidase activity) within the myocardium after reperfusion was not reduced by prior depletion of fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic defibrination with ancrod does not protect canine myocardium from reperfusion injury. 170 37

Disposal of heparin is accomplished rapidly by the normal liver, but the effects of ischemia, flushing and hypothermia during hepatic transplantation have not been investigated before. The results of the present study showed that neither laparotomy, hypothermia nor insertion of the portosystemic bypass seemed markedly to affect the coagulation profile, but autograft associated with 30 to 45 minutes of warm ischemia resulted in a twofold prolongation of the t1/2 heparin as calculated from sequential measurements of the activated clotting time. Unexpectedly, the storage of livers for four hours in EuroCollins solutions seemed to result in more rapid disappearance of heparin than in animals after laparotomy. After hepatectomy, the clearance of heparin was delayed for two hours but, thereafter, the slope of the disappearance resembled that in sham operated animals. Autograft and allograft of livers in normal pigs that did not receive transfusion were also associated with changes in fibrinolysis and declining levels of fibrinogen together with severe intraoperative bleeding problems and rapid death on the operating table in 30 per cent of the pigs. While administration of heparin alone did not appear to precipitate these changes, use of the drug after dissection, mobilization and storage of the liver may release other tissue factors that activate fibrinolysis.
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PMID:Heparin as the cause of coagulopathy which may complicate grafting of the liver. 180 3

The thromboxane-receptor antagonist, SQ 30,741, may be used as adjuvant therapy for thrombolysis and has also been shown to have antiischemic activity that is independent of its thrombolytic activity. Since tissue-type plasminogen activator (t-PA) and SQ 30,741 may be administered simultaneously, we determined whether the antiischemic effects of SQ 30,741 can be potentiated by t-PA. This was accomplished by combining doses of t-PA and SQ 30,741, which alone were not cardioprotective. Anesthetized dogs were subjected to left circumflex coronary artery occlusion for 90 minutes and reperfusion for 5 hours. The dogs were treated during reperfusion with a dose of t-PA that caused approximately a 30% reduction in plasma fibrinogen alone or in combination with 1.5 mg/kg + 0.4 mg/kg/hr SQ 30,741, which started 10 minutes after initiation of ischemia. At these doses, neither t-PA nor SQ 30,741 alone significantly reduced infarct size (57% +/- 6%, 50% +/- 10%, 57% +/- 6% of the left ventricular area at risk for vehicle controls, t-PA, and SQ 30,741 respectively); however, combination treatment resulted in a significant reduction in infarct size (37% +/- 5% of the left ventricular area at risk). Higher doses of t-PA and SQ 30,741 alone significantly reduced infarct size. The protective effects of t-PA and SQ 30,741 occurred without altering peripheral hemodynamic status. No differences in collateral or reperfusion blood flow were observed between groups. Thus although SQ 30,741 may act to improve the efficacy of thrombolysis, t-PA may in turn enhance the antiischemic activity of SQ 30,741 or at least reduce the threshold dose.
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PMID:The combined antiischemic effects of the thromboxane receptor antagonist SQ 30,741 and tissue-type plasminogen activator. 182 8

Hypertension is a major contributor to cardiovascular morbidity and mortality, increasing risk threefold. It predisposes to every clinical manifestation of coronary heart disease, now the most common and lethal outcome. It is as relevant a risk factor in the elderly as in the young. Risk is proportional to the degree of blood pressure elevation without a discernible critical value. Cardiovascular sequelae do not derive chiefly from the diastolic component, and isolated systolic hypertension confers increased risk at all ages. Hypertension tends to cluster with other cardiovascular risk factors, which must be taken into account in evaluating the risk and in choosing treatment. The excess cardiovascular risk in hypertension is concentrated in those with an increased total/high density lipoprotein cholesterol ratio, glucose intolerance, cigarette smoking, elevated fibrinogen, and electrocardiogram abnormalities. Left ventricular hypertrophy (LVH) is a common feature of hypertension and an ominous harbinger of cardiovascular sequellae. Electrocardiographic evidence of LVH, when manifested by repolarization abnormalities and voltage elevations, is particularly hazardous, reflecting not only anatomical hypertrophy but also ischemia. Electrocardiogram-LVH adds to cardiovascular risk associated with X ray or echocardiographic evidence of anatomical LVH. Because of a tendency to ventricular ectopy, LVH is associated with increased risk of sudden death. Electrocardiogram-LVH can be corrected or avoided by control of hypertension and weight reduction. The efficacy of correcting LVH remains to be demonstrated but benefits seem likely.
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PMID:Hypertension, hypertrophy, and the occurrence of cardiovascular disease. 183 77

To determine which therapeutic procedure is most appropriate for which type of aortic dissection, we investigated 146 cases of acute aortic dissection. In the group with dissection of the ascending aorta, 58.6% of patients given medical therapy and 48.8% of patients given surgical therapy died. In the group with dissection of the descending aorta, 14.0% given medical therapy and 50.0% given surgical therapy died. High mortality in the medical group with type A dissection was caused by delayed operation. Better survival was achieved in treated than surgically treated patients with acute distal dissection. In patients with cardiac tamponade, aortic regurgitation, hemothorax/hemo-mediastinum, visceral ischemia and peripheral ischemia, mortalities following medical treatment were fairly high. Surgical treatment brought on improvement in mortality in these groups. However, in the cases complicated by renal dysfunction, the mortality in the surgical group was higher than that in the medical group. 42 patients (28.8%) had no evidence of any complication and only 6 (14.3%) died. In 20 cases (47.6%) of uncomplicated dissection, no blood flow was observed in the false lumen. In cases with open false lumen, the following abnormal findings were more conspicuous: thrombocytopenia, decreased level of fibrinogen, increased fibrin degradation product and soluble fibrin monomer complex. However, these changes seem to be minimal in cases with thrombosed false lumen. The measurement of coagulation factors may be one useful method to determine which therapeutic procedure is most suitable.
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PMID:Medical vs surgical treatment of acute aortic dissection in an intensive care unit. 189 14

A femoroperoneal bypass using a cryopreserved human saphenous allograft was performed on a patient who presented with critical ischemia of the left lower extremity. The patient died of myocardial infarction 48 hours later and the graft was examined histologically. There was karryorhexis and focal neutrophilic infiltrate in the media underlying a layer of fibrin on the intimal surface. Immunoperoxidase studies showed nonspecific luminal deposition of immunoglobulins and fibrinogen. The histologic changes that occur in cryopreserved venous allografts are similar in experimental and human material and may be the result of anoxia of the vessel wall rather than immunologic mechanisms.
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PMID:Biologic fate of cryopreserved human saphenous allografts: case report and hypothesis. 193 38

The safety and efficacy of a new regimen of intravenous recombinant tissue-type plasminogen activator (rt-PA) potentially suitable for either pre- or in-hospital administration were assessed in 60 patients with acute myocardial infarction in an open label coronary angiographic study. The regimen consisted of a 20-mg bolus dose followed 30 min later by a delayed infusion of 80 mg over 2 h. This regimen was designed to facilitate prehospital administration of rt-PA. Infarct-related artery patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow) was observed in 40 of 53 patients at 60 min (75.5%, 95% confidence intervals [CI] 61% to 84%) and in 55 of 60 patients at 90 min (91.7%, 95% CI 80% to 95%) after the rt-PA bolus. By 90 min the majority of patients (55%) exhibited TIMI grade 3 flow; infarct artery patency at 120 min was 84.9%. During hospitalization definite recurrent ischemia occurred in nine patients (15%); nonfatal recurrent infarction was noted in one (1.7%). Four patients (6.7%) experienced major bleeding, including one with intracranial bleeding. There were seven deaths (11.7%). Mortality was significantly influenced by the occurrence of cardiogenic shock, which was present in five patients at the time of enrollment. Blood fibrinogen levels were obtained before and during rt-PA infusion. At baseline and 30 and 150 min after the bolus dose, the mean fibrinogen level (+/- SD) was 284.83 +/- 77.39, 237.96 +/- 76.92 and 192.04 +/- 57.82 mg/dl, respectively. Compared with the baseline value, there was a significant (p less than 0.05) decrease in fibrinogen at both 30 and 150 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of a new regimen of intravenous recombinant tissue-type plasminogen activator potentially suitable for either prehospital or in-hospital administration. 196 Mar 29

When conventional treatment of patients with early clinical reinfarction after thrombolytic therapy fails, mechanical revascularization may be attempted. An alternative strategy, repeat thrombolytic infusions, is reported. Fifty-two patients with acute myocardial infarction were treated with one or two additional thrombolytic infusions of recombinant tissue-type plasminogen activator (rt-PA) because of nonsustained ischemia after initial treatment with rt-PA or streptokinase. Thirty-five patients received the second infusion within 1 h of the first; 13 patients received the second infusion 1 to 72 h after the first and 4 patients received it later during their hospitalization. Bleeding complications occurred in 10 patients (19%); however, most of these were minor (no intracranial bleeding) and only 2 patients required blood transfusion. In 14 patients in whom the decrease in fibrinogen and plasminogen levels was measured after the first and second infusions, this decrease was only 25% and 63%, respectively--only slightly higher than the 22% and 53% decreases measured in 63 patients who had only one rt-PA infusion. In 44 patients (85%), the acute ischemia resolved completely within 1 h after initiation of the second infusion. In 23 patients (44%), pain and ST segment elevation did not recur and invasive coronary intervention was avoided. Thus, repeat rt-PA infusions can stabilize a substantial number of patients with acute reinfarction and, even when relief is temporary, repeat rt-PA infusions can minimize myocardial damage while patients await mechanical revascularization.
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PMID:Repeat infusion of recombinant tissue-type plasminogen activator in patients with acute myocardial infarction and early recurrent myocardial ischemia. 212 Mar 9

The pathogenesis of branch retinal vein occlusion has not been completely clarified. The role of abnormal blood viscosity in the appearance and evolution of the disease has recently been advocated. We studied 54 patients with long-standing branch retinal vein occlusion from a hemorrheologic point of view. Depending on the extension of retinal ischemia, two subgroups were identified. Hematocrit, blood and plasma viscosity, whole blood filterability, cell deformability, and fibrinogen levels were investigated. Thirty-five subjects of similar age, sex, and risk factors of diabetes and hypertension served as controls. Our results showed that blood viscosity is higher in patients with occlusion and particularly in those with severe retinal ischemia. Statistical analysis showed a direct correlation between blood viscosity and hematocrit.
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PMID:Branch retinal vein occlusion: the pathogenetic role of blood viscosity. 222 10

Myofiber injury-repair was studied in the rat following blunt trauma to the lower leg in order to understand how the inflammatory and regenerative responses of muscles are altered when myofiber rupture is accompanied by bleeding and clotting reactions. A contusion injury to the muscles of the lower hindlimb of the rat was induced by applying an impact force of 4.7 N-m/cm2 to one leg. The gastrocnemius and soleus muscles were removed bilaterally and evaluated by histochemical and immunohistochemical techniques to document myofiber, vascular, and connective tissue alterations for several days following insult (6-120 hr). A significant increase in wet weight of the gastrocnemius muscle was noted 24 hr postinjury as fluid accumulation and bruising were evident in the muscles resulting from bleeding and inflammation. Vascular disruption was confirmed by the localization of some plasma constituents (fibrinogen, albumin, and complement C3) throughout the interstitial space and even inside some of the damaged myofibers. Inflammation was present and persisted for 5 days as evidenced by continued mast cell degranulation and increased vascular permeability. Using antibodies to identify specific proteoglycans which appear or disappear at various times during muscle regeneration, muscle repair could be followed. The repair process required approximately 10 days for restoration of morphologically intact myofibers. Thus, myofiber repair processes appear to be maintained even after disruption of the vascular system and ischemia following blunt trauma.
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PMID:Extracellular matrix changes following blunt trauma to rat skeletal muscles. 230 15


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