Nutritional status, cardiac and hepatic carbohydrate in the infant rat

Heggeness, FW

doi:10.1152/ajplegacy.1968.215.3.644

Cited by 3 publications

(4 citation statements)

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“…It has long been known that liver glycogen is relatively high in the fetus and then rapidly falls during the first 24 h after birth, only to gradually rise again with maturation. The developmental time course for change in liver glycogen that we found is similar to that previously reported in mice and other species (5,20,37). Noteworthy is the close similarity between SWR and BALB/c mice in this regard.…”

Section: Discussionsupporting

confidence: 88%

“…Noteworthy is the close similarity between SWR and BALB/c mice in this regard. These observations contrast with the observed changes in cardiac glycogen and is in keeping with observations by others, indicating that regulation of glycogen metabolism is highly organ specific (18,20,37). It is well known that cardiac glycogen is also elevated in the fetus but, unlike liver glycogen, the postnatal decrease is gradual (37).…”

Section: Discussionsupporting

confidence: 86%

“…Consistent with these past observations, our present findings confirm that cardiac glycogen content is substantially lower in SWR compared with BALB/c weanling mice. Although cardiac glycogen in adult and infant mice was comparable to previously reported values, of particular relevance was the present observation in SWR mice that glycogen reaches a developmental nadir at 21 days and at this point is well below levels previously reported for mice and other species (4,18,20,35,42). Assuming that a critical level of myocardial glycogen may be needed for successful autoresuscitation, such a nadir during maturation could explain the previously documented period of vulnerability ranging from 18 to 23 days of age in SWR mice.…”

Section: Discussionsupporting

confidence: 77%

“…Lateoccurring increases in hypoxic redistribution of perfusion may also increase cardiac efficiency during repeated anoxic exposures (17). Also, it is known that depletion of cardiac glycogen rapidly promotes increased glycogen synthesis (20,29). Glycogen synthesis occurring during the brief recovery periods after autoresuscitation may have been sufficient to compensate for the glycogen metabolized during anoxia.…”

Section: Discussionmentioning

confidence: 99%

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Failure of autoresuscitation in weanling mice: significance of cardiac glycogen and heart rate regulation

Deshpande

Khurana

Hansen

et al. 1999

Journal of Applied Physiology

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"Autoresuscitation" (AR) is the spontaneous recovery from hypoxic apnea by gasping. We examined aspects of heart function in two situations: 1) the maturationally acquired failure of AR that is characteristic of SWR, but not BALB/c, weanling mice and 2) AR failure in BALB/c mice induced by repeated exposures to anoxia. We determined maturational changes in heart and liver glycogen. Unlike liver glycogen levels, heart glycogen levels in SWR mice differed from those in BALB/c mice. They were consistently much lower throughout maturation and reached a nadir during the brief period when SWR weanling mice are vulnerable to AR failure. Also, rate of cardiac glycogen utilization in vulnerable SWR mice was lower than that of same-aged BALB/c mice and was nil during the latter one-half of the gasping stage when heart function is critical for AR success. Therefore, because glycogen utilization reflects cardiac work, heart failure could explain AR failure in SWR weanlings. Additionally, the increase in hypoxic heart rate that occurs with maturation is developmentally delayed in SWR mice, and this may contribute to their AR failure. Cardiac glycogen was not fully depleted in BALB/c mice during repeated anoxic exposures, indicating other reasons for AR failure. We view these findings as a potential model for the age-related peak in incidence of sudden infant death syndrome.

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Section: Discussionsupporting

confidence: 88%