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

We compared moderate (29 degrees C.) and profound (5 degrees C.) (ice chips) cardiac hypothermia for myocardial preservation during aortic cross-clamping for 30 or 60 minutes in a canine right heart bypass preparation. Ventricular function deteriorated significantly at 29 degrees C. but not at 5 degrees C. Maximum dp/dt declined only after 60 minutes of ischemia at 29 degrees C., and Vmax decreased after one hour at either temperature. Lactate and pyruvate washout were greater after 29 degrees C., and pyruvate production persisted after 60 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C., and total coronary flow remained elevated after 60 minutes of ischemia at 29 degrees C. Coronary flow distribution was not altered by hypothermia. Ultrastructural changes were primarily time dependent and not temperature dependent. Ice-induced subepicardial injury was not evident in the ultrastructure or by flow distribution. Sixty minutes of profound topical cardiac hypothermia is moderately well tolerated by the canine heart, but functional and structural alterations are evident.
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PMID:Topical cardiac hypothermia for myocardial preservation. 87 Jul 64

The ability of the lung to decrease blood flow to an atelectatic lobe and to increase flow to normal after reinflation was investigated with a model using left lower lobe atelectasis (LLLA) in the dog. The change in the shunt fraction QS/Qt with continuing LLLA was assumed to represent a change in blood flow to the LLL. With LLLA the Qs/Qt rose from 0.112 to 0.172 and then decreased to 0.119 by the end of 2 hours at the rate of -17%/hour. Reversal of atelectasis for varying times demonstrated that the pulmonary vasoconstrictive response persisted for at least 4 hours after reinflation of LLLA. With LLL ischemia for 1 and 2 hours followed by LLLA, Qs/Qt decreased, but at a rate less than the controls, whereas after hemorrhagic shock with venous reinfusion and LLLA, the Qs/Qt did not decrease. When hemorrhagic shock was followed by arterial reinfusion, 60% had a normal response to LLLA; 40% did not. There was no difference in PVR in these two groups. Pulmonary extravascular water in both groups was the same as in controls. Infusion of NE after 3 hours of LLLA caused Qs/Qt to rise from 0.125 to 0.248, comparable to the value immediately after onset of LLLA. EPi had similar results. Catecholamines may restore blood flow to the atelectatic lobe by causing a maximum generalized pulmonary vasocontriction or by overexpansion of the pulmonary blood volume secondary to peripheral vasoconstriction and thereby abolish any differential in pulmonary vascular resistance across the lung. The early hypoxemia of adult respiratory distress syndrome may arise not on the basis of any intrinsic lung pathology but rather as the result of a normal response of the lung to increased catecholamines.
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PMID:The nature of failure of pulmonary adaptation to atelectasis. 87 60

Ischemia in the isolated perfused rat heart resulted in an increase in coronary vascular resistance. Studies were undertaken to determine the effect of hyaluronidase and methylprednisolone on this increase in resistance as well as on glycolytic rate and mechanical function of ischemic hearts. Neither hyaluronidase nor methylprednisolone affected the rate of glucose utilization in working perfused control or ischemic rat hearts. However, both agents prevented a reduction in coronary flow during a 2-hour ischemic period. Associated with the higher coronary flows were higher tissue concentrations of creatine phosphate and lower concentrations of lactate. These agents also prevented accumulation of tissue water in the ischemic hearts. Such changes would appear to be beneficial to the ischemic heart, although mechanical function of post-ischemic hearts was not enhanced by the presence of either hyaluronidase or methylprednisolone. The results, however, suggest that the reduction in myocardial infarct size noted with hyaluronidase and methylprednisolone may be due to their prevention of further reduction of coronary flow in marginally eschemic tissue.
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PMID:Effect of hyaluronidase and methylprednisolone on myocardial function, glucose metabolism, and coronary flow in the isolated ischemic rat heart. 89 Aug 92

Organ perfusion methods offer a number of advantages in biologic studies but require full characterization before application. Two new methods for perfusing rat testes were characterized and compared with recirculating hemicorpus system. These preparations, selective and isolated testicular perfusion, are nonrecirculating and consequently, allow direct measurement of testosterone secretion. In both systems, testosterone production was a fuction of the dose of human chorionic gonadotropin in the perfusion medium up to 1000 mIU per ml which appeared to be inhibitory. The isolated testis method, in comparison with the selective, is more sensitive to human chorionic gonadotropin, requires less perfusion medium, maintains normal blood flow rates and water content, and is associated with no ischemia at commencement of perfusion. However, this system does not retain normal levels of ATP and GTP after 3 hr of perfusion. Whereas both procedures may be used for studies of testosterone secretion and androgen receptors, the inability to maintain testicular ATP and GTP levels indicates that present methods are not suitable for study of processes dependent upon high energy phosphate metabolism.
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PMID:Evaluation of methods for perfusing rat testes. 90 14

The effect of warm ischemia on the transmembrane transport of potassium in dog kidney slices was studied by measurement of the uptake of 42K. The requirement for steady-state conditions concerning the intracellular potassium concentration was thereby studied. The total potassium content in the slices was found to be constant between 120 and 180 min incubation at both 25 and 37 degrees C. The cell water calculated from the total tissue water and 14C-inulin space in the dog kidney slices amounted to 38 ml-100 g wet weight-1 at 37 degrees C and 45 ml-100 g wet weight-1 at 25 degrees C and was found to remain constant for the incubation interval 120--180 min. The major part of the tissue uptake of 42K could be described by one single mono-exponential function under these conditions. The transmembrane influx at 37 degrees C calculated by using a modified Keynes formula amounted to 1.70 mmol K+-kg wet weight-1-min-1 after no warm ischemia and to 0.89 mmol K+-kg wet weight-1-min-1 after 2 h warm ischemia. The corresponding values for incubation at 25 degrees C were 1.26 and 0.77 mmol K+-kg wet weight-1-min-1, respectively. In the slices incubated at 25 degrees C, the potassium content was higher and the sodium content lower than in slices incubated at 37 degrees C.
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PMID:Transmembrane fluxes of potassium in dog kidney slices. A quantitation of the effect of warm ischemia. 92 4

The pathogenesis of acute gastric mucosal lesions produced by distension of the rat stomach was studied. One hour of distension with 0.1 N HCl, but not saline, produced lesions in the glandular stomach in all rats. Histologic studies revealed marked thinning of the mucosa plus thrombus formation in the ulcerated area. Gastric distension with 8 ml HCl (per 100 g body weight) produced severe lesions, 4 ml minimal lesions and 2 ml no lesions. Intragastric pressure in the 8-ml group remained above 110 mm H2O for the first 10 min. Distension with 8 ml acid/100 g body weight for just 10 min resulted in significant lesion formation. Acid distension did not cause generalized disruption of the gastric mucosal barrier to H+ back-diffusion. It appears that an intragastric pressure of over 110 mm H2O for 10 min damages the mucosa by pressure (with thinning) and ischemia (with thrombosis), resulting in decreased resistance to acid peptic digestion and consequent acute lesion formation.
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PMID:Mucosal lesions due to gastric distension in the rat. 93 Sep 7

Reperfusion following myocardial ischemia has been postulated to cause myocardial edema resulting in increasing interstitial pressure and retardation of the microcirculation. If ischemia then is repeated, the additional insult results in increasing edema and possible infarction. In order to test this hypothesis, 15 pigs were placed on cardiopulmonary bypass with coronary perfusion maintained at 100 mm. Hg by a separate pump through the clamped aortic root. Coronary flow and vascular resistance were recorded. Distribution of coronary blood flow was monitored by injection of radioactively labeled microspheres (15 mu). Myocardial extravascular water was measured by simultaneously determining myocardial intravascular water with radioactive iodinated serum albumin (RISA) and total myocardial water with tritiated water (THO). Three 30 minute periods of myocardial ischemia and 5 minutes of coronary perfusion produced (1) a loss of the reactive hyperemic response to ischemia (coronary vascular resistance increased--from 0.295 +/- 0.024, control, to 0.366 +/- 0.042, after anoxia--rather than decreasing with reactive hyperemia induced vasodilatation); (2) a significant maldistribution of coronary flow away from the endocardium (endocardial: epicardial perfusion ratio 1.10 +/- 0.05, control, to 0.69 +/- 0.08, following ischemia, p less than 0.05); and (3) significant myocardial edema. Myocardial extravascular water rose from 46.4 +/- 1.7 ml. per 100 Gm., control, to 52.6 +/- 2.0 ml. per 100 Gm., after ischemia (p less than 0.05), whereas intravascular myocardial volume did not change significantly. Both light and electron microscopic examination of the postischemic myocardium shows interstitial and intracellular edema with typical ischemic changes at a cellular and subcellular level. The significant increase in myocardial extravascular water content associated with this injury supports the concept that myocardial reperfusion plays a role in its development.
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PMID:Myocardial reperfusion, a cause of ischemic injury during cardiopulmonary bypass. 94 Oct 98

A possible protective effect of glucocorticoids on the ischemic myocardium was investigated in in situ dog hearts subjected to regional ischemia and in isolated rat hearts subjected to global ischemia. In the whole-animal preparation, the left anterior descending coronary artery (LAD) was occluded for 3 hours, or for 2 1/2 hours followed by 30 minutes of reperfusion. Dexamethasone phosphate was randomly administered (20 mg. per kilogram intravenously) after 15 minutes of ischemia. Its effects were studied on the following: (1) myocardial cell membrane integrity, using electron microscopic examination of tissue biopsies treated with colloidal lanthanum; (2) myocardial water content, measuring the wet/dry weight of myocardial tissue; (3) ischemic injury, by a count of fuchsinophilic cells at light microscopy. In isolated rat hearts, ischemia was produced by a 60 per cent reduction of coronary flow. Randomized hearts were perfused for 2 hours with dexamethasone, 15 mg. per milliliter in buffered salt solution. Study included determination of tissue water content and coronary vascular resistance. Lanthanum was confined to the extracellular spaces in normal dog myocardium, but it was found all intracellularly after 3 hours of ischemia or after reperfusion. This was associated with morphologic changes characteristic of irreversible cell injury. In the hearts treated with dexamethasone, lanthanum remained excluded from the cells, water content was less (p less than 0.005), and fuchsinophilia less severe (p less than 0.005). Likewise, water content was less (p less than 0.005) and the increase in coronary vascular resistance resulting from ischemia less severe (p less than 0.005) in the dexamethasone-treated isolated rat hearts. Thus dexamethasone administered in pharmacologic doses, early, appeared to stabilize the cell membrane, limit myocardial edema, and reduce the severity of injury, both during ischemia and upon reperfusion.
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PMID:Glucocorticoid protection of the myocardial cell membrane and the reduction of edema in experimental acute myocardial ischemia. 96 99

A study by pulsed NMR techniques in living liver tissue has led to the discovery that the observed longitudinal relaxation decay behavior is strongly multicomponent. After death of the experimental animal, the relaxation decay curves evolve toward a single-component behavior. These changes can also be observed within a few minutes after the liver is excised and placed in a test tube, and they involve a high degree of quantitative and qualitative regularity and reproducibility. An excellent description of all observed NMR behavior is obtained from a dynamic two-compartment model. Rapidly relaxing volumes exchange water molecules with slowly relaxing volumes; associating only an increasing water molecule exchange rate with increasing ischemia accounts in quantitative detail for all observed changes. The exchange-rate values and their variation with tissue deterioration are in good agreement with that estimated for intra- to extracellular water exchange as limited by cell-membrane osmotic permeabilities. Possible applications of these results in different biomedical areas are discussed.
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PMID:NMR relaxation behavior in living and ischemically damaged tissue. 100 99

The perfused rat heart was used to assess the possible contribution of glycolytically produced ATP to the maintenance of the action potential in the normoxic heart, and to the maintenance of membrane integrity in the underperfused, ischemic heart. During normoxia, pyruvate (10 mM) was nearly as able as glucose (10 mM) to maintain the normal action potential. During ischemia (reduction of perfusion pressure of Langerdorff heart from 100 to 20 cm H2O), total tissue values of ATP and creatine phosphate were similar in pyruvate and in glucose hearts. However, pyruvate-perfused hearts had higher tissue levels of cyclic AMP during the ischemic period, and during the reperfusion period they had an increased release of lactate dehydrogenase and an increased incidence of arrhythmias when compared with glucose hearts. It is proposed that these differences can be related to a higher rate of production of glycolytic ATP. The anatomical, biochemical, and pharmacological evidence favoring a cytoplasmic compartment of ATP located in relation to the cell membrane is reviewed.
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PMID:Glycolytic ATP and its production during ischemia in isolated Langendorff-perfused rat hearts. 103 48


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