Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since sub-endocardial ischemia is the consequence of a discrepancy between the blood demand and supply of oxygen at this level, the study of the myocardial performance by the measurement of the endocardial viability ratio (E.V.R.) is both useful and possible during anesthesia. E.V.R. is the ratio between the oxygen supply and demand of the myocardium. It is equal to the diastolic pressure time index (D.P.T.I.) over the tension time index (T.T.I.). Measurements are made at different times, by means of the arterial pressure and the left atrial pressure, as well as with the Datascope-E.V.R. Computer. During gradual morphine administration (0.5-1-1.5 mg/kg) and if no major surgical stress occurs, E.V.R. remains excellent and stable (1.46 - 1.48 - 1.43). It deteriorates more or less (1.29 - 1.09) during tachycardia or hypertension. Within the hour following the end of extracorporeal circulation, E.V.R. significantly improves (1.04 - 1.06 - 1.09 - 1.23). Although E.V.R. measurement is easy during cardiac surgery, it is impossible to carry out in case of arrhythmia. While morphine anesthesia induces no variation in E.V.R., tachycardia or hypertension require the addition of therapeutic drug. Within one hour following the end of extra-corporeal circulation, E.V.R. measurement shows improved endocardial viability, although the hemodynamic parameters undergo no significant change.
Acta Anaesthesiol Belg 1978 Dec
PMID:Measurement of endocardial viability ratio (E.V.R.) during anesthesia for cardiac surgery. 75 39

Preservation of left ventricular function with various potassium-based cardioplegic solutions has been considered to be effective for at least 60 minutes during occlusion of the ascending aorta. The purpose of this study was to define the limits of protection offered by potassium alone. A single bolus of 150 ml of potassium (24 mEq per liter) in normal saline solution at 30 degrees C was injected in the aortic roots of foxhounds at the initiation of periods of 45 minutes, 60 minutes, and 75 minutes of aortic occlusion at a core temperature of 30 degrees C. Data derived from postischemic recovery phase ventricular function curves and force-velocity relations demonstrated excellent protection during 45 minutes of ischemia, inconsistent protection at 60 minutes, and poor protection at 75 minutes.
Ann Thorac Surg 1978 Dec
PMID:Limits of myocardial protection with potassium cardioplegia. 75 64

Six weeks after placement of an ameroid constrictor on the circumflex coronary artery, blood flow in a collateral region was compared with flow in myocardium supplied by normal arteries during cardiopulmonary bypass (80 mm Hg). Myocardial blood flow was determined using radionuclide-labeled microspheres (8 to 10 mu) before 10 minutes of ischemic arrest and after 1, 5, and 10 minutes of reperfusion. The retrograde circumflex pressure was monitored continuously and served as an additional index of perfusion of the collateral region. During reperfusion, endocardial flow in the collateral region remained unchanged despite a threefold increase in a similar layer having normal arteries (p less than 0.01). Following ischemic arrest, mean transmural and subendocardial hyperemic responses both persisted for longer than 10 minutes in normal regions. Simultaneously, peripheral circumflex pressures decreased at 1 and 5 minutes of reperfusion (p less than 0.001) but returned to control within 10 minutes. Persistently elevated endocardial flow in the normal arteries and the absence of a hyperemic response in the collateral region during an associated decrement in retrograde circumflex pressure may indicate incomplete flow repayment even after 10 minutes of reperfusion. Marked transmural flow imbalances despite adequate coronary perfusion pressures suggest that intermittent ischemic arrest may cause cumulative ischemia, and this occurrence may be detrimental especially in collateral regions of myocardium.
Ann Thorac Surg 1978 Dec
PMID:The effects of intermittent ischemic arrest on the perfusion of myocardium supplied by collateral coronary arteries. 75 65

The metabolic consequences of low-temperature kidney preservation were investigated. A comparison was made between kidneys which were immediately preserved and kidneys which had been ischemic for 1 hour. Two types of preservation techniques were used: (1) continuous perfusion with oxygenated plasma as described by Belzer and (2) a single flush with potassium-containing perfusate as suggested by Collins. Slices of renal cortex were removed at varying times during preservation and analyzed for a variety of metabolic intermediates. ATP levels were markedly reduced from normal. The Belzer technique was associated with higher ATP levels and ischemia lowered the ATP level. Kidneys perfused by the Belzer technique had lower ADP levels than those by the Collins method. Preservation caused marked elevation of tissue lactate, irrespective of ischemia or the technique used. We conclude that low temperature kidney preservation has profound effects on cellular metabolism. Therefore, the measurement of metabolic intermediates may provide a rational approach to the prediction of organ survival.
J Lab Clin Med 1976 Dec
PMID:Metabolic consequences of low-temperature kidney preservation. 79 69

Stress ulcers are multiple, superficial erosions which occur mainly in the fundus and body of the stomach. They develop after shock, sepsis, and trauma and are ofter found in patients with peritonitis and other chronic medical illness. Stress ulcers should be differentiated from reactivation of chronic duodenal or gastric ulcers. Cushing's ulcer following head injury, or drug-induced gastritis. Digestive symptoms are usually absent, hemorrhage is the most common manifestation, and perforation and obstruction are rare. The presence of luminal acid and ischemia are necessary for the production of stress ulcer, while disruption of the gastric mucosal barrier by refluxed duodenal content may contribute to the pathogenesis. Endoscopy is the mainstay of the diagnostic procedure, and angiography should be used if endoscopy fails to identify the bleeding lesions. Medical management should include volume replacement, nasogastric aspiration, and the use of antacid. Selective intraarterial infusion of pitressin has shown encouraging preliminary results. Surgical treatment is reserved only for those patients who continue to bleed despite all medical management. The operation of choice is open to question. We prefer vagotomy, pyloroplasty, and oversewing the ulcers as an initial operation. Since the result of all forms of therapy has been poor, it seems resonable to try to prevent ulcer development. The use of vitamin A, hyperalimentation, and growth hormones is still in an experimental stage. Large clinical studies with case control are necessary before recommendations can be made. The use of potent and frequent antacid to buffer the gastric content has shown promising results; however, these observations need to be confirmed in a properly controlled and randomized study.
Surg Clin North Am 1976 Dec
PMID:Stress ulcers: their pathogenesis, diagnosis, and treatment. 79 64

Bilateral cervical autotransplantation of canine kidneys is described for comparative study of renal preservation techniques. Data are obtained from kidneys preserved by (1) initial intravascular flushing with modified Collins' C3 solution (Ursol) followed by cold storage, and (2) pulsatile perfusion (MOX 100). Preharvest condition of the donor and ischemia times are identical, thus eliminating major sources of potential data variation. Renal function studies performed at periodic intervals demonstrated better initial function for machine preservation but no difference after one to two-month period.
Urology 1976 Dec
PMID:Bilateral cervical transplantation of canine kidneys for study of canine renal preservation. 79 40

The free fatty acid (FFA) and triacylglycerol content and composition are compared in the mouse and toad brain during ischemia. Mouse brain FFA are rapidly increased after decapitation, the maximal production rates being attained within the first minutes. Free arachidonic and stearic acids undergo the highest increases, followed by palmitic, oleic and docosahexaenoic. In contrast, toad brain FFA only changes significantly several hours after decapitation. Triacylglycerols remain virtually unmodified in the amphibian brain during ischemia, whereas in the mammal they are partially decreased, reaching a nearly steady level at about 10 min. This triglyceride breakdown may represent a part, but cannot account for all the changes taking place in FFA. Uneven contributions to the FFA are shown for their counterparts in triacylglycerols. Although the neutral glycerides could be the source of free palmitic acid, they are not responsible for the increases in arachidonic and stearic acids. It is suggested that FFA mainly arise from polar lipid deacylation and a relationship is suggested between the slowness of FFA changes and the higher resistance of poikilotherms to oxygen deprivation.
Brain Res 1975 Dec 12
PMID:Differential lipid deacylation during brain ischemia in a homeotherm and a poikilotherm. Content and composition of free fatty acids and triacylglycerols. 81 Feb 21

The pars convoluta of the proximal tubules of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of complete ischemia produced by clamping of the aorta. The same ischemia periods were also examined after 24 hrs of blood reflow. It was found that the vast majority of the cells of pars convoluta survived 60 min of ischemia as seen after 24 hrs of reflow. The following pattern of changes were observed at time intervals up to 60 min: progressive clumping of chromatin, progressive distortion of microvilli with bleb formation, increasing dilatation and finally vesiculation of rough-surfaced endoplasmic reticulum and initially condensation and later high amplitude swelling of mitochondria. It is concluded that these subcellular changes are compatible with cell survival. Also tubule cells containing swollen mitochondria with small flocculent densities are potential candidates for survival. 120 min of ischemia was associated with marked mitochondrial swelling with large flocculent densities, severe cell damage and necrosis and was not compatible with cell survival. A working hypothesis is presented relative to the pathogenesis of acute renal failure caused by complete ischemia.
Virchows Arch B Cell Pathol 1975 Dec 19
PMID:Studies on the pathogenesis of ischemic cell injury. II. Morphological changes of the pars convoluta (P1 and P2) of the proximal tubule of the rat kidney made ischemic in vivo. 81 77

The pars recta of the proximal tubule of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of ischemia produced by clamping of the aorta. Also the effects of 24 hrs of blood reflow following the same ischemia periods were determined. The maximal changes occurring after ischemic periods of up to 60 min included: marked cell swelling, swelling of the inner compartments of the mitochondria, swelling of the endoplasmic reticulum and of microvilli, pronounced chromatin clumping in the nuclei and distortion of the Golgi apparatus. These cell changes were reported to be reversible in the previous paper of this series. After 24 hrs of blood reflow it was found that with increasing periods of primary ischemia, ranging from 15 to 120 min, an increasing number of pars recta tubules cells were undergoing necrosis. Theses findings indicate that some additional mechanism other than the initial ischemia per se must be responsible for the progressive cellular damage leading to the necrosis. This is in contrast to the pars convoluta of the proximal tubule, which does not undergo further degenerative changes after the primary ischemia has been ended. The "no reflow" phenomenon may satisfactorily explain the necrosis seen in the pars recta segments following various periods of ischemia after 24 hrs of arterial renal reflow.
Virchows Arch B Cell Pathol 1975 Dec 19
PMID:Studies on the pathogenesis of ischemic cell injury. III. Morphological changes of the proximal pars recta tubules (P3) of the rat kidney made ischemic in vivo. 81 78

Rat pancreatic slices were incubated at 37 degrees C in vitro, in order to determine if complete ischemia would reproduce the subcellular alterations seen in human pancreatic acinar cells following shock. The ultrastructural alterations observed were similar to those seen in humans and in animal models of hypovolemic shock. These changes ranged from dilated endoplasmic reticulum and swollen mitochondria (reversible changes) to mitochondrial flocculent densities and later stages (evidence of cell death). In this in vitro study the pancreas remained in an apparently reversible stage longer than liver, heart, kidney, and brain treated similarly. However, once the pancreatic cells died, necrotic breakdown occurred very rapidly, perhaps due to intracellular release of lysosomal and zymogen granule hydrolases.
Virchows Arch B Cell Pathol 1975 Dec 19
PMID:Cellular and subcellular effects of ischemia on the pancreatic acinar cell: in vitro studies of rat tissue. 81 79


<< Previous 1 2 3 4 5 6 7 8 9 10