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

Myocardial cationic electrolytes were determined at regular time intervals up to 24 hours after coronary artery ligation in the dog. Replicate electrolyte ratios were computed for different areas of the heart at each time interval. For purposes of statistical analysis, ratios from two border areas and four areas remote from the infarct were pooled as values for ZONE B and ZONE N, respectively, and compared with those from the infarct proper, ZONE I. Ischemia-induced tissue Mg++/Ca++ changes paralleled those of K+/Na+ with respect to time course and zonal variations. In ZONE I, both K+/Na+ and Mg++/Ca++ fell precipitously during the first hour, and the falls became more gradual thereafter, approac hing those of extracellular fluid at 24 hours. Changes in ZONE B, which appeared normal histologically, followed a similar downward trend but differed in magnitude from those in ZONE I (P smaller than 0.01). Changes in ZONE N were small but did not always overlap values in sham-operated dogs. It was concluded that lowered tissue K+/Na+ and Mg++/Ca++ were sensitive, but not specific, indices of myocardial ishemia, and multiple samplings of ionic ratios were essential for proper interpretation of ischemia-induced myocardial electrolyte derangements.
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PMID:Time course and zonal variations of ischemia-induced myocardial cationic electrolyte derangements. 112 91

The mechanism of sodium retention by the kidney in rats with ligation of the common bile duct was studied with micropuncture techniques. 10-14 days after bile duct ligation, rats showed positive sodium balance and ascites formation. Measurements of renal blood flow and glomerular filtration rate yielded values that were not different from those in normal control animals. Likewise, single nephron filtration rte of surface nephrons was the same in the experimental rats as in the controls. Sodium reabsorption, however, was markedly increased in the proximal convoluted tubule, as well as in segments beyond the proximal convolutions. Single nephron filtration fraction, calculated from measurements of efferent arteriolar and arterial hematocrits, was significantly elevated in the cortical nephrons, even though whole kidney filtration fraction was the same as in normal rats. The calculated protein concentration of cortical peritubular blood was higher in the bile duct-ligated rats than in the normal controls. The observations are consistent with the view that sodium retention is the result of enhanced reabsorption primarily by cortical nephrons. The enhanced reabsorption can be accounted for by relative cortical ischemia due to efferent arteriolar vasoconstriction with the consequent elevation of peritubular colloid oncotic pressure.
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PMID:A micropuncture study of renal salt and water retention in chronic bile duct obstruction. 112 34

Twenty-four dogs were divided into five groups. Under pentothal sodium anesthesia, those in the control group received no further manipulation; another group underwent laparotomy only; and dogs in the last three groups had induced pancreatitis, intestinal ischemia and duodenal perforation, respectively. An analysis was made of serum and peritoneal lavage fluid in the dog of each group at 30 minute intervals for four and one-half hours. Parameters which were significantly elevated in dogs with pancreatitis compared with other groups included fluid amylase, lactate dehydrogenase, proteolytic activity and intestinal alkaline phosphatase and serum amylase. We judge that these biochemical differences in the lavage fluid, when taken with the physical characteristics of the fluid and the clinical symptoms, can significantly aid the clinician in arriving at the diagnosis of acute pancreatitis.
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PMID:Use of peritoneal lavage in the diagnosis of experimental acute pancreatitis. 112 80

Previous studies by the author have demonstrated a hyperemia in the lateral funiculus of the Rhesus spinal cord following experimental traumatic spinal cord injury which has sufficient to render the animals permanently paraplegic. This absence of ischemia in the lateral funiculus, coupled with a reappraisal of available data from other investigators, has prompted the author to formulate a theory of primary neuronal dysfunction to explain the observed pathophysiology. It is suggested that the initial injury causes a pathologic biomolecular rearrangemant within the neuronal membrane which interferes with its ability to restrict sodium conductance at rest,nd in effect, makes the membrane nonexcitable.
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PMID:The neuronal theory of experimental traumatic spinal cord dysfunction. 115 48

To assess the effects of sodium nitroprusside (5-10 mug/min) on total and regional cardiac performance, energetics, and lactate metabolism during acute ischemia, studies were performed in 21 open-chest dogs. For studies of regional function and metabolism, length gauges were sutured to the epicardial surface and an epicardial vein adjacent to the artery to be occluded was cannulated. Following occlusion of the left anterior descending coronary artery, cardiac output, mean arterial pressure, epicardial vein blood flow, and systolic shortening of the ischemic segment decreased significantly, In the blood samples from the ischemic zone, but not in those from the coronary sinus, lactate extraction shifted to production. In seven control dogs these alterations persisted throughout the experiment. In 14 animals treated with nitroprusside, cardiac output increased while peripheral resistance and mean arterial pressure decreased. Systolic shortening in the ischemic segment increased from 1.10 +/- 0.24 (SEM) to 1.77 +/- 0.30 mm (P less than 0.005). In eight dogs, regional venous outflow increased from 1.9 +/- 0.1 to 3.0 +/- 0.4 ml/min despite a slight reduction in mean arterial pressure. Concomitantly, regional negative lactate balance was reduced from -61.0 +/- 20.0 to -23.2 +/- 5.7% (P less than 0.05). These results indicate that nitroprusside significantly improves both total cardiac performance and the mechanical performance of regional ischemic myocardium. Moreover, this improvement in mechanical function occurred concomitantly with apparent increase in regional perfusion and reduction in lactate production, suggesting that nitroprusside simultaneously alleviates ischemia.
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PMID:Hemodynamic and metabolic effects of sodium nitroprusside on the performance and metabolism of regional ischemic myocardium;. 115 36

The cortical evoked potential of the two cerebral hemispheres of the cat is taken as the parameter of brain function; its course is studied during strangulation which determines its disappearance, and especially during strangulation release (recovery phase). Under these experimental conditions, the injection of 9% NaCl solution in each carotid does not modify the symmetry of recovery in the two cerebral hemispheres. The unilateral injection of increasing doses of 1,6-dimethyl-8beta-(5-bromonicotinoyl-oxymethyl)-10alpha-methoxyergoline tartrate (nicergoline) (20 to 400 mug) produces more rapid recovery on the treated side. This is also the case for the unilateral injection of 40 mg of sodium malonate. Observation of this effect in the hypoventilated, hypercapnic animal, with an already dilated cerebral network suggests that the mechanism of the protection afforded is not due to vasodilatation of the cerebral network produced by either of the two products. The effect of nicergoline disappears when a previous i.v. injection of sodium malonate has inhibited anoxic depolarization of the cellular membrane and inhibited the fall in cerebral ATP caused by ischemia. It would thus appear that the anti-ischemic properties of nicergoline, acting at the level of the central nervous system, are due to an effect on the cellular membrane or to an inhibiting effect on the metabolism of the brain cell. Supplementary experiments, involving the use of more specific pharmacological reagents should allow its action to be localized at the level of the membrane and/or of cellular metabolism.
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PMID:Study of the protection on afforded by nicergoline against the effects of cerebral ischemia in the cat. 117 43

The subendocardial to subepicardial gradient in the severity of ischemia following acute coronary occlusion is described. The effects of mild, moderate, and severe ischemia on cell structure and function are compared in summary form, and special attention is given to the effects of severe ischemia on myocardial cells. The characteristics of reversible and irreversible ischemic injury are defined in biologic terms. The failure of cell volume regulation in cells which have entered an irreversible state of ischemic injury is demonstrated by the use of free-hand slices in vitro. Irreversibility is associated with structural defects in the plasma membrane and is reflected in an increased slice inulin-diffusible space, increased slice H2O and Na+ content, and failure of the tissue to maintain the high K+ and Mg2+ levels characteristic of normal left ventricular myocardium. Defective cell membrane function is an early feature of irreversible ischemic injury and may be a primary event in the genesis of the irreversible state.
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PMID:Ischemic tissue injury. 118 Mar 31

This study was intended to define the early early electrolyte and water abnormalities of ischemic myocardium in the intact anesthetized dog. We have defined the appropriate circumstances for using 52Cr-ethyelendiamineletraacetate as an extracellular marker during ischemia and have discerned no change in this space at a time when tissue water increments were observed, by 15 min of ischemia. Calculated on the basis of cell dry weight, the cell sodium increment exceeded potassium loss in this early period of ischemia. This is consistent with the view that interference with energy metabolism reduces the pumping of sodium from the cell. The enhanced entry of sodium is associated with a gain of water, initiating events that effect irreversibility.
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PMID:Myocardial cell electrolytes and water during acute ischemia. 120 75

Impaired metabolism interferes with the active extrusion of intracellular sodium and results in intracellular edema. In the brain and regionally in the kidney, elevation of extracellular osmolality is accompanied by a reduction of ischemic cell swelling and improvement of reflow of blood after arterial occlusion. Studies were therefore performed to examine the effect of elevation of extracellular osmolality on ischemic myocardial physiology and by morphologic examination on the extent of acute injury and subsequent necrosis. Under conditions of controlled hemodynamics, administration of hyperosmotic mannitol resulted in improvement of function of the canine heart with regional ischemia, a lessening of the extent of ischemic injury assessed by electrocardiographic ST segment mapping, and improved total and collateral blood flow. Metabolic studies under conditions of controlled hemodynamics revealed that hyperosmotic mannitol reduced the myocardial oxygen requirement of the ischemic heart. Mannitol dilated large collateral conductance vessels in addition to improving blood flow through the region of myocardial ischemia. Under conditions of ischemia induced by a prolonged reduction in coronary perfusion, hyperosmotic mannitol attenuated the progressive rise in vascular resistance. Direct morphologic examination of areas of myocardium subjected to total interruption of blood flow followed by reflow of blood revealed swelling of both myocardial and capillary endothelial cells early during the reflow period. The extent of swelling was substantially reduced with elevation of the extracellular osmolality with mannitol. Simarilty, osmolality elevation strikingly reduced the extent of eventual myocardial necrosis following prolonged periods of reflow of blood.
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PMID:Effects of hyperosmotic mannitol in reducing ischemic cell swelling and minimizing myocardial necrosis. 125 68

Studies on animals implicating reflux of bile salts in formation of "stress ulcer" often are suspect because of the inordinately high intragastric concentrations of bile salts used to induce experimental acute gastric mucosal damage. We studied reflux of bile salt in 11 patients after operation. Nine refluxed bile salts in a mean intragastric concentration of 1.87 +/- 0.24 mM. (range, 0.34 to 4.88 mM.). In the present study, therefore, the ulcerogenic potential of physiologic concentrations of bile salts was evaluated. With use of vascularized, chambered canine gastric mucosa, groups of animals were studied during three consecutive periods. Group A = topical acid test alone (ATS) during periods 1, 2, and 3; Group B = (1) ATS, (2) ATS, (3) ATS + vasopressin (VP = 0.1 U per Kg.-min. via the splenic artery); Group C = (1) ATS, (2) ATS + topical 1 mM. sodium taurocholate (TC), (3) ATS + 1 TC + VP; Group D = (1) ATS, (2) ATS + 2 TC, (3) ATS + 2 TC + VP; Group E = (1) ATS (2) ATS + 5 TC, (3) ATS + 5 TC + VP. Parameters evaluated were (1) net fluxes H+, Na+; (2) electrical potential difference (PD); (3) clearance of aminopyrine, a measure of mucosal blood flow (MBF); and (4) formation of lesions, graded zero to six by an independent observer who used photographs. In nonischemic mucosa, bile salts produced no ulcers, a significant concentration-dependent increase in H+ "back diffusion" and fall in PD, and a noncentration-dependent increase in MBF. In ischemic mucosa, the combination of topical acid, topical bile salts, and mucosal ischemia was acutely ulcerogenic. The severity of mucosal injury was dependent on the concentration of bile salt (y = 0.108 + 1.53x, r = 0.90, p less than 0.01). These data indicate that acute mucosal damage occurs in the presence of physiologic concentrations of bile salt, i.e., those routinely found in the gastric contents of postoperative patients.
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PMID:Acute gastric mucosal ulcerogenesis is dependent on the concentration of bile salt. 127 70


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