Improved tolerance to ischemia in hypertrophied myocardium by preischemic enhancement of adenosine triphosphate

Rb, Peyton; P, Van Trigt; Gl, Pellom; Rn, Jones; Jd, Sink; As, Wechsler

doi:10.1016/s0022-5223(19)39508-x

Cited by 33 publications

(2 citation statements)

References 10 publications

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“…12 Likewise interventions that replenish ATP levels after ischemia have been demonstrated to improve myocardial functional recovery after ischemia. 13 In a canine model, Silverman and colleagues 2 created a chronic hypoxia model by anastomosing the left atrium to the pulmonary artery. This study showed no baseline adenine nucleotide differences in hearts of cyanotic versus the acyanotic animals.…”

Section: Discussionmentioning

confidence: 99%

Does the degree of cyanosis affect myocardial adenosine triphosphate levels and function in children undergoing surgical procedures for congenital heart disease?

Najm

Wallen

Belanger

et al. 2000

The Journal of Thoracic and Cardiovascular Surgery

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Section: Discussionmentioning

confidence: 99%

Does the degree of cyanosis affect myocardial adenosine triphosphate levels and function in children undergoing surgical procedures for congenital heart disease?

Najm

Wallen

Belanger

et al. 2000

The Journal of Thoracic and Cardiovascular Surgery

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“…The hypertrophied heart is damaged more rapidly than control hearts when subjected to total ischemia. We (2), as well as others (7,58), have shown that when the hypertrophied heart is subjected to total cessation of blood flow, the time to development of ischemic contracture is shorter than in control hearts. In addition, if reflow is instituted at the time of peak contracture, functional recovery is less and release oflactate dehydrogenase, a cytoplasmic enzyme, is greater (I).…”

Section: Response Of the Hypertrophied Heart To Injurymentioning

confidence: 91%

The Myocardial Cell: Normal Growth, Cardiac Hypertrophy and Response to Injury

Bishop

1990

Toxicol Pathol

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Development and growth of cardiac muscle tissue is controlled by a variety of intrinsic and extrinsic factors. Fetal growth is by hyperplasia, is strongly governed by inherent factors and is only slightly modified by external environmental factors. The number of cell divisions is species-dependent and normally stops shortl~after birth. Developing blood volume and pressure dictate the hypertrophic stage of normal growth, and this may be further modified by abnormal hemodynamic and humoral factors. Connective tissue, neural and vascular components of the myocardium mature along with the myocyte, and alterations in these structures profoundly affect myocyte function. Hypertrophy beyond normal growth is the response of the myocyte by increased protein synthesis to various stimuli including hemodynamic, humoral and ischemic factors. Injury to normal and hypertrophied myocardium may vary due to structural and metabolic adaptations of hypertrophied tissue, such as connective tissue proliferation, vascular supply alterations and glycolytic metabolic potential. Ischemic effects influence not only cell necrosis, but also hypertrophy and congestive myocardial failure.

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Effects of Hypoxia and Ischemia on Intracellular Calcium and Relaxation: Studies in the Aequorin-Loaded Whole Heart Model

Morgan¹,

Harada²,

Meissner³

et al. 1994

Diastolic Relaxation of the Heart

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Improved tolerance to ischemia in hypertrophied myocardium by preischemic enhancement of adenosine triphosphate

Cited by 33 publications

References 10 publications

Does the degree of cyanosis affect myocardial adenosine triphosphate levels and function in children undergoing surgical procedures for congenital heart disease?

Does the degree of cyanosis affect myocardial adenosine triphosphate levels and function in children undergoing surgical procedures for congenital heart disease?

The Myocardial Cell: Normal Growth, Cardiac Hypertrophy and Response to Injury

Effects of Hypoxia and Ischemia on Intracellular Calcium and Relaxation: Studies in the Aequorin-Loaded Whole Heart Model

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