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)

We examined specimens of skin overlying the sacral region, among the most common sites of bedsores, from patients with amyotrophic lateral sclerosis (ALS) and controls, and found that in ALS patients, collagen fibrils had a greater density and became more tightly packed with the duration of illness. Our results suggest that the increased density of collagen fibrils may protect the skin of ALS patients from pressure ischemia, a major cause of bedsore formation.
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PMID:Increased dermal collagen density in amyotrophic lateral sclerosis. 334 11

To evaluate myocardial tissue changes using two-dimensional (2D) echocardiography, several approaches were attempted. 1. Quantitative evaluation of the myocardial echo intensity by computerized image processing in patients with old anteroseptal myocardial infarction: 2D echocardiograms of the parasternal long-axis view were converted to digital images to measure the echo intensity of the regions of interest (ROI) placed in the interventricular septum (IVS), the left ventricular posterior wall (LVPW), the left ventricular cavity, and the pericardium. The mean value of the echo intensity was compared with that of the pericardium (maximum echo intensity) and of the left ventricular cavity as the minimum. In 12 normal subjects, the relative echo intensity of the IVS was 0.40 +/- 0.05 (mean +/- SE), whereas it was 0.71 +/- 0.06 in 11 patients with old MI (p less than 0.001). Color display facilitated the visual recognition of the numerical differences in echo intensities. 2. Evaluation of the myocardial echo intensity in acute phase of myocardial infarction: In nine normal elderly persons, the relative echo intensity of IVS was 0.29 +/- 0.14, and there was no significant change in the early stage (three to seven days) of acute infarction (0.31 +/- 0.14). Two weeks later, however, a significant increase was noted (0.61 +/- 0.10) (p less than 0.01), probably due to an increase in collagen fibers. 3. Changes of the myocardial echo intensity in acute myocardial ischemia: Two-dimensional echocardiograms were recorded in nine open-chest dogs using 3 and 5 MHz transducers before and 10 min, 1 hr, 3 hrs, and 6 hrs after coronary artery ligation. With the 5 MHz transducer, the echo intensity of the ischemic myocardium was decreased after 10 min and was remarkable after 1 hr (0.24 +/- 0.08), and restored in six hrs. These changes could not be detected using the 3 MHz transducer. 4. An in vitro study for assessment of ultrasonic attenuation in the canine infarcted myocardium: The frequency dependency of ultrasonic attenuation of the resected canine myocardium in the frequency region of 2 MHz to 7 MHz was estimated one and two weeks after coronary artery ligation. The distributions of attenuation characteristics were nearly consistent with those of collagen contents determined histologically. In conclusion, we demonstrated that acute and chronic ischemia of the myocardium influences the transmission and reflection of ultrasound. By applying this property, ultrasonic tissue characterization may become a useful tool for detecting myocardial ischemia in the near future.
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PMID:[Ultrasonic tissue characterization in diagnosing myocardial infarction]. 342 30

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.
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PMID:Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy. 343 79

Four patients with pyoderma gangrenosum were treated with hyperbaric oxygen to prepare the wounds for skin grafting. Each wound responded to a course of daily hyperbaric oxygen with reduction of infection and increased capillary angiogenesis. During follow-up periods of 12 to 30 months, all wounds remained healed. Although the exact etiology of pyoderma gangrenosum is unknown, vasculitis with wound ischemia and infection are prominent components. Inspired oxygen partial pressures of 1100 to 1300 mmHg elevate wound oxygen tension despite relative ischemia. The impaired intracellular bacterial killing of hypoxic leukocytes is corrected during each day's 2-hour bolus of hyperbaric oxygen. Daily wound oxygenation increases collagen production by fibroblasts to support capillary angiogenesis.
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PMID:Pyoderma gangrenosum: skin grafting after preparation with hyperbaric oxygen. 354 80

The effects of chronic fluoride excess in the mouse were studied by means of polarizing microscopy in combination with a special staining technique employing Sirius red F3B, a dye which renders collagen fibrils sharply visible. It was observed that changes occur in three renal areas: the interstitium, the intrinsic vasculature and Bowman's capsule. The collagen content of each area increases after about 100 days of the total fluoride exposure of 280 days had elapsed. Although Bowman's capsule was thickened, the glomerular tufts and the nephrons showed edematous swelling and degeneration. A concept is developed to illustrate how early inflammatory response to the chemical effects of fluoride excess leads to vascular injury, parenchymal ischemia and fibrosis.
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PMID:Response of the renal supporting tissues to chronic fluoride exposure as revealed by a special technique. 372 97

Ten weeks old male Sprague-Dawley rats were used. One mg/kg of a calfskin type III collagen was injected into a tail vein under pentobarbital anesthesia, and the electrocardiogram (ECG) was recorded via leads I, II and III for 10 min. Abnormal ECG patterns, i.e., ST-T changes and incidence of arrhythmia, were shown after collagen injection, and some rats suffered cardiac arrest. Oral administration of (E)-7-phenyl-7-(3-pyridyl)-6-heptenoic acid (CV-4151), a thromboxane synthetase inhibitor, at the dose of 10 mg/kg two hr before the collagen injection made the ST-T changes small, and it reduced the incidence of cardiac arrest. The effect of CV-4151 was greater than that of 30 mg/kg of ticlopidine with the same type of treatment. Neither CV-4151 nor ticlopidine had any affect on collagen-induced decreases in the blood platelet count. However, plasma thromboxane (TX) B2 level in the CV-4151-treated group was very low in comparison with those in both the control and ticlopidine-treated groups at 10 min after the collagen injection. These findings indicate that TXA2 may contribute, at least partly, to the collagen-induced ECG changes and indicate that CV-4151 might be a favorable agent for the prevention of TXA2-mediated cardiac ischemia.
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PMID:[Antagonism of collagen-induced ECG changes in rats by a thromboxane synthetase inhibitor, CV-4151]. 375 13

This study was carried out to evaluate the mechanism of action of a reticuloendothelial (RE)-depressing substance. This RE-depressing substance was obtained from the plasma of dogs subjected to 3 hr of intestinal ischemia. RE-depressing substance was partially purified by dialysis and reverse-phase column chromatography. The assay of RE-depressing activity was based on the depression of the rate of clearance of colloidal carbon from the blood of rats or mice. The effect of RE-depressing substance on three other RE system (RES) test particles (gelatinized lipid emulsion, formalinized sheep erythrocytes, and IgM-coated erythrocytes) was determined. RE-depressing substance did not affect the clearance rate or the organ localization of these three test particles. Therefore, RE-depressing substance affected only the clearance of colloidal carbon. Since platelet aggregation has been shown to contribute to the clearance of colloidal carbon, the effect of RE-depressing substance on platelet aggregation was evaluated. RE-depressing substance depressed in vitro platelet aggregation induced by ADP or collagen. It was concluded that the effect of RE-depressing substance on the clearance of colloidal carbon was due to a depression of platelet aggregation rather than to a depression of hepatic macrophage phagocytic function.
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PMID:Reticuloendothelial-depressing substance: studies on the mechanism of action. 386 28

Abnormal myocardial composition in diabetes mellitus has been described, but the effects on ventricular vulnerability have not been defined. We have assessed the susceptibility to arrhythmias in a canine model after 1 yr of mild diabetes induced by alloxan. Since physical conditioning can affect metabolic abnormalities in diabetes, this intervention has also been evaluated. Group 1 served as controls and groups 3 and 4 were diabetic. Animals in the latter group as well as nondiabetic controls of group 2 were exercised on a treadmill for the last 8 mo of the experiment. After 1 yr, anesthesia was induced with chloralose for vulnerability studies. The ventricular fibrillation threshold of 24.4 +/- 1.9 mA in group 3 was significantly less than in normals (45.1 +/- 2.2). Spontaneous arrhythmias were also more prevalent in diabetics during acute ischemia (group 3-A). Increased ventricular vulnerability after epinephrine infusion was present in the sedentary diabetes despite normal ventricular function responsiveness. In a superfused preparation of myocardium, resting membrane potential and action potential amplitude were normal in diabetics, and beta-adrenergic stimulation shortened repolarization more than in controls. Myocardial collagen concentrations, which included an interfibrillar distribution on morphologic examination, were increased in group 3. In the trained diabetics of group 4 the basal vulnerability thresholds and responses to epinephrine were normal. While myocardial collagen levels were normal, cholesterol and triglyceride increments persisted. Thus, in mild experimental diabetes, enhanced susceptibility to arrhythmias exists; this susceptibility may be based on a combination of nonhomogenous collagen accumulation affecting local conduction and increased electrophysiologic sensitivity to catecholamines.
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PMID:Arrhythmia susceptibility and myocardial composition in diabetes. Influence of physical conditioning. 394 64

We studied the effect of nucleus pulposus (NP) on platelet aggregation. Our in vitro experiments showed that NP extract produced platelet aggregation and the addition of collagenase to the NP extract abolished this response. It was further shown that chymopapain did not affect the activity of the extract. We assume that collagen is the active platelet aggregant in the NP extract. Intravascular release of collagen may cause platelet aggregation, vascular obstruction, ischemia, and cord necrosis in a patient with acute transverse myelitis. Intradiskal chymopapain is known to cause transverse myelitis and it is possible that collagen released during the action of the enzyme initiates a similar chain of events.
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PMID:Possible role of collagen in transverse myelitis and chymopapain-induced paraplegia. 396 20

Chronic renal failure and its sequelae, particularly secondary hyperparathyroidism, may be associated with spontaneous quadriceps tendon ruptures. This is a report of two cases of bilateral spontaneous simultaneous quadriceps tendon ruptures in uremia and a review of the literature. The level at which the tendon ruptures is inconstant. Light microscopy reveals nonspecific changes of degeneration and calcification. Under electron microscopy, the structure and maturity of collagen fibers are normal. The ruptures occur in patients younger than 40 years of age who reject medical treatment (i.e. oral phosphate binder) and have long-standing renal disease (mean = 12.3 years). The predisposing causes of rupture are unknown. An abnormality of collagen metabolism, ischemia, direct effects of parathormone, and dystrophic calcification are some of the possible contributory factors.
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PMID:Quadriceps tendon ruptures in uremia. 397 53


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