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)

In previous reports from this laboratory, we have proposed that stress ulceration complicating hemorrhagic shock results from a gastric mucosal energy deficit due to shock-induced mucosal ischemia. We reasoned that if this hypothesis were correct, an agency known to augment the severity of stress ulceration would be expected to have an adverse effect on gastric mucosal energy metabolism. Others have shown that the severity of stress ulceration developing in animals subjected to hemorrhagic shock is increased by introducing bile salts into the stomach; conversely, the development of stress ulceration can be prevented by ligation of the pylorus or of the common bile duct. We have studied the influence of sodium tauurocholate on the respiration of gastric mucosal mitochondria and on gastric mucosal ATPase. We have also evaluated the influence of the intragastric introduction of taurocholate on the mucosal energy depletion produced by shock. The data presented in this report indicate that taurocholate uncouples oxidative phosphorylation of gastric mucosal mitochondria and inhibits gastric mucosal ATPase. The shock-induced gastric mucosal energy deficit was significantly more severe in the presence of added intragastric taurocholate.
Am J Dig Dis 1976 Dec
PMID:Mechanism of stress ulcer: influence of sodium taurocholate on gastric mucosal energy metabolism during hemorrhagic shock and on mitochondrial respiration and ATPase in gastric mucosa. 13 60

Occlusion of the celiac, superior mesenteric, and inferior mesenteric artery has been studied in 46 patients treated by operation. The condition was acute and was caused by embolic obstruction of the superior mesenteric artery in four cardiac patients and detachment of the inferior mesenteric artery in two patients during removal of infrarenal abdominal aortic aneurysms. The condition was chronic and involved two or all three of the vessels in 40 patient. Embolic obstruction caused severe abdominal pain but few physical signs early in the process,, but the picture of an acute abdomen indicating bowel gangrene developed in a few hours. Ischemia from inferior mesenteric detachment was observed at operation. Patients with chronic obstruction had abdominal pain, weight loss, and diarrhea. Patients with embolic obstruction were treated successfully by embolectomy, and patients developing intraoperative sigmoid ischemia were treated by reattachment of inferior mesenteric arteries to aortic graft. Various procedures were employed in patients with chronic multiple obstruction. However, graft bypass using Dacron tubing was preferable because of its simplicity and because the frequently (48%) associated occlusive disease and aneurysm of the distal aorta were treated at the same time. Confining operation to the abdomen significantly reduced the magnitude of operation and eliminated risks in this age group. Of the 46 patients, 91% survived and were relieved of their symptoms despite associated disease. The 5-year survival rate in this group of patients was 62%.
Surgery 1977 Dec
PMID:Celiac axis, superior mesenteric artery, and inferior mesenteric artery occlusion: surgical considerations. 14 29

Injuries of the major visceral arteries are among the more difficult to manage and rarely occur without serious associated injuries. Sixty-six patients are presented with injuries to the celiac, superior, and inferior mesenteric arteries. Fifty-three injuries resulted from gunshot wounds, nine from stab wounds, and four from blunt trauma. Operative management included vessel ligation in 11 patients, arteriorrhaphy in 43, resection and end-to-end anastomosis in six, Dacron graft interposition in four, and aortic reimplantation in two. Twenty-three patients died, 16 from failure to control hemorrhage. In two patients failure to restore adequate visceral circulation resulted in bowel ischemia and infarction. The successful management of patients with visceral arterial injuries is dependent upon rapid and adequate exposure followed by primary repair or revascularization utilizing available surgical techniques.
Surgery 1978 Dec
PMID:Injuries to the visceral arteries. 15 81

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
J Pediatr 1979 Dec
PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

Although corticosteroids have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure. The few reports regarding the use of steroids in myocardial ischemia have been conflicting. This study was undertaken to determine if a pharmacologic dose of the glucocorticoid methylprednisolone would protect the heart during ischemic cardiac arrest. A randomized double-blind study was performed in 25 dogs. Biochemical and hemodynamic parameters were assessed during and after cardiopulmonary bypass and after 30 minutes of ischemic cardiac arrest. Animals were divided into two groups. Group I served as controls and consisted of dogs injected intravenously with the vehicle of methylprednisolone 18 hours and 1 hour prior to experiment. Group II comprised dogs injected with methylprednisolone, 30 mg. per kilogram, IV, at the same time periods. Blood pH, gases, and electrolytes were measured; aortic, left atrial, and left ventricular pressures were monitored; the first derivative of the left ventricular pressure (dp/dt max.) was also determined. Arterial and coronary sinus blood samples were assayed for lactate levels and activity of the lysosomal enzyme, beta-glucuronidase. Left ventricular muscle was assayed for the nucleotides cyclic adenosine 3',5' monophosphate (AMP) and cyclic guanosine 3',5' monophosphate (GMP). Following restoration of coronary flow, mean aortic and left ventricular systolic pressures and left ventricular contractility as determined by dp/dt max. and dp/dt max./IP were depressed in both groups as expected but were significantly higher in Group II than in Group I (p less than 0.05). An increase in levels of both cyclic nucleotides occurred in each group during ischemia, but this increase in cyclic GMP was significantly greater in Group I (p less than 0.05). beta-glucuronidase activity and myocardial potassium loss as determined in coronary sinus blood were both significantly greater in Group I than in Group II (p less than 0.05). Results of this study demonstrate that pretreatment with a pharmacologic dose of methylprednisolone significantly enhances cardiac recovery after ischemia. Lysosomal membrane stability and modulation of cyclic GMP levels may be critical determinants in the mechanism of cardiac ischemia.
J Thorac Cardiovasc Surg 1975 Dec
PMID:Protective effect of methylprednisolone on the heart during ischemic arrest. 17 23

Reporting 14 own cases symptomatology and treatment of the common ischemic syndromes of the extremities (Volkmann's contracture, thumb adduction contracture respectively contracture of the intrinsic hand muscles and anterior tibial syndrome) including the regularly concomitant nerve lesions are discussed. Edema and compression beyond the primary ischemia are essential factors in pathogenesis of nerve and muscle lesions. The electromyographic examination is helpful in diagnosis, prognosis and treatment of the severe sequelae of nerve and muscle. Since late diagnosis yields poor therapeutical results, early recognition of ischemic states and prophylaxis are most important.
Z Orthop Ihre Grenzgeb 1975 Dec
PMID:[Ischemic contractures of muscle and nerve lesions (author's transl)]. 17 1

By use of highly sensitive radioimmunoassays, 3':5'-cyclic AMP (cAMP) and 3':5'-cyclic GMP (cGMP) were measured in individual layers of light- and dark-adapted rabbit retinas, and the effects of ischemia were determined. In light-adapted retinas, cGMP levels ranged 50-fold, with over 90% of the total concentrated in the photoreceptor cells. The layer of outer segments contained 95 mumol/kg of dry weight, or three times the concentration present in the remainder of the photoreceptor cell layers. By contrast, levels of cAMP varied only 4-fold; the lowest level (6 mumol/kg of dry weight) was found in the outer segment layer and the highest level (22 mumol/kg of dry weight) in the inner segment layer of the photoreceptor cells. Dark adaptation elevated cGMP levels only in retinal layers containing photoreceptor cells, and the greatest proportional increase was observed in the synaptic layer of photoreceptor cells. Dark adaptation also caused increases of cAMP that were restricted to the outer plexiform and outer nuclear layers. Ischemia lowered cGMP levels, but only in retinal layers containing photoreceptor cells, and elevated cAMP levels, primarily in the inner layers of the retina. The effects of ischemia were greater in the dark-adapted than in light-adapted retinas. These results indicate that cGMP and cAMP levels in retina are influenced by the light adaptational state, that ischemia markedly modifies these processes, and that the effects of both light exposure and ischemia are regionally selective.
Proc Natl Acad Sci U S A 1976 Dec
PMID:Distribution of 3':5'-cyclic AMP and 3':5'-cyclic GMP in rabbit retina in vivo: selective effects of dark and light adaptation and ischemia. 18 39

After prelabeling the adenine nucleotides (ATP, ADP, AMP) of isolated perfused guinea pig hearts with either 14C-adenine or 14C-adenosine for 35 min, labeled adenosine, inosine, hypoxanthine and cyclic 3'5'-AMP (cAMP) were continuously released into the cardiac perfusate. Determination of the specific activities (SA) of the adenine nucleotides, cAMP, and their breakdown products (adenosine, inosine, hypoxanthine) in tissue and perfusate revealed: Under steady state conditions the SA of adenosine and cAMP in the perfusate were of the same order of magnitude and proved to be many times higher than the SA of the respective precursor adenine nucleotides. This difference was observed regardless whether adenine or adenosine was used as prelabeling substances. The SA of inosine and hypoxanthine in the perfusate were constantly lower than the SA of adenosine. Cardiac ischemia of 6 min, which resulted in a markedly increased formation of adenosine, led to a pronounced decrease in the SA of adenosine released from the heart. Our findings provide evidence that at least two different adenine nucleotide compartments of the heart severe as precursors for the formation of adenosine and cAMP, one characterized by a high, the other by a lower SA. Under normoxic conditions adenosine and cAMP released into the cardiac perfusate are derived mainly from a nucleotide fraction of high SA, which appears to be rather small. During ischemia a second compartment of much lower SA in addition contributes to the formation of adenosine.
Pflugers Arch 1976 Dec 28
PMID:Compartmentation of cardiac adenine nucleotides and formation of adenosine. 18 85

The rapid i.v. administration of digitalis has recently been shown to cause a substantial increase in coronary vascular resistance in the normal heart. This neurogenically mediated decrease in coronary blood flow would be potentially detrimental if it occurred during ischemia. The present study evaluates the effects of i.v. acetylstrophanthidin and digoxin on coronary vascular resistance during acute global ischemia in 29 dogs anesthetized with chloralose and urethane. Under these conditions, 0.5 mg of i.v. acetylstrophanthidin in 15 dogs resulted in erratic increases in coronary vascular resistance. The peak rise was 12+/-5% above control (P less than 0.01). In 7 of the 15 dogs, the initial erratic rise in coronary vascular resistance culminated in a steep rise associated with acute elevation in left ventricular end-diastolic pressure, which in four dogs terminated in ventricular fibrillation. During the nonischemic control periods, the peak rise in coronary vascular resistance with acetylstrophanthidin was 16+/-1% above control (P less than 0.01). In five dogs, prior alpha adrenergic receptor blockade with phenoxybenzamine prevented the rise in coronary vascular resistance with acetylstrophanthidin during ischemia. Similar erratic increases in coronary vascular resistance were observed with i.v. digoxin (1 mg) during ischemia in three dogs. In two of these dogs, there was a progressive rise in coronary vascular resistance associated with elevation of left ventricular end-diastolic pressure and ventricular fibrillation. The increase in coronary vascular resistance with digoxin during ischemia was abolished with phenoxybenzamine in two additional dogs. Thus, i.v. digitalis in the ischemic heart results in potentially detrimental increases in coronary vascular resistance mediated through alpha adrenergic receptor stimulation.
J Clin Invest 1977 Dec
PMID:Neurogenic coronary vasoconstrictor effects of digitalis during acute global ischemia in dogs. 19 18

The fluorescence of the reduced form of the endogenous pyridine nucleotide nicotinamide adenine dinucleotide was used to map regions of ischemia in cat brain. A remarkably microheterogeneous pattern of increased fluorescence resulted from a critical level of incomplete cerebral ischemia. The fluorescence pattern suggests that ischemia occurs initially in microwatershed zones between penetrating cerebral arteries.
Science 1977 Dec 02
PMID:Regions of cerebral ischemia located by pyridine nucleotide fluorescence. 20 Oct 26


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