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Alterations in canine submaximal exe...

Roche, Brian Michael.

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Alterations in canine submaximal exercise VO2-kinetics and neurohormones during the evolution of heart failure produced by rapid ventricular pacing.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Alterations in canine submaximal exercise VO2-kinetics and neurohormones during the evolution of heart failure produced by rapid ventricular pacing./
Author:	Roche, Brian Michael.
Description:	66 p.
Notes:	Source: Dissertation Abstracts International, Volume: 61-05, Section: B, page: 2422.
Contained By:	Dissertation Abstracts International61-05B.
Subject:	Biology, Veterinary Science. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9971627
ISBN:	059976712X

Alterations in canine submaximal exercise VO2-kinetics and neurohormones during the evolution of heart failure produced by rapid ventricular pacing.
Roche, Brian Michael.

Alterations in canine submaximal exercise VO2-kinetics and neurohormones during the evolution of heart failure produced by rapid ventricular pacing. - 66 p.

Source: Dissertation Abstracts International, Volume: 61-05, Section: B, page: 2422.

Thesis (Ph.D.)--The Ohio State University, 2000.

Reduced exercise capacity is a well-known concomitant of heart failure. Rapid ventricular pacing is an often-used method for studying pathophysiology and therapy of heart failure in dogs. Although many hemodynamic and neuroendocrine parameters have been used to quantify the severity (degree) of heart failure, health care professionals consider exercise capacity as a function that correlates strongly with severity of compromise of ventricular function characteristic of heart failure. It is thought that among the parameters of exercise capacity, maximal oxygen consumption, maximal CO2 production and respiratory exchange ration (CO2:O2) at maximal exertion are the most important; but recently investigators have suggested that the rate of achieving a plateau in oxygen consumption while performing 4 minutes of submaximal, constant exercise is a simple and reproducible estimate of aerobic capacity.

ISBN: 059976712XSubjects--Topical Terms:

1021733
Biology, Veterinary Science.

Alterations in canine submaximal exercise VO2-kinetics and neurohormones during the evolution of heart failure produced by rapid ventricular pacing.
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100 1 $a Roche, Brian Michael. $3 1907190
245 1 0 $a Alterations in canine submaximal exercise VO2-kinetics and neurohormones during the evolution of heart failure produced by rapid ventricular pacing.
300 $a 66 p.
500 $a Source: Dissertation Abstracts International, Volume: 61-05, Section: B, page: 2422.
500 $a Adviser: Robert Hamlin.
502 $a Thesis (Ph.D.)--The Ohio State University, 2000.
520 $a Reduced exercise capacity is a well-known concomitant of heart failure. Rapid ventricular pacing is an often-used method for studying pathophysiology and therapy of heart failure in dogs. Although many hemodynamic and neuroendocrine parameters have been used to quantify the severity (degree) of heart failure, health care professionals consider exercise capacity as a function that correlates strongly with severity of compromise of ventricular function characteristic of heart failure. It is thought that among the parameters of exercise capacity, maximal oxygen consumption, maximal CO2 production and respiratory exchange ration (CO2:O2) at maximal exertion are the most important; but recently investigators have suggested that the rate of achieving a plateau in oxygen consumption while performing 4 minutes of submaximal, constant exercise is a simple and reproducible estimate of aerobic capacity.
520 $a The hypotheses of this study were; (1) increasing severity of heart failure, produced by rapid ventricular pacing, results in an increase in time required for oxygen consumption to reach steady state, and (2) to determine the values of neurohormones during progressive increases in rapid ventricular pacing.
520 $a Mature, male hound dogs were instrumented with a programmable pacemaker. The dogs were then exercised at 3.7 mph 8% grade for 4 continuous minutes. Expired gas samples were collected every 10 seconds. Twenty-eight milliliters of blood was drawn at baseline and for each level of pacing for evaluation of neurohormones. Every three weeks the pacemaker's rate was increased (180, 200 and 220bpm) and the dogs were re-evaluated.
520 $a Shortening fraction decreased with each level of pacing. The time to intersection point was not different at any level of pacing, showing a trend of elongation at 220bpm. Atrial natriuretic peptide and norepinephrine increased significantly with each level of ventricular pacing. Dopamine increased with each level of pacing, becoming significant at 200bpm.
520 $a In conclusion, the rapid ventricular pacing model employed in this study induces an evolution of heart failure in dogs.
590 $a School code: 0168.
650 4 $a Biology, Veterinary Science. $3 1021733
650 4 $a Biology, Animal Physiology. $3 1017835
690 $a 0778
690 $a 0433
710 2 0 $a The Ohio State University. $3 718944
773 0 $t Dissertation Abstracts International $g 61-05B.
790 1 0 $a Hamlin, Robert, $e advisor
790 $a 0168
791 $a Ph.D.
792 $a 2000
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9971627