4 edition of Myocardial buffering capacity & hydrogen ion accumulation during global ischemia found in the catalog.
Myocardial buffering capacity & hydrogen ion accumulation during global ischemia
Thesis (M.Sc.) -- University of Toronto, 2001.
|Series||Canadian theses = -- Thèses canadiennes|
|The Physical Object|
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In this cohort study myocardial blood flow values were established for global rest and stress MBF and global MFR for time-efficient 13 NH 3 myocardial PET/CT with residual activity correction in patients without a history of CAD from a regular cohort of cardiac (out) patients who showed no signs of ischemia on the performed 13 NH 3 myocardial Cited by: 4. Myocardial ischemia occurs when the supply of oxygen is inadequate for the metabolic demand of the myocardium. Measurements of myocardial perfusion (O 2 supply) and myocardial oxygen consumption (MVO 2) may provide accurate assessments of this balance in the heart. Two important parameters for oxygen delivery are myocardial blood flow (MBF) and Cited by:
A recent study sought to determine the impact of plasma potassium concentration for patient survival following myocardial infarction. Current guidelines emphasize the importance of avoiding hypokalemia, advising that patients diagnosed with myocardial infarction should be given potassium supplements, if necessary, to maintain serum potassium in. Myocardial infarction (MI) refers to tissue death of the heart muscle caused by ischaemia, that is lack of oxygen delivery to myocardial is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Unlike the other type of acute coronary syndrome, unstable angina, a myocardial infarction occurs when there is cell Causes: Usually coronary artery disease.
Abstract—The hemodynamic abnormalities and neurohumoral activation that accompany congestive heart failure (CHF) might be expected to impair the increase in coronary blood flow that occurs during study was performed to determine the effects of CHF on myocardial oxygen consumption and coronary blood flow during exercise. Coronary blood flow was measured in chronically Cited by: Intracellular proton accumulation. When compared with control, both NKCCC (P during data in Fig. 1 demonstrate that at the end of 40 min of ischemia, pH i was higher in CCC hearts than in control hearts [NKCCC ( ± ) vs. HKCCC ( ± ) vs. control ( ± )]. In terms of pH i, neither cardioplegia Cited by:
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During myocardial ischemia, accumulation of end products from anaerobic glycolysis (hydrogen ions (H(+)), lactate) can cause cellular injury, consequently affecting organ function. The cells'. Calculation of glycolytic rate from 31p spectra during ischemia, when myocardial buffering capacity is known, has been previously described by Wolfe, Gilbert, and BrindleP Glycolytic rates in ischemic perfused rat hearts were confirmed in those studies by using I H spectroscopy to monitor lactate accumulation.
Progressive acidosis is a constant finding in global myocardial ischemia and is associated with reduced myocardial contractility after ischemia. The hypothesis tested in these experiments was that imidazole (pKa = at 37° C), a commonly used buffer in physiology and microbiology, would provide superior buffering capacity when used in lieu of bicarbonate (pKa = at 37° C) in a cardioplegic by: In early myocardial ischemia we find a number of salient electrical and ionic alterations.
This article reviews action potential shortening, K accumulation, and contractile failure. Enhanced K efflux during early myocardial ischemia has been attributed to a number of mechanisms, including: the inhibition of active K uptake, osmotic changes, efflux of K ions linked to anion extrusion, cation Cited by: 8.
The time required for myocardial oxygen utilization to recover from 12 minutes of warm ischemia was studied in 15 sheep. Five control animals had 42 minutes of cardiopulmonary bypass at 37°C with the heart beating and vented.
In 10 experimental animals, the aorta was clamped for 12 minutes during bypass with the heart. Cardioplegia, or myocardial protection — the latter expression is the more precisive one — is a very complex procedure.
It is not only the aim to arrest the heart by suppression of its electrical and mechanical activities, that means ‘cardioplegia’, but to protect the heart against ischemia induced by: 7.
In 2 large clinical trials (Guard During Ischemia Against Necrosis [GUARDIAN] and Evaluation of the Safety and Cardioprotective Effects of Eniporide in Acute Myocardial Infarction [ESCAMI]), no overall clinical benefit was detected after NHE-1 inhibition in acute coronary syndromes.
18,19 A cardioprotective effect was detected after eniporide Cited by: During ischemia and hypoxia, the coronary circulation is unable to deliver metabolic substrates to the heart to support aerobic metabolism. Under these conditions, the heart is able to utilize glycogen (a storage form of carbohydrate) as a substrate for anaerobic production of ATP and.
Hydrogen Sulfide Mitigates Cardiac Remodeling During Myocardial Infarction via Improvement of Angiogenesis. Natia Qipshidze, Naira Metreveli, Paras K. Mishra, David Lominadze, Suresh C.
Tyagi. Departments of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, Kentucky- Introduction. Heart failure (HF) is a frequent complication of myocardial infarction (MI).
Several factors, such as recurrent myocardial ischemia, infarct size, ventricular remodeling, stunned myocardium, mechanical complications, and hibernating myocardium influence the appearance of left ventricular systolic dysfunction with or without clinical HF after MI.
Cited by: Start studying Myocardial ischemia. Learn vocabulary, terms, and more with flashcards, games, and other study tools. sympathetic stimulation may initially cause vasoconstriction, but also increases HR and FOC, resulting in increased myocardial oxygen consumption and autoregulation-induced vasodilation Describe the typical clinical.
Myocardial buffering capacity. Total myocardial buffering capacitycan be defined as the resistance to pH changewhen an acid load isdelivered to or removedfrom the cell.
There are two major components: (1) intrinsic buffering capacity and (2) the capability of the cell to extrude hydrogen ions or import bicarbonate.
Anaerobic. Myocardial hypertrophy has been shown to lead to increased susceptibility to ischemia with accelerated loss of high-energy nucleotides, greater accumulation of H+. Myocardial hypothermia increases autophagic flux, mitochondrial mass and myocardial function after ischemia-reperfusion injury Stefanie Marek-Iannucci 1 Amandine Thomas 1Author: Stefanie Marek-Iannucci, Amandine Thomas, Jean Hou, Annunziata Crupi, Jon Sin, David J.
Taylor, Lawr. Start studying Myocardial Ischemia. Learn vocabulary, terms, and more with flashcards, games, and other study tools. Search. (during exercise?) bpm (decrease myocardial wall stress, decrease myocardial O2 demand decreasing preload) Nitroglycerin.
injury during reperfusion after regional myocardial ischemia and, in particular, on the important role of the polymorphonuclear leukocyte as a primary medi- ator of reperfusion injury due to its capacity to generate reactive species of oxygen.
This study was supported by the National Institutes of Health, Heart. Myocardial injury is common in patients without acute coronary syndrome, and international guidelines recommend patients with myocardial infarction are classified by aetiology.
The universal definition differentiates patients with myocardial infarction due to plaque rupture (type 1) from those due to myocardial oxygen supply-demand imbalance (type 2) secondary to other acute by: A close link between heart failure (HF) and systemic insulin resistance has been well documented, whereas myocardial insulin resistance and its Cited by: Nearly complete brain ischemia during normoglycemia results in selective neuronal destruction and lactate accumulation to a level up to 13 mmol/kg neocortex (Pulsinelli and Duffy, ).
In contrast, equivalent ischemia under hyperglycemic conditions produces necrosis of all tissue elements and lactate accumulation to greater than 19 mmol/kg (Pulsinelli et al., ).Cited by: Estrogen limits intracellular proton accumulation during ischemia.
The data in Fig. 2 are consistent with the hypothesis that acute E2 limits the accumulation of protons in ischemic myocardium (P during by:. The purpose of this study was to measure myocardial buffering capacity and adenosine triphosphate utilization rates in the newborn animal in vivo during hypothermic circulatory arrest and by: 9.After min of global ischemia, myocardial pH decreased to +/- in Group I and +/- in Group II (P less than ).
Blood cardioplegia was most effective during the first hour of aortic cross clamp when myocardial pH rose by +/- pH by: Introduction. After acute myocardial infarction (MI), mortality risk of an individual patient can be estimated at the point of care by clinical risk scores that include variables showing evidence of MI, e.g.
ST-segment deviation and elevated cardiac enzymes, co-morbidities, e.g. renal impairment, or abnormal physiology, e.g. systolic blood pressure and heart rate.
1–3 The degree of left Cited by: