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)

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
 ...
PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

We measured total and regional cerebral blood flow (CBF, rCBF) and cerebral metabolic rate (CMR) of oxygen (O2), glucose (G), and lactate (L) levels for 4 h after 16 min global brain ischemia in rhesus monkeys with and without post-insult thiopental therapy. Eleven monkeys weighing 4-5 kg anesthetized with 1 percent halothane, 66 percent nitrous oxide and 33 percent oxygen, were subjected to 16 min global brain ischemia by a combination of trimethaphan hypotension (to a mean arterial pressure of 50 torr) and a high pressure (1500 torr) neck tourniquet. Post-ischemia, 7 monkeys were untreated (controls) and 4 received thiopental 90 mg/kg infused intravenously over 60 min, beginning at 5 min post-ischemia. Total CBF and rCBF were measured by continuous monitoring of cerebral venous (torcula) and parietal-occipital (external scintillation) 133Xe activity, respectively, after intra-innominate artery injection of 500 micronCi 133Xe in saline. In control monkeys, hyperemia in rCBF, but not in total CBF was observed at 6-7 min post-ischemia, whereas both total CBF and rCBF increased in thiopental treated monkeys. The hyperemia in thiopental treated monkeys coincided with an increase in CMRG without a proportional increase in CMRO2 or lactate levels. Indeed, CMRO2 was depressed in the first 30 min post-ischemia. At 30 min post-ischemia, CMRO2 rose to twofold greater than pre-ischemia in control monkeys, but only to pre-ischemic levels in thiopental treated monkeys. The data suggest that thiopental therapy improves distribution of brain blood flow and brain glucose uptake early post-ischemia and depresses CMRO2 later post-ischemia.
 ...
PMID:Brain blood flow and metabolism after global ischemia and post-insult thiopental therapy in monkeys. 11 95

The effects of ischemia on myocardial adenine nucleotide metabolism and coronary flow during cardiac hypertrophy were studied in 140 rats and 20 guinea pigs, respectively. During increased periods of ischemia, the initially lower ATP contents decreased significantly as did the initially elevated ADP levels, whereas AMP, adenosine, and inosine, and hypoxanthine showed a continually rising elevation compared with the normal hearts. The sum of ATP, ADP, AMP, and their degradation products in the hypertrophied myocardial tissues started to decline after 5 min of ischemia. The remainder was found in the 0.9% NaCl solution in which the rat hearts were incubated, in the form of hypoxanthine, which was the largest fraction, followed by inosine and adenosine, which was the lowest fraction. In normal hearts, these changes occurred only after 60 min of ischemia. The coronary flow of the isolated guinea pig hearts increased significantly with decreasing content of the oxygen gas phase in the Krebs-Henseleit perfusion medium. These changes were more significant in normal than in hypertropheid hearts despite the clear initial elevations of the coronary flow in these hearts at 95% oxygen saturated perfusion, as well as the essential increases of the adenosine content in the myocardial tissues and in the perfusates during the development of the hypoxemia. Consequently, these results significantly demonstrate the curtailed compensation possibilities of hypertrophied hearts for the maintenance of their functions during the development of ischemia in comparison with normal hearts, a factor obviously caused by the ineffecient utilization of their energy supply even without ischemia.
 ...
PMID:Effects of ischemia on adenine nucleotide metabolism and coronary flow during cardiac hypertrophy. 12 92

Regional ischemia results in infarction even in the presence of residual oxidative metabolism. Although glycolytic flux is relatively inhibited at the level of phosphofructokinase, glucose competes more effectively than does free fatty acid for the residual oxygen supply. Glycogen is not the major energy source until effective collateral flow is virtually zero.
 ...
PMID:Estimated glycolytic flux in infarcting heart. 13 60

Uncontrolled hypertension increases the workload of the left ventricle causing the development of hypertrophy and an increase in myocardial oxygen consumption that may precipitate ischemia because of inadequate oxygen delivery related to accelerated coronary atherosclerosis. Control of the hypertension should prevent the further development of hypertrophy, delay the development of fibrosis and possibly also slow the rate of development of atherosclerosis. Furthermore, when myocardial function is impaired because of hypertrophy or other myocardial diseases, the level of blood pressure becomes an important determinant of left ventricular performance. Regardless of the level of arterial pressure, vasodilator drugs that lower arterial pressure may result in marked improvement in left ventricular performance and relief of symptoms of left ventricular failure. Therefore, control of blood pressure in the presence of heart disease may involve treatment of normotensive patients to bring them into a lower normotensive range as well as the more traditional treatment of hypertensives to bring them into the normotensive range. Although this scenario is consistent with conventional wisdom and clinical experience, intricacies of the relationship between hypertension, hypertrophy, myocardial oxygen delivery, atherosclerosis and intramyocardial blood flow distribution remain poorly understood. Until these aspects of the natural history of heart disease are better worked out therapy will remain largely empirical.
 ...
PMID:Heart disease in the hypertensive patient. 14 Feb 80

Myocardial ischemia occurs when there is an imbalance between myocardial oxygen demand and supply, and it is usually entirely or predominantly subendocardial. Animal experiments have shown that relative subendocardial ischemia (a reduced inner:outer flow ratio) can be predicted quite accurately from the ratio of two pressure-time areas:DPTI, the area between diastolic aortic and left ventricular pressures, and SPTI, the area beneath the systolic left ventricular pressure curve. Although the importance of relating supply and demand is obvious, care is needed in applying the results of these animal experiments to man. Recent work has shown that the critical DPTI:SPTI ratio below which subendocardial ischemia occurs is about 0.4 to 0.5 rather than 0.7 to 0.8, as originally reported. On the other hand, the critical ratio may be raised to an unknown extent by myocardial edema or hypertrophy, or by thickened or narrowed coronary arteries. Furthermore, the critical ratio is not independent of absolute coronary diastolic pressure: It is much lower than 0.4 when coronary pressures are high, perhaps because intramyocardial diastolic pressures are much higher than once thought. Further work is required to allow an important physiologic concept to be used in making decisions about patients with heart disease.
 ...
PMID:The myocardial supply:demand ratio--a critical review. 14 25

The article deals with oxidation of different substrates, intensity of glycolytic and glycogenolytic processes in mitochondria and homogenates of dog liver with its 2-hour exclusion from circulation under conditions of endotracheal ether-oxygen narcosis. It was established that already 30-60-minute ischemia causes a decrease in intensity of succinate, alpha-ketoglutarate oxidation and acceptor respiration, inhibiton in the activity of the citrate cycle enzymes; succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, isocytrate dehydrogenase. The activity of NAD-dependent malate dehydrogenasedehydrogenase and Mg2+-ATPase as well as intensity of NADN oxidation in mitochondria increase. After 2-hour ischemia the activity of Mg2+-ATPase, cytochrome oxidase and peroxidase lowers. A sharply developed glycogenolysis is accompanied by inhibition of phosphorylase activity and a two-fold stimulation of the glycolytic reactions. Peculiarities in regulation of enzymatic reactions under conditions of ischemia and their role in origin of metabolism disturbances in the liver are under discussion.
 ...
PMID:[Carbohydrate metabolism in the liver in acute ischemia]. 17 60

Classical forms of degenerative changes of neurocytes, defined by Nissl and Spielmeyer as neuronal diseases were produced experimentally in rats. The individual neuronal changes were induced with the aid of X-ray irradiation, TET administration, ligation of the carotid artery followed by oxygen deficient breathing (anoxia), and by sectioning of the sciatic nerve. The so produced experimental models of neuronal diseases were the subject of morphological and cytochemical studies with special attention payed to enzymic and autoradiographic reactivity. Basing on the results of performed investigations, the author inferred that from a pathogenetic point of view, not all of the respective forms of neuronal diseases postulated by the classification of Nissl and Spielmeyer can be regarded as separate, distinct forms of degenerative changes. From the results obtained it would appear that pathogenetically distinct are only the following diseases: acute nerve cell swelling, shrinkage of perikaryons, homogenizing changes of Purkinje cells and axonal degeneration. The so called severe disease as well as the ischemic disease should be regarded as transitory forms of neuronal changes developing from shrunken neurocytes. It has also been suggested that the pathogenesis of homogenizing changes in Purkinje cells is distinct from that responsible for the development of ischemic changes in the course of cerebral anoxia and ischemia. This suggestion is substantiated by the observed differences in cytoenzymic reactivity between homogenized Purkinje cells and ischemically changed neurocytes.
 ...
PMID:Histochemistry of neuronal degenerative changes. 17 15

Fluorescence emission of reduced nicotinamide adenine dinucleotide (NADH) from the surface of perfused rat hearts was photographed to provide a two-dimensional recording of NADH levels. Sodium Amytal inhibition of NADH oxidation resulted in a homogeneous increase in NADH fluorescence, while lowering perfusion pressure from 55 to 10 torr caused a heterogeneous increase in NADH fluorescence, reflecting the heterogeneous oxygen delivery at this low pressure. Local ischemia resulted in a well-defined region of high NADH fluorescence that corresponded to the region of ischemic inslut. The sharp transition between the ischemic and normoxic areas demonstrated that the hypoxic interface separating the two areas must be quite small.
 ...
PMID:Ischemic areas in perfused rat hearts: measurement by NADH fluorescence photography. 18 43

Using a time-sharing fluorometer-reflectometer, pyridine nucleotide (NADH) and flavoprotein (Fp) fluorescence, as well as reflected light at the excitation wavelength, were measured and correlated with the electrical activity of an awake cerebral cortex. Exposure of the rat to a nitrogen atmosphere (anoxia) led to an increase in signals representing the reduction of pyridine nucleotides and flavins, with very similar kinetics. Inducement of partial ischemia by bilateral carotid artery ligation led to an increase in NADH, accompanied by a very small effect on the electrical activity (ECoG). In most animals, 2-3h after ligation, the ECoG became flat or depressed. Exposure of this ischemic cerebral cortex to KC1 solution caused depression of the electrical activity without metabolic response probably due to the limitation of oxygen supply. The metabolic state of an awake cerebral cortex was identified by exposing the brain to various levels of oxygen, epileptoform activity, spreading depression, hyperbaric pressure of oxygen and an uncoupler. From our results we conclude that the awake cerebral cortex is close to the resting state, state 4, rather than to the active state, state 3.
 ...
PMID:Brain energy metabolism of the conscious rat exposed to various physiological and pathological situations. 18 22


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