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

Systemic hypertension (secondary to aortic coarctation) produces in monkeys, multifocal brain lesions where capillaries show increased diameter, endothelial degeneration and deposition of collagen and other substances in the basement membrane. In one animal, capillary changes were detected as early as 8 weeks after induction of hypertension. Similar capillary alterations were demonstrated in brain samples of hypertensive humans obtained at autopsy. We suggest that the above abnormalities may be the result of successive episodes of regional ischemia and/or hyperperfusion. Validation of these observations requires careful evaluation of additional human and animal brains.
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PMID:Arterial hypertension injures brain capillaries. Definition of the lesions. Possible pathogenesis. 679 8

Proteins central to normal wound repair, including collagen and proteoglycans, were extracted during postoperative mesothelial regeneration, then the quantitation was correlated to macroscopic observations of normal peritoneal reepithelialization and/or postoperative adhesion formation. Sixty-three New Zealand white female rabbits of reproductive age were prospectively assigned to either Group A, untreated control; Group B, which received intramuscular injections of ibuprofen, 70 mg/kg per injection (immediately and 6 hr after surgery); or Group C, which received 5 intramuscular injections of ibuprofen (4 hr before surgery, and immediately, 6, 12, and 18 hr after surgery). The right uterine horn underwent one of three standardized surgical traumas: (1) abrasion of the peritoneal surface with a scalpel until punctate bleeding developed, (2) ischemia of the uterine horn by removal of the collateral blood supply (devascularization), (3) crushing of the uterine horn by cross clamping for 3 min with a Kelley hemostat. Thereafter, 10 microCi of C-14-labeled glucosamine and 10 microCi of C-14-labeled proline were injected into the marginal ear vein of each rabbit. All rabbits underwent a laparotomy on the fifth postoperative day for evaluation of adhesion formation and tissue biopsy for protein extraction. No reduction in adhesion formation was found using a 2-dose postoperative treatment regimen. However, using a 70 mg/kg X 5-doses regimen in the immediate perioperative interval, a significant reduction in both adhesion formation and severe adhesion formation (both P less than 0.025) were found following standardized surgical injury. The extent of adhesion formation was correlated with the extractable glycosaminoglycan and collagen concentrations. As determined by recovered glucosamine and proline, a positive correlation was apparent between the severity of adhesion grade and formation of new glycosaminoglycans or collagens. Thus, ibuprofen appears to inhibit adhesion formation through suppression of fibroproliferative inflammation.
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PMID:Biochemical evaluation of postsurgical wound repair: prevention of intraperitoneal adhesion formation with ibuprofen. 683 8

Morphological examinations of 72 autopsy observations of the disseminated intravascular blood coagulation (DIVBC) syndrome (a combination of microthrombosis in renal glomeruli, adrenals, gastrointestinal tract and other organs with the hemorrhagic syndrome) led to a conclusion on the role of DIVBC in the formation of cortical renal necroses. All the observations presented capillary thrombosis of the renal glomeruli the extent and dissemination of which had influenced the size of cortical necroses. Cortical ischemia in early stages is manifested by nephrothelium dystrophy followed at 3-5 days by the development of necrosis of the tubules, glomeruli, and stroma. The formed cortical necroses of the kidneys (CNK) are demarkated, their healing occurs at the expense of the interstitial tissue, whose cells proliferate, and later collagen genesis is observed. Scars from CNK have been shown to contain tubules with an undifferentiated epithelium.
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PMID:[Characteristics of kidney involvement in disseminated intravascular coagulation (morphogenesis of cortical necrosis)]. 686 Jan 65

Platelet aggregation and circulating platelet aggregates (CPAs) were evaluated in 18 patients with myeloproliferative disorders, both with and without thrombocytosis. No specific patterns of platelet aggregation were detected, but 11 of 18 patients demonstrated abnormal aggregation to epinephrine, nine of 18 had abnormal aggregation to adenosine diphosphate, and seven of 18 had abnormal aggregation to collagen. There was no definitive correlation of bleeding episodes with abnormal aggregation. However, significant bleeding was observed in a patient with a platelet count of 1,500,000/cu mm and abnormal aggregation. The aggregation defects persisted despite lowering of platelet count. Evidence of increased circulating platelet aggregates and normal platelet aggregation was seen in two patients, one of whom had transient cerebral ischemic attacks relieved by antiplatelet therapy, with return of the CPA index to normal. In two patients with digital ischemia, claudication, and angiographic evidence of peripheral vascular disease, no laboratory evidence of increased circulating platelet aggregates was observed, but one patient had regression of symptoms with antiplatelet therapy.
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PMID:Abnormal platelet function in myeloproliferative disorders. 689 52

Experimental myocardial infarction has been induced in rats by isoprenaline pretreatment and progress of the lesions has been observed histologically at intervals over a period of 6 weeks. This revealed transition from extensive ischaemic degeneration to apparently complete recovery of much of the affected muscle, leaving lesser areas of necrotic cells to become replaced by dissecting collagen-fibre scars. Isolated perfused preparations of affected and normal hearts were used to give electrocardiogram records. Oscilloscope photographs were measured. Ischaemia was associated, typically, with enlarged Q waves and decreased R and S waves, plus evidence of bundle branch block. These abnormalities abated as lesions resolved, leaving residual Q enlargement and arrhythmias, consistent with persistent scarring.
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PMID:Abnormal electrocardiographic activity revealed by isolated rat heart preparations at various times after experimental myocardial infarction. 726 Sep 82

The sciatic/tibial/plantar nerve complex of normal aged rats displays striking morphological changes that are most pronounced distally. Nerve fiber abnormalities include: (a) large numbers of axonal glycogenosomes, mitochondria, dense membranous bodies, and decorated particles; (b) adaxonal Schwann cell processes sequestering portions of axoplasm; (c) swollen demyelinated and remyelinated axons, some encircled by supernumerary cellular processes; and (d) collagen pockets, denervated Schwann cell columns, and empty basal laminae. Abnormalities a and b were encountered with increasing frequency on descent through the tibial and plantar nerves. Abnormalities b, c, and d were found in lateral and medial plantar nerves, where they were associated with an enlarged endoneurial space. Found in animals kept in cages with smooth or wire-mesh floors, the incidence of these changes increased with advancing age. They are attributed to trauma and ischemia from chronic pressure on the plantar nerve.
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PMID:Peripheral nerve abnormalities in aging rats. 746

Although the autonomic nervous system has been implicated in the formation of ventricular fibrillation, the precise mechanism by which this is mediated remains undetermined. In particular, the role of second messengers, generated by beta-adrenoceptor activation, has been postulated to mediate the pro-arrhythmic effects of the sympathetic nervous system. Thus, a 2 min occlusion of the left circumflex coronary artery was initiated during the last minute of exercise in canines with healed myocardial infarctions (produced by ligation of left anterior descending artery). Fifteen dogs were found to be susceptible to the formation of ventricular fibrillation while 17 animals were resistant. Nine resistant dogs were treated with the phosphodiesterase inhibitor isobutylmethyl xanthine (IBMX, 1 mg/kg) in combination with an infusion of 8-bromo-cAMP (100-150 micrograms/kg/min beginning 45 min prior to exercise). Heart rate and left ventricular dP/dtmax significantly increased, but failed to elicit, arrhythmias during the exercise and ischemia test. Nine resistant animals were also treated with the adenylate cyclase activator forskolin, (100 micrograms/kg), which provoked the same hemodynamic changes as the cyclic AMP infusion but also failed to induce ventricular fibrillation. Both forskolin (n = 3) and IBMX (n = 3) induced large increases in myocardial cAMP levels (control 5.2 +/- 0.5, forskolin 8.1 +/- 0.8 pmol/mg non-collagen protein; control 5.0 +/- 0.8, IBMX 6.8 +/- 0.3 pmol/mg non-collagen protein). Ten resistant animals were treated with the beta-adrenoceptor agonist isoproterenol (1-10 micrograms/kg/min), which failed to cause ventricular fibrillation despite significant increases in the hemodynamic parameters described above. Finally, experiments were repeated after 8-bromo-cAMP infusion and IBMX pretreatment in 8 susceptible animals with pharmacologic denervation (atropine+propranolol+prazosin). In spite of hemodynamic increases indicative of an increase in myocardial cyclic AMP levels, arrhythmias were not re-introduced. These data suggest that changes in cAMP may not be responsible for ventricular fibrillation in this model of sudden cardiac death.
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PMID:Effect of interventions that increase cyclic AMP levels on susceptibility to ventricular fibrillation in unanesthetized dogs. 751 86

We investigated the ability of a newly developed calcium and serotonin (5-HT2) antagonist, nexopamil, to protect the heart from ischemia- and reperfusion-induced myocardial injury. Anesthetized open-chest minipigs were subjected to 1 h left anterior descending coronary artery (LAD) occlusion and 3-h reperfusion. Thirty minutes before occlusion, one group of pigs (n = 7) received nexopamil (0.1 mg/kg intravenously, i.v.) and another group (n = 9) received vehicle. Nexopamil reduced infarct size (IS: tetrazolium stain) from 47 +/- 4% (vehicle) to 21 +/- 7% of the ischemic area (p < 0.05). In nexopamil-treated pigs, this was paralleled by reduced release of creatine kinase (CK) into coronary venous blood. In addition, nexopamil prevented reperfusion-associated myocardial contracture. Nexopamil decreased left ventricular peak pressure (LVPP) and pressure rate index (PRI) immediately before coronary occlusion by 11 and 18%, respectively. Coadministration of methoxamine (2 mg/kg, n = 6) with nexopamil increased LVPP and PRI to values of vehicle-treated pigs but did not prevent reduction in infarct size or CK activity in plasma. During reperfusion, neutrophil granulocytes showed increased formation of reactive oxygen metabolites (chemiluminescence) after stimulation with zymosan. Neutrophil counts in coronary venous blood were significantly reduced at 3 h reperfusion. Both changes were attenuated in nexopamil-treated pigs. Coronary occlusion resulted in increased platelet reactivity in coronary venous blood (collagen-induced aggregation) that was prevented by nexopamil. Nexopamil significantly increased the transcardiac (coronary venous-arterial) concentration gradients of 6-oxo-prostaglandin F1 alpha (PGF1 alpha) without changing thromboxane (B2 (TBX2) concentrations, indicating a selective increase in cardiocoronary PGI2 formation. Nexopamil reduces myocardial injury in reperfused ischemic myocardium. Besides calcium channel blocking activity, inhibition of ischemia-induced neutrophil activation and enhanced endogenous PGI2 formation may be factors contributing to the beneficial effects of nexopamil.
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PMID:Protection of reperfused ischemic pig myocardium by nexopamil, a new combined Ca2+ and serotonin antagonist. 752 84

We tested the hypothesis that acute, intravenous (i.v.) magnesium (Mg2+) supplementation would protect against myocardial stunning in an in situ swine model of regional ischemia and reperfusion and that a concomitant inhibitory effect on platelet aggregation would be elicited. An open-chest model was used, with transient occlusion of the left anterior descending coronary artery (LAD) for 8 min. Regional contractile function was assessed by measuring wall thickening fraction with epicardial Doppler crystals. One control group (n = 6) and two treatment groups were studied: group I (n = 6) received 750 mg MgSO4 before occlusion; group II (n = 6) received 1 g MgSO4 after the occlusion. Both protocols produced significant hypermagnesemia. In group I, platelet aggregation was measured before and after Mg2+ treatment using platelet-rich plasma (PRP) and various agonists (ADP 5 and 10 mM and collagen 1 mg/ml). As compared with controls, both treatment groups experienced significantly less postischemic dysfunction, with systolic function returning more quickly to baseline. Furthermore, platelet aggregation was significantly decreased immediately after Mg2+ infusion. Inhibition of platelet aggregation induced by Mg2+ treatment occurs concomitantly with significant amelioration of postischemic myocardial dysfunction.
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PMID:Effects of magnesium supplementation in a porcine model of myocardial ischemia and reperfusion. 752 43

Acute myocardial infarction can produce alterations in the topography of the left ventricle both in the infarcted and remote areas. These changes as a whole, have been termed ventricular remodelling. Attention has been focused on myocyte alterations due to the remodelling process, but the myocardial wall also contains fibroblasts, which produce collagen and elastin fibers, and endothelial and smooth muscle cells which are the main constituents of the vascular wall. In left ventricular hypertrophy, a form of myocardial remodelling, structural changes of myocytes, cardiac interstitium as well as the coronary microcirculation have been found (vascular remodelling). In vivo, the function of coronary microcirculation can be evaluated by measuring myocardial blood flow and coronary reserve. In fact the study of coronary reserve in patients with left ventricular hypertrophy disclosed microcirculatory dysfunction which probably represents the functional counterpart of the structural changes already described. Positron emission tomography (PET) can noninvasively quantitate myocardial blood flow and coronary reserve in humans. Recently studies with PET disclosed microcirculatory alterations also in patients with coronary artery disease (CAD) in the absence of gross myocardial hypertrophy. In particular, after myocardial infarction, coronary vasodilator capacity has been shown to be impaired not only in the infarcted areas but also in the remote ones subtended by angiographically normal vessels. A blunted coronary reserve has been identified with PET also in remote regions from ischemia in patients with stable angina and single vessel CAD.
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PMID:[Microcirculation and remodelling]. 763 67


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