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

A microscopic histopathological study was done on 500 full-eyelid-thickness surgical specimens: 25 with the diagnosis of senile ectropion and 25 with that of senile entropion. Five different staining techniques were used. There appears to be significantly more orbicularis and Riolan's muscle ischemia, atrophy, and collagen fragmentation with ectropion than with entropion. Entropion shows more septal and tarsal atrophy. In both conditions, the skin and conjunctiva show chronic inflammation and scarring as a constant feature. Statistical significance at the 1% level was present for all six characteristics studied. These histopathological changes, if not etiological, are at least concomitant features differentiating senile ectropion from entropion at the microscopic tissue level.
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PMID:Senile ectropion and entropion: a comparative histopathological study. 5 35

Nine cases of microemboli of arterial origin to the upper extremity are reported. The source of emboli in five of these cases was in the subclavian artery compressed by osseous anomalies in the thoracic outlet. Three aneurysms, one in a subclavian vein graft and two traumatic false aneurysms in the hand, were also noted to be the sources of distal emboli. One unproved case of emboli from an atherosclerotic plaque of the subclavian artery is also reported. Chronicity of symptoms and delay in operation are often noted and lead to difficulties in surgical management. The compressing osseous structures causing the vascular lesion in the thoracic outlet syndrome must be resected, along with removal of the source of emboli. Cervicodorsal sympathectomy is often needed in cases of extensive thrombosis and/or long-standing ischemia. Embolectomy is usually a futile procedure when the main arterial trunk contains old, organized thrombus. Differential diagnostic problems between collagen vascular disease, vasculitis, vasospastic disease, and microembolic disease in cases of unilateral Raynaud's phenomenon are pointed out.
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PMID:Ischemia of the upper extremity due to noncardiac emboli. 56 Jan 30

An ulnar nerve biopsy from a patient with purely neural leprosy of the borderline tuberculoid group, who developed ulnar and median paralysis after 2.5 years of DDS therapy, was examined using light and electron microscopes. The nerve parenchyma was largely replaced by collagen fibrils. There were many onion bulbs similar to those seen in hypertrophic neuropathies. Bizarre fibroblasts such as those seen in hereditary sensory neuropathy were also demonstrated. A few Schwann cells contained M. leprae. It is suggested that considerable proliferation of fibrous tissue may be a reactive phenomenon in response to the continued presence of fragmented M. leprae and their products. Ischemia following a marked progressive increase of intraneural collagen is an important cause of atrophy of Schwann cells followed by segmental demyelination and necrosis of the axons in this healed leprosy patient.
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PMID:Progressive nerve lesion in a disease-arrested leprosy patient. An electron microscopic study. 56 56

Radiation necrosis is a significant complication of surgery for previously irradiated head and neck malignant neoplasms. We used hyperbaric oxygen therapy (HBO) as adjunctive therapy in 52 cases of radiation necrosis. Thirty-nine cases involved the head and neck. Nineteen of 23 cases of osteoradionecrosis of the mandible remain arrested after as much as two years of follow-up. Fifteen of the 16 cases of soft-tissue radionecrosis of the head and neck were successfully managed with HBO therapy as an adjunct to surgery and antibiotics. Fibroblastic proliferation, collagen formation, and capillary budding require at least 20 to 30 mm Hg of wound Po2. This effect can be achieved in wounds that are rendered hypoxic by radiation endarteritis and ischemia with high-dose or hyperbaric oxygenation.
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PMID:Hyperbaric oxygen. A new adjunct in the management of radiation necrosis. 76 Jul 15

From many observations made at autopsy it is apparent that thrombosis in a coronary artery is usually, if not always, associated with rupture of an atheromatous plaque. The sequelae of such rupture include hemorrhage into the plaque with further narrowing of the lumen, formation of an occlusive thrombus or of a non-occlusive thrombus. A developing thrombus in an artery undergoes fragmentation with showering of the distal microcirculation by aggregates of platelets possibly with some admixture of fibrin. In many cases of sudden cardiac death associated with severe atherosclerotic stenosis of the coronary vessels, an occlusive thrombus is not found and the myocardium shows no morphological lesion or else focal patchy early damage in the subendocardial region. One possible mechanism that might explain these findings is microembolism from mural nonobstructing coronary thrombus. Such a mechanism is well established in transient ischemia of the brain and retina related to ulcerated atheroma of the internal carotid artery. Experimental observations indicate that platelet aggregates in the myocardial circulation cause arrhythmias, sudden death, vasculitis, and myocardial ischemic damage. Induction of an occlusive coronary artery thrombus is associated with development of an infarct involving the full thickness of the myocardium. A nonocclusive thrombus is associated with either no myocardial damage or focal subendocardial ischemic injury. It is possible that further aggregation of platelets may facilitate the extension of infarction subsequent to an occlusive event, although there is little evidence on this point. A number of clinical studies show increased platelet reactivity to agents causing aggregation, such as norepinephrine or collagen, in subjects experiencing thromboembolic episodes. It seems unlikely, however, that in vitro tests of platelet function can identify or predict clinical arterial thrombotic disease, although studies of platelet survival and turnover may be more helpful. There is also evidence that platelet survival may be prolonged by drugs having a therapeutic benefit in coronary artery disease and arterial thromboembolism. There is a need for better designed and coordinated clinical trials and for better experimental approaches to explore the relationships among coronary thrombosis, embolsim of the myocardial microcirculation, myocardial ischemia, and sudden death.
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PMID:Platelet aggregation secondary to coronary obstruction. 76 18

The acute and chronic changes produced in canine femoral arteries by ischemia and by perfusion with D10W were examined by light and by scanning electron microscopy. Mild changes of injury characterized by medial and adventitial inflammation and an increase in intimal lining cells occur following 30 minutes of perfusion with return to a normal microscopic appearance within one week. Perfusion for 6 hours produces significant injury to the entire arterial wall, as evidenced by depletion of cells and elastin from the media, replacement with collagen, and eventual fibrosis. The intimal surface is replaced by a layer of spindle cells which appear to originate in the media. The internal elastic membrane is flattened and thrombosis is prominent, particularly in areas where medial fibrosis is severe. Many of the vascular changes produced by perfusion injury may persist for 3 months and some may even by permanent. A period of 6 hours of ischemia also produces similar but less prominent alterations in vascular morphology which return to near-normal appearance within 8 weeks.
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PMID:Serial changes in arterial endothelium following ischemia and perfusion. 85 Aug 70

The pathogenesis of Bell's palsy is presented as retrograde epineurial compression edema with ischemia of the facial nerve. Although the etiology is unknown, an attractive theory is vasospasm, from any cause, along any facial nerve branch, with the chorda tympani, perhaps, the usual primary involvement. Retrograde vascular distension and edema, within the epineurium of the bony facial canal, compresses the nerve from outside its perineurial sheath. The compression force may be mild or severe, resulting in varying degrees of reversible or irreversible ischemic degeneration of myelin sheaths and axons, with varying degrees of cellular reaction to myelin breakdown. The edema may be resorbed, leaving reversible or irreversible nerve damage, or may stimulate collagen formation within the epineurium, with persisting fibrous compression (entrapment) neuropathy of the facial nerve. This concept is consistent with the varying results of Bell's palsy, and depends on the severity and duration of edema, and whether fibrosis occurs within the epineurium of the facial canal. Epineurial fibrosis also results in disturbance of metabolic exchange through the epineurial-perineurial-endoneurial tissues, and may ultimately result in obliteration of vascular drainage. Two temporal bone cases of Bell's palsy, one occurring ten years before death, with residual paralysis, and one two years before death, with clinical recovery, are added to the previously described four cases in the literature, three of early Bell's palsy, and one of remote palsy with almost complete recovery.
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PMID:Pathogenesis of Bell's palsy. Retrograde epineurial edema and postedematous fibrous compression neuropathy of the facial nerve. 88 28

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79

Clinical and experimental studies on primary tendon healing are reviewed and correlated. Emphasis is placed on the importance of blending the extratendinous and intratendinous elements of tendon healing to obtain optimal functional results. Studies which demonstrate the ability of tendon cells to metabolize, proliferate, and secrete collagen when isolated from paratendinous tissue are cited along with those which demonstrate the importance of the microcirculation of the tendon in tendon healing. Those factors which interfere with intratendinous healing are discussed, such as invasive suture techniques, tension on the area of repair, and interference with segmental blood supply within zone II. The importance of the synovial sheath and synovial fluid in nourishing tendon cells and the effect of ischemia in stimulating the ingrowth of adhesions are brought out. Discussion includes such factors involved in the postoperative management of tendon repairs as those which affect the strength of tendon repairs and quantitative and qualitative methods of modifying adhesion formation.
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PMID:Primary tendon healing: a review. 92 31

To determine whether platelets play a part in the pathogenesis of transient cerebrovascular ischemia, we studied 22 patients with transient ischemia, 18 control patients and 38 normal subjects. Platelet aggregation and [14C]-serotonin release by ADP, epinephrine and collagen were normal in all patients, as were plasma coagulation assays, except for shortened partial thromboplastin times in the patients with transient ischemia. Platelet coagulant activities concerned with initiation and early stages of intrinsic coagulation were increased two to three times in 12 patients with transient ischemic attacks with normal serum lipids and normal in the 10 others with Type IV hyperlipoproteinemia. These results indicate an association between platelet coagulant hyperactivity and transient ischemic attacks in a group of patients with normal serum lipids.
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PMID:Platelet coagulant activities and serum lipids in transient cerebral ischemia. 95 87


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