Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

Urokinase, the plasminogen activator from human urine, produces a dose-dependent increase in blood flow in the canine superior mesenteric artery when injected intraarterially at doses from 10(-1) to 10(3) units kg-1. This vasodilation persists despite blockade of beta-adrenergic and histamine H1 and H2 receptors as well as inhibition of plasminogen activation, suggesting that these mechanisms are not involved. Infusion of urokinase at 10(2) CTA (Committee on Thrombolytic Agents) units kg-1 min-1 does not produce a sustained vasodilation, but is effective in achieving complete lysis of thrombi within 100 min in the superior mesenteric arterial circulation. Increasing the dose slightly to 125 CTA units kg-1 min-1 results in unwanted clotting abnormalities without attaining a vasodilator level. Decreasing the dose to 75 CTA units kg-1 min-1 still results in complete thrombolysis. In contrast to the results in the femoral circulation, the dose required for fibrinolysis-thrombolysis does not overlap with that for vasodilation in the superior mesenteric artery. Nevertheless, these experiments provide some basis for the use of intraarterial urokinase infusion in the treatment of nonocclusive mesenteric ischemia and, perhaps, thrombotic occlusion of the superior mesenteric artery.
...
PMID:Vasodilation, fibrinolysis, and thrombolysis with intraarterial infusion of urokinase in the canine superior mesenteric artery. 9 90

A common although infrequently recognized complication associated with the use of a pneumatic tourniquet is profuse bleeding from the wound after deflation of the tourniquet. The purpose of this study was to determine whether intravascular coagulation and fibrinolysis could be induced in subhuman primates by tourniquet ischemia, and whether this phenomenon could be altered by pretreatment of the animal with heparin. It was shown that, after 2(1/2) hours of tourniquet ischemia, (400 mmHg) to one lower limb, fibrinogen levels were significantly lower (p < .005), antithrombin III levels were significantly lower (p < .05), plasminogen levels were significantly lower (p < .05), fibrin split products significantly higher (p < .025) and fibrinopeptide A levels were significantly higher (p < .02) than values measured simultaneously in the control limbs. After pre-treatment with sodium heparin, 30 units/kg, there was no change in antithrombin III levels or fibrinogen levels, but fibrin split products in the experimental limbs were significantly elevated (p < .05) when compared to control limbs. In both groups the abnormal levels returned to control levels 5-30 minutes after tourniquet deflation. We conclude that intravascular coagulation and fibrinolysis develop within ischemic subhuman primate limbs during tourniquet ischemia. Pretreatment with heparin prevents the consumption of fibrinogen and antithrombin III but does not prevent the increase in fibrin split products which was observed. It is possible that intravascular coagulation and fibrinolysis contribute to post tourniquet bleeding.
...
PMID:Intravascular coagulation and fibrinolysis within primate extremities during tourniquet ischemia. 11 39

Following liver transplantation, the decision to retransplant in cases in which graft function is marginal must be taken early. Plasma coagulation factor monitoring was evaluated as an early predictor of graft failure requiring retransplantation in the first posttransplant week. Plasma levels of fibrinogen, factors V, VII, VIII, IX, antithrombin III, protein C, and plasminogen were measured in all patients at 0, 12, 24, 48, 72, 96, and 120 hours posttransplant in 46 patients who received 56 grafts and results were compared between livers that failed early (group 1) and those that functioned adequately (group 2). Six grafts were included in group 1: one patient died before retransplantation, four were retransplanted once, and one patient was retransplanted twice. Three grafts had primary nonfunction (PNF), 2 had obstructed portal veins, and 1 had a long period of warm ischemia during the initial transplant. In group 1, plasma levels of factor V were significantly lower than in group 2 at 24, 48, and 72 hours posttransplant (21.2% +/- 14.2%, 12.4% +/- 4.5%, and 13.0% +/- 5.0% v 39.1% +/- 23.9%, 48.8% +/- 31.9%, and 60.9% +/- 25.9%; P less than .05, P less than .01, and P less than .005, respectively). Similarly, plasma levels of factor VII were significantly lower in group 1 over the same period of time (7.3% +/- 2.7%, 4.2% +/- 1.8%, and 4.7% +/- 2.5% v 27.4% +/- 17.1%, 34.1% +/- 21.6%, and 34.8% +/- 18.6%, respectively; P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Coagulation plasma factor levels are early indicators of graft nonfunction following liver transplantation in children. 150 Oct 1

Pharmacologic lysis of occlusive, ischemia-producing thrombi has become widely accepted during the past decade. New developments in this field have centered around increasing the efficacy of the known plasminogen activators while employing methods to minimize the risk of hemorrhage and decrease the incidence of rethrombosis. Such methods have included the use of thrombus-directed antibodies linked to plasminogen activators, increased plasminogen (substrate) concentration at the thrombus site, anticoagulant and antiplatelet therapy to prevent thrombus propagation and reformation following lysis, and combination plasminogen activator therapy designed to increase efficacy and safety. These new strategies have been extensively tested in vitro and in a variety of animal models. As we have indicated, extrapolation of such results to human patients cannot be done with confidence. However, the strategies are based on sound rationale and the reported findings should serve as the basis for controlled human trials.
...
PMID:New developments in thrombolytic therapy. 154 May 36

With intravenous thrombolysis mortality of acute myocardial infarction can be significantly reduced, not only in the first hours after the onset of symptoms, but also up to 24 hours. The open infarct related coronary artery is important concerning long-term clinical outcome. If thrombolysis can be administered within the first three to six hours, limitation of infarct size and preservation of left ventricular function contribute to an impressive reduction in mortality. Long-term assessments of clinical outcome have surprisingly shown that the prognosis is much more dependent upon patency of the infarct related artery than from the time to treatment. Since a correlation is suspected between the degree of residual stenosis and the clinical course, recurrence of ischemia, reinfarction, hemodynamic instability and death, and the fact that mortality is highest within the first three days after thrombolysis the emphasis of numerous investigations has been on possibilities of PTCA in the acute stage of myocardial infarction. The application of interventional techniques was tested at different times within the progression of myocardial infarction. PTCA can be applied as primary, direct therapy without thrombolysis, immediately and during intravenous thrombolysis, following successful pharmacological recanalisation, as rescue-PTCA for failed thrombolytic therapy, delayed and as a prophylactic measure up to until days after the infarction or later when accompanied by careful observation of the patient, when limited to few indications with spontaneous or stress-related angina pectoris, hemodynamic instability or predetermined angiographic criteria. Important results have been gathered by the larger studies of the last few years, TAMI, ECSG, and TIMI as well as by numerous smaller investigations, about the pathophysiology and treatment of myocardial infarction. Despite different study design, the three larger trials have come to the same conclusion regarding PTCA and rt-PA thrombolysis, early PTCA is without advantage compared to a deferred treatment; the acute results are usually worse and the clinical course more complicated. It must be mentioned however, that major problems still remain unresolved: primary or direct angioplasty, PTCA in combination with non-fibrin specific plasminogen activators, as well as rescue-PTCA after failed thrombolysis. Specially, 90 minutes after thrombolysis 23 to 44% of the coronaries are still occluded, depending on the plasminogen activator, and there is no non-invasive procedure to detect this patient-group and to advise further treatment. Due to the high mortality rate within the first three days attempts of treatment are concentrated on this time-span.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:[PTCA in acute myocardial infarct: primary, immediate, delayed or elective?]. 154 50

In this paper the Authors illustrate their experience of loco-regional fibrinolytic medical treatment in patients suffering from acute thrombotic-type ischemia of the lower limbs. The clinical, ultrasonographic and angiographic criteria leading to the choice of this form of treatment rather than surgery are examined. The Authors outline the reasons which led them to give preference to the use of plasminogen tissue activators (rt-PA) rather than other fibrinolytic agents; the results obtained are evaluated not only in terms of immediate permeability but also in relation to the additional procedures required to ensure a correct therapeutic iter. In conclusion, the paper underlines the need to assess the indications for this type of therapy with great care since "washing" the distal vascular bed may be decisive for successful treatment even in the event of possible future surgery.
...
PMID:[Effects of fibrinolytic therapy in acute ischemia of the lower limbs]. 163 Jun 69

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)
...
PMID:Therapeutic defibrination with ancrod does not protect canine myocardium from reperfusion injury. 170 37

Various substances (saline solution, dextran, heparin, proteinase inhibitors, etc.) have been investigated to determine their influence on adhesion prevention, but until recently the results were controversial and lacked any implication for clinical use. The analysis of intraperitoneal plasminogen activating factor (PAA) and the fibronectin production rate of peritoneal macrophages promises new aspects of adhesion formation and prevention. The results of studies show a close correlation between ischemia/infection and the decrease of PAA as well as increased adhesion formation in patients (endometriosis) with increased fibronectin production by peritoneal macrophages.
...
PMID:[Prevention of adhesions by intraperitoneal administration of substances in abdominal interventions]. 198 79

Protein C content and plasminogen activity were measured in plasma from 100 horses with signs of colic. Data were analyzed by grouping horses 4 ways. Each horse was allotted to 1 of 2 outcome groups (survivors and nonsurvivors), 1 of 3 broad-category diagnosis groups (inflammatory disorders, strangulating obstructions, and all other gastrointestinal disorders), and 1 of 2 clinical management groups (medical and surgical). In a fourth grouping, all horses (although numbers of horses included in each subgroup were small) were assigned either to specific diagnostic groups that had high expectation for activated hemostasis (intestinal ischemia, endotoxemia, jugular thrombosis, peritoneal adhesions, and laminitis) or to a control group, in which active hemostasis was unlikely. Within 2 to 24 hours after admission, nonsurvivors developed lower protein C content than did survivors. Protein C content and plasminogen activity became low during hospitalization in horses with strangulating obstructions and in horses having surgery. The results from the grouping by specific diagnosis must be considered pilot data because the numbers of horses in each subgroup were small. Although not statistically significant, trends were noticed in protein C and plasminogen: (1) horses with intestinal ischemia and endotoxemia developed low protein C content and plasminogen activity, (2) protein C content became low in horses that developed peritoneal adhesions or laminitis, and (3) plasminogen activity became low in horses that developed jugular thrombosis. Low protein C content or low plasminogen activity, or both, may be useful as predictors for outcome and for these specific complications of equine colic.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Use of newly developed assays for protein C and plasminogen in horses with signs of colic. 201 48

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.
...
PMID:Repeat infusion of recombinant tissue-type plasminogen activator in patients with acute myocardial infarction and early recurrent myocardial ischemia. 212 Mar 9


1 2 3 4 5 6 7 8 Next >>

---