Year: 1996
Type: dissertation
Abstract: Myocardial ischemia, inadequate coronary perfision relative to demand, is a leading cause of death in North America.Ischemia suppresses the oxidation of glucose and fatty acids and accelerates glycolysis in the cardiomyocytes.One serious consequence of this is the generation of a substantive proton load and the inhibition of transporters which normally serve to negate it in these cells.Epidemiological and experimental evidence indicate that exercise training reduces both the occurrence of ischemia (primary prevention) and the degree of post ischemia myocardial damage (secondary p~evention or rehabilitation).Tne mechanisms for this protective effect, however, are not known.One possibility through which training-induced adaptations may aliow the heart to cope better with an hypoxiclischemic insult is an adaptation in cardiomyocyte H ' handling.A traininginduced increase in H' intracellular buffering capacity (Pi) and/or the activity of N~'-H+ exchanger, a paramount cardiomyocyte pH regulator, may serve as a protective adaptation.The studies in this thesis, therefore, sought to assess if exercise training can induce adaptations in cardiac H' handling.Intracellular buEering capacity (Pi) and the rate of ~a " -& exchange (NHE) using single isolated cardiomyocytes from sedentary control (C) and exercise trained (T) rats were determined.All experiments were conducted in HC03--free Tyrode's solution ( p a 7.4 @ 37•‹C) in myocytes loaded with IS pM of the plTi fluorophore C -S N M -I AM.Cardiomyocyte pHi was determined by exciti~lg the cells at 510 nm and measuring the fluorescent emissions at 580 and 640 nm.Intracellular buffering capacity was determined by exposing the cardiomyocytes to a solution of 20 rnM N&CI, 5 mM BaC12 and 1.5 m M amiloride (A) for 120 s.The [NH4CI], was then sequentially reduced at 120 intervals to 10, 5, 2.5, 1.25, and finally 0 mM NH4CI.Pi was calculated using the equation: Pi= A(Nl&)i/ApHi.To study NHE kinetics, the NM4CI (20 mM) prepulse technique was used both in the presence (+A) and absence (-A) of 1.5 mM I would like to thank the members of my masters committee, Drs.Glenn Tibbits and Wade Parkhouse.Especially to my Senior Supervisor, Dr. Glen Tibbits, I am greatly indebted for his dedication and commitment to this study.I am also gratefid
Source: Summit (Simon Fraser University)
Author: Vennetia R. Danes
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1487473475