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)

Ageing of the arterial wall is defined as the age-related structural and functional changes in arteries. These changes include distension of the lumen, kinking of the artery, and rigidity of the arterial wall. Distension of the arterial luminal diameter with hardening of the arterial wall causes chronic ischemia in peripheral tissues, leading to age-related deterioration of the organs. The ensuing pathological modification in blood circulation is mainly linked to the decrease in the elastic recoil of the arteries and to the increasing difficulty of pumping systolic blood volume towards the periphery. This results in increased systolic blood pressure in the elderly and an increasing load on the ageing heart. Age-related changes in elastic arteries are characterized as degenerative changes in the SMCs of the media associated with depositions of collagen fibers and the fragmentation of elastic fibers. Data obtained from in vivo experiments indicate that the susceptibility of aged arteries to atherogenic stimuli might be related to intrinsic cellular changes with age. Substances that can regulate the function of vascular wall cells may be continuously present in the vessel walls, perhaps as components of super-extracellular matrix complexes. One type of substance is the functional domain structure of extracellular matrix molecules exposed to specific receptors or binding proteins on the surface of the cells. The role of extracellular matrices, especially elastin, on cultured vascular cells has been discussed.
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PMID:[Arterial ageing of aorta and atherosclerosis--with special reference to elastin]. 764 69

Oxygen inhalation in a chamber at the pressure exceeded 0.2 MPa produces some positive effects, that are explored for therapeutic purposes at about 30 years. Oxygen increases bactericidal capacity of leukocytes, reduces tissue edema, protects intracellular ATP, maintain tissue oxygenation even in the absence of hemoglobin. Stimulates fibroblast replication, increases collagen production, stimulates arborisation of capillaries into ischemic tissue, protects from lipid peroxidation. These properties of oxygen are exploit in acute, life threatened conditions and in various chronic ischemias. Hyperbaric oxygen therapy as an adjuvant together with conservative and invasive therapy methods helps to decrease morbidity, work incapability, invalidisation and mortality in oclusive and inflammatory arteriities, diabetic gangrene and other forms of clinical leg ischemia. The use of hyperbaric oxygenation will become increasingly common as more hyperbaric facilities are established.
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PMID:[Hyperbaric oxygen therapy]. 767 Dec 82

The photochemical reaction between rose bengal and light (540 nm) produces thrombotic occlusion in rat coronary artery. We have now developed an experimental myocardial infarction (MI) model by photochemically induced thrombosis (PIT) in rats and investigated the mechanisms responsible for the induction of MI. PIT in the coronary artery induced myocardial ischemia, which was determined by tissue oxygen tension (tpO2), and resulted in MI. Pretreatment with a thromboxane (TX) A2-receptor antagonist, vapiprost, prevented a decrease in myocardial tpO2 and markedly reduced the MI area, although vapiprost inhibited collagen-induced platelet aggregation by 30% ex vivo. An ADP-induced platelet aggregation inhibitor, clopidogrel, also reduced the MI area. In contrast to vapiprost, clopidogrel inhibited collagen-induced platelet aggregation by 90% ex vivo. Pretreatment with a 5-HT2-receptor antagonist, ketanserin, which did not inhibit collagen-induced platelet aggregation ex vivo, prevented the decrease in myocardial tpO2 and reduced the MI area. These results suggest that TXA2, 5-HT and ADP play a role in the induction of MI and that platelet aggregation and other factors induce ischemia in this model.
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PMID:An experimental myocardial infarction model in the rat and its properties. 774 45

Berberine (Ber) 20 mg.kg-1.d-1 for 1, 3, or 5 d inhibited platelet aggregation induced by ADP, arachidonic acid (AA) and collagen (Coll) in rats with 24 h reversible middle cerebral artery occlusion (MCAO), and the platelet adhesiveness was inhibited as well. Using radioimmunoassay method, the thromboxane B2(TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) contents in rat plasma were measured 24 h after MCAO. The results indicate that the TXB2 levels after drug treatment were lower than those in ischemia control rats, but the 6-keto-PGF1 alpha levels showed no obvious difference between the two groups. The same dose of Ber was also shown to inhibit thrombosis formation. This suggests that the decline of platelet aggregation and decrease of TXB2 content may be one of the important factors involved in the anti-cerebral ischemia effect of Ber.
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PMID:[Effects of berberine on platelet aggregation and plasma levels of TXB2 and 6-keto-PGF1 alpha in rats with reversible middle cerebral artery occlusion]. 778 38

Studies on the stress response of isolated myocytes have gained great importance in the understanding of the response of the heart as an organ after, for instance, ischemia. However, the possible role of the extracellular matrix on these effects has thereby been neglected. The recently developed model system of neonatal heart cells cultured on a collagen gel, characterized by a high coherence of contractions, has been used to study the effects of this more in vivo-like collagen environment on the heat shock response of the myocytes as compared to 'normally used' monolayer cultures. After four days differences were found in the heat-induced synthesis of HSPs of cells grown by the two culturing procedures. The degree of induction of different HSPs appeared to be directly related to the basic level of synthesis of these HSPs under the used culturing conditions. In collagen gel-grown cultures the basic level of synthesis as well as the heat-induced synthesis of HSP84 and HSP100 was decreased, for HSP60 both were increased, and for HSP70 no differences were found compared to the monolayer cultures. Our results suggests that the collagen matrix has a regulatory role in the synthesis of HSPs.
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PMID:HSP synthesis of neonatal rat heart myocytes is regulated by a collagen environment. 779 Jul 39

Acute dysvascular limb in young adults is a rare entity. Diagnosis is often difficult because symptoms are not recognized as ischemic. The most common causes of this condition are premature atherosclerosis, thromboangiitis obliterans, microemboli, popliteal entrapment syndrome, collagen vascular disease, Takaysu's arteritis, and coagulopathy. A case study is presented to illustrate the disease process. A systematic approach to diagnosis, consisting of history and physical examination, palpation and auscultation of peripheral pulses at rest and following exercise, and noninvasive vascular examination at rest and following exercise, is recommended. Suggestion of an ischemic condition following noninvasive studies should be followed up with an arteriogram. The prognosis is dependent on the underlying etiology of the ischemia, early detection, and appropriate treatment.
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PMID:Acute dysvascular limb in a young adult. A case study. 785 53

Ischemia-induced systolic dysfunction has been ascribed to changes in cellular excitation-contraction coupling and diastolic dysfunction because of disruption of the extracellular collagen matrix. Therefore, systolic and diastolic pressure-volume relationships and O2 consumption were determined before and after 5 min of global ischemia in isolated blood-perfused porcine hearts. The slope of the systolic pressure-volume relationship was 7.2 +/- 0.6 (SE) mmHg.ml-1.100 g-1 (n = 18) at baseline and did not change during reperfusion, but the systolic volume intercept shifted from 1.0 +/- 0.4 ml/100 g at baseline to 3.7 +/- 1.4, 4.1 +/- 1.1, and 4.2 +/- 0.9 ml/100 g at 15, 30, and 60 min of reperfusion, respectively (all P < 0.05). The diastolic volume intercept was 8.2 +/- 0.7 ml/100 g at baseline and remained unchanged during reperfusion. Therefore, the difference of the systolic-diastolic volume intercepts, an index of elastic recoil forces, was decreased to 57 +/- 8, 49 +/- 7, and 47 +/- 9% of baseline values (P < 0.05). The shift of the systolic pressure-volume relationship was accompanied by a transient decrease of contractile efficiency (slope of O2 consumption-pressure-volume-area relationship) at 15 min of reperfusion (from 43 +/- 6 to 27 +/- 7%). We hypothesize that the rightward shift of the systolic pressure-volume relationship was compatible with a decrease of elastic-restoring forces, probably induced by alterations in the extracellular collagen matrix and/or the cytoskeleton, and thereby our data imply that left ventricular dysfunction of postischemic myocardium does not result solely from disturbances in excitation-contraction coupling.
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PMID:Loss of elastic recoil in postischemic myocardium induces rightward shift of the systolic pressure-volume relationship. 794 2

Abnormally shaped arteries were found in the intestines of 17 of 62 patients (27%) with Hirschsprung's disease. The histological characteristics of abnormal arteries included proliferation of collagen fibers and smooth muscle cells in the adventitia. The incidence of abnormal arteries in each type of aganglionosis was as follows: 25% (13 of 51) in short-segment aganglionosis; 0% (0 of 6) in long-segment aganglionosis; and 80% (4 of 5) in total-colon or extensive aganglionosis. The older the patients were at the time of resection, the higher the incidence of abnormal arteries (< 1 year old, 15%; 1-3 years old, 38%; > 3 years old, 75%). The abnormally shaped arteries were mostly located in the histological transitional zone. These findings suggest the following possibilities: (a) the craniocaudal migration of ganglion cells was interrupted by intestinal ischemia in the presence of abnormal arteries in utero; (b) an ischemic episode caused both the disappearance of neural cells and dysplasia of the artery; (c) the ganglion cells were destroyed by mild ischemia caused by the abnormal arteries; or (d) the tension caused by mechanical expansion resulted in a change in the vascular walls in the transitional zone.
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PMID:Abnormally shaped arteries in the intestine of children with Hirschsprung's disease: etiological considerations relating to ischemic theory. 801 68

Eight hearts with pulmonary atresia with intact ventricular septum were studied grossly and microscopically. The right ventricle was composed of inlet, infundibular, and trabecular portions in two hearts, without trabecular portions in three hearts, and consisted of an inlet part only in another three hearts. Pulmonary atresia was classified as membranous in two hearts; the other six hearts had muscular atresia. The left ventricle showed a range of abnormalities, albeit mostly discrete. A mitral valve with short tendinous chords was present in four hearts; one of these had a cleft mitral valve. All hearts (except the heart of a 1-day-old neonate) had a prominent subaortic septal bulge. All hearts had left ventricular hypertrophy, which exceeded twice the standard deviation of normal in two patients. None of the hearts had histologic features of hypertrophic cardiomyopathy. The density of intramyocardial coronary arteries was normal in each patient, but medial thickening (20 to 100 microns diameter arteries) had occurred in four patients. Signs of acute myocardial ischemia (hydropic cell swelling) were present in all; one heart (the oldest case of 6 months) contained areas of replacement fibrosis and calcifications indicative of previous infarction. Quantification of the volume density of endomysial (interfiber) collagen (Picrosirius red microspectrophotometry) showed high levels in all, within the range of normal in five patients, but exceeding twice the standard deviation of normal in three patients. In all cases the values obtained in the subendocardial layers were higher than those obtained subepicardially. The observations show that the left ventricle in hearts with pulmonary atresia with intact ventricular septum contains abnormalities that may render the left ventricle less capable to cope with a volume load. The high values of endomysial (interfiber) collagen suggest chronic ischemia in relation to left ventricular hypertrophy as the main mechanism involved. Therefore, as a late consequence, the left ventricle could be the limiting factor for long-lasting successful surgical intervention.
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PMID:Disease of the left ventricle in pulmonary atresia with intact ventricular septum. The limiting factor for long-lasting successful surgical intervention? 802 53

Symptomatic occlusive disease of the subclavian arteries, not associated with thoracic outlet syndrome, is an uncommon problem with a paucity of literature related to the appropriateness of bypass graft selection and long-term patency for revascularization. Between 1985 and 1993, 9 patients (3 men and 6 women) underwent 13 carotid brachial bypasses for chronic severe upper-extremity ischemia. Ages ranged from 47 to 75 years (mean 65). Three patients had documented collagen vascular disease, 1 had radiation arteritis, and 4 had bilateral disease requiring staged arterial reconstruction. Indications for operation included severe exercise-induced ischemia in two limbs (15%), rest pain in eight (62%), and gangrene or infection, or both, in three (23%). Two bypasses were performed for failed prior reconstructions. Inflow originated from the carotid artery (4 proximal and 9 bifurcation), and distal anastomoses were made to a disease-free section of brachial artery. Reinforced 6 mm thin-wall polytetrafluoroethylene (PTFE) grafts were used in all operations. No operative mortality or major upper-extremity amputation was associated with the procedure, although digital amputations were performed in four instances. Follow-up ranged from 4 to 83 months with a mean of 38 months. The 5-year primary patency rate, by life-table analysis, was 92%. Our results showed excellent long-term patency when prosthetic grafts were used for carotid brachial bypass, because of excellent runoff and the relatively short graft length required.
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PMID:Carotid brachial bypass for treating proximal upper-extremity arterial occlusive disease. 805 29


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