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)

General and vascular surgeons are consulted occasionally to evaluate young adults with ischemia of the lower extremity. Between 1975 and 1985, 51 adults under 40 years of age who had arterial occlusive disease of the lower limb were managed. Although premature atherosclerosis was the most common problem (50%), claudication or limb-threatening ischemia also resulted from other sources (thromboembolism, popliteal artery entrapment, Buerger's disease, collagen vascular disease, and Takayasu's arteritis). Identifying the exact cause was sometimes difficult. The authors were impressed with the number of young adults who had delay in diagnosis and treatment (30 patients, 59%) before referral for a surgical opinion. In this paper, the attempt has been made to uncover the reasons for delayed diagnosis and to suggest a systematic approach that should lead to early recognition of lower extremity ischemia in this age group.
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PMID:Lower extremity arterial disease in young adults. A systematic approach to early diagnosis. 405 11

The histologic fate of venous grafts used for coronary artery bypass has been observed with light and electron microscopy in dogs. Endothelial damage and thrombosis were chiefly limited to the first postoperative week. The muscular media uniformly suffered extensive necrosis and inflammatory cell infiltration during the first week. Its smooth muscle cells either hypertrophied, died or underwent apparent fibroblastic transformation, with eventual fibrous replacement, to a variable degree, of the vein wall. Vascular wall ischemia due to interruption of vasa vasorum during transplantation appears to initiate these medial changes. Much more slowly, intimal thickening by myointimal cells and collagen may reduce the graft lumen to a variable extent.
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PMID:Histologic fate of the venous coronary artery bypass in dogs. 500 48

12 patients with digital ischemia due to collagen vascular disease were treated with repeated infusions of low molecular weight dextran at intervals from 5 to 6 weeks. The patients were followed clinically and by capillary microscopy. In 5 patients an increased capillary blood flow was seen by capillary microscopy. The clinical changes consisted of a lower number of ulcers in 5 of 9 patients with ulcers and a reduction of cold intolerance in 8 of the 12 patients studied. 4 patients had no improvement at all from the treatment. A determination of dextran-reactive antibodies was also performed.
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PMID:Low molecular weight dextran therapy for digital ischemia due to collagen vascular disease. 617 63

The beneficial effects of lodoxamide tromethamine (U42585E) have been examined in a canine model of myocardial ischemic injury. Lodoxamide was infused 20 mg/kg/h i.v. starting 30 min before occlusion of the proximal left circumflex coronary artery (LCX) and continuing through 90 min of ischemia. Lodoxamide produced a significant reduction in ultimate infarct size measured at 24 h by postmortem tetrazolium perfusion staining. Infarct size expressed as a percent of the anatomical area at risk was 21.7 +/- 2.7 in the treated group vs. 47.0 +/- 3.1 in the control group (mean +/- SEM). No significant difference in area at risk was observed between treated and control groups. Salvage occurred primarily in subepicardial and midmyocardial tissue without apparent lateral protection. Histological examination confirmed gross results of postmortem staining. The protection appeared to be unrelated to myocardial oxygen demand since no hemodynamic differences between groups were observed at the time of occlusion of throughout the 24-h experimental course. Concurrent studies of ex vivo platelet aggregation showed no effect of lodoxamide on adenosine diphosphate (ADP), collagen, and arachidonic acid-induced aggregation. In vivo antithrombotic effects were evaluated in four conscious dogs by inducing LCX thrombosis with low-amperage stimulation (50 microA for 24 h) of the intimal surface. Occlusive thrombi occurred in all four dogs and were similar to controls. These results suggest that lodoxamide reduces myocardial ischemic injury by a mechanism unrelated to oxygen demand or antiplatelet effects.
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PMID:Effects of lodoxamide on ischemic reperfused myocardium. 617 41

The function of blood platelets sampled from the coronary sinus and the superior vena cava was studied in 50 men with coronary artery disease at rest and during pacing-induced angina. At rest, a lower platelet aggregation and retention response was found in coronary sinus compared with vena caval blood. This may be due to refractoriness after previous platelet stimulation or to release of platelet inhibitors in the coronary circulation. During pacing-induced angina, lactate levels indicated that blood was sampled from ischemic myocardium in only 27 of the patients. Pacing-induced angina influenced platelet function differently in blood from ischemic and nonischemic regions. Adenosine diphosphate- and collagen-induced aggregation, platelet retention and plasma beta-thromboglobulin levels remained unchanged in blood from ischemic myocardium during pacing, but increased in blood from nonischemic regions. Thus, factors other than ischemia activated platelets in the coronary circulation during tachycardia-induced stress.
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PMID:Effects induced on blood platelets in ischemic and nonischemic myocardium. 622 28

The neurovascular supply to the pigeon's extensor digitorum communis muscle was disrupted. The muscle spindles were studied by light and electron microscopy to determine whether their degeneration was compatible with regeneration by activation of satellite cells within an intact spindle capsule. The denervation and ischemia induced intrafusal muscle fiber necrosis and degeneration of the sarcolemma and basal lamina. The muscle fibers in the equatorial region were often absent and their sites were indicated by collagenous caps which usually covered the sensory nerve terminal regions. These collagenous caps enclosed amorphous material derived from the intrafusal fibers and degenerating mitochondria from the sensory terminals. In this equatorial region, the basal lamina was present only under the collagenous cap and was disrupted elsewere . The cells of the muscle spindle capsule were more sparse or absent, but the collagen content had increased. The sheath lacked continuity, containing numerous gaps. These observations indicate that the basal lamina does not remain intact, and regeneration may not occur by activation of satellite cells within the former basal lamina, as reported for regenerating rat muscle spindles. This suggests that the mechanisms of regeneration of muscle spindles in rat and pigeon muscle may not be similar.
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PMID:Ischemic degeneration of the avian muscle spindle. 623 37

The use of stemmed patches and tubes from the seromuscular layer of the colon wall to replace part of the ureter has proven unreliable because of complications such as urinary leakage and invagination, fibrosis, bone formation, shrinkage and disappearance of the intestinal wall due to ischemia and necrosis, causing hydronephrosis and pyelonephritis. The use of tubes and patches of tanned and untanned collagen, implanted in order to study the ingrowth of urothelium and possibly muscle cells, resulted in fibrosis, bone formation, rejection of the material and, in the case of the tubes, complete obstruction with hydronephrosis and destruction of the kidney.
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PMID:Ureter replacement by collagen and seromuscular parts of the large bowel in dogs. 647 2

Thromboxane A2 (TxA2) may aggravate myocardial ischemia by inducing vasoconstriction and platelet aggregation in small coronary vessels, whereas prostacyclin (PGI2) counteracts these effects. Acetylsalicylic acid (ASA) inhibits the formation of TxA2 as well as PGI2, whereas dazoxiben, a thromboxane synthetase inhibitor, reduces TxA2 formation selectively. In 25 patients with coronary artery disease, 2 identical atrial pacing stress tests were performed: before and after the administration of dazoxiben (200 mg) in 15 patients and before and after ASA (250 mg) in 10. The ischemic response, quantified by coronary sinus and aortic lactate levels and by ST depression, was significantly reduced after administration of dazoxiben (p less than 0.02) but not after ASA. Heart rate at rest, myocardial extraction of free fatty acids and the arteriovenous oxygen difference was unaffected by medication. Both drugs reduced TxB2 levels to the same extent, whereas collagen-induced aggregation was more reduced after ASA than after dazoxiben. The effect of dazoxiben on ischemia was probably a result of inhibited TxA2 and preserved PGI2 production, which increased blood flow to ischemic regions.
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PMID:Effects of a selective thromboxane synthetase inhibitor, dazoxiben, and of acetylsalicylic acid on myocardial ischemia in patients with coronary artery disease. 653 40

The in-vivo effects of the new antithrombotic compound nafazatrom on experimental thrombosis of the left circumflex coronary artery, on hemodynamics and on ultimate infarct size were studied in pentobarbital-anesthetized, open-chest dogs. Coronary artery thrombosis was induced by low amperage stimulation (150 microA, DC for 6 hr) of the circumflex artery intimal lining. The effects of oral pretreatment of 1%-Tylose suspension as drug diluent and 5 mg/kg nafazatrom plus vehicle were determined. Both agents were administered twice a day before onset of current stimulation. In the drug vehicle group, coronary thrombosis caused severe hemodynamic alterations, e.g. blood pressure and left ventricular pressure decrease, as well as reduction in the LV dP/dtmax associated with increases in end-diastolic filling pressure and heart rate. Time to coronary artery occlusion was delayed by nafazatrom (5.2 +/- 1.1 vs 3.1 +/- 0.4 hr, p less than 0.05). Smaller blood pressure and LV dP/dtmax reductions and minor heart rate and filling pressure increases around the time of thrombus formation suggested cardioprotection with the drug. Smaller R wave changes and S-T segment elevation indicated minor ischemia at the time of occlusive coronary artery occlusion in nafazatrom-treated hearts (24 +/- 0.5 vs 72 +/- 7% ST segment elevation, p less than 0.01). Thrombus wet weight was 18.4 +/- 2.6 mg in the nafazatrom group, but 63.7 +/- 3.1 mg in controls (p less than 0.01). Thus, ultimate infarct size was smaller in nafazatrom-treated hearts as related to left ventricular mass (8.4 +/- 1.4 vs 32.3 +/- 3.1%, p less than 0.02) or to the occluded artery perfusion area at risk for infarction (16 +/- 3.4 vs 53 +/- 6.2%, p less than 0.05). No ex-vivo effect of nafazatrom on collagen-induced platelet aggregation was observed. These results may indicate efficacy of the drug in prevention of acute coronary artery disease as one cause of ischemic jeopardy of the myocardium and/or therapeutic value in coronary artery spasm.
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PMID:The effects of oral nafazatrom (= BAY g 6575) on canine coronary artery thrombosis and myocardial ischemia. 661 99

Recently, a reduction in postoperative adhesion formation in rabbits which received high-dose ibuprofen (280 mg/kg/day) treatment in the perioperative interval was reported. Because these results could have resulted from a nonspecific effect of ibuprofen, the effects of ibuprofen on peritoneal injury in a time and dose response fashion was evaluated. Seventy rabbits were assigned to seven groups. All rabbits received a dose of ibuprofen 1 hr prior to surgery. The time of the second dose was either 8 or 12 hr after the surgical procedure; 8 hr for groups A, C, and E; 12 hr for groups B, D, and F (A, B: 70 mg/kg; C, D: 35 mg/kg; E, F: 17.5 mg/kg, respectively). Thereafter, rabbits received further dosing every 6 hr to complete a total 10-dose regimen. Group G served as a nontreatment control. Surgical injury was induced by either abrasion or ischemia of the right uterine horn. Immediately after closing the incision, 10 muCi of 14C-labeled glucosamine and 10 muCi of 14C-labeled proline were injected into each rabbit. All rabbits underwent a second laparotomy on the fifth postoperative day for evaluation of adhesion formation. Uterine tissue adjacent to the site of uterine healing was excised for determination of glycosaminoglycan and collagen concentration. In the nontreatment control group G, 5 of the 10 rabbits had severe grade 2 adhesions at the time of second laparotomy, 3 had grade 1 filmy adhesions, and 2 had no adhesions. This is in marked contrast (P less than 0.025) to the group that received ibuprofen at 70 mg/kg/day with the first postoperative dose 8 hr after surgery (group A). In this group, no rabbits had severe grade 2 adhesions, 3 rabbits had filmy grade 1 adhesions, and 7 rabbits were free of pelvic adhesions. A gradual tendency towards more adhesions and more severe adhesions was apparent in groups B-F as the dose of ibuprofen was decreased and the time of first postoperative injection was prolonged. The recovery of 14C-labeled glucosamine from the glycosaminoglycan extraction demonstrated a positive correlation between the cpm recovered and the severity of adhesions formed. Groups A and B had, overall, the lowest ratios of glucosamine (1.47 +/- 0.08 and 1.56 +/- 0.09, respectively) which were statistically different from the nontreatment control group G (1.76 +/- 0.11, P less than 0.05). There was also a positive correlation between the formation of severe adhesions and the ratio of 14C-labeled proline recovered by collagen extraction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ibuprofen inhibition of postsurgical adhesion formation: a time and dose response biochemical evaluation in rabbits. 669 77


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