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Oxygen transport across the lifespan of male Sprague Dawley rats
被引:0
作者:
Nugent, William H.
[1
]
Golub, Aleksander S.
[1
]
Pittman, Roland N.
[2
]
Song, Bjorn K.
[1
]
机构:
[1] Song Biotechnol LLC, Baltimore, MD 21030 USA
[2] Virginia Commonwealth Univ, Med Coll Virginia, Dept Physiol & Biophys, Richmond, VA 23298 USA
关键词:
Aging;
Sprag Dawley rat;
Spinotrapezius muscle;
Microcirculation;
Oxygen;
Phosphorescence quenching method;
SKELETAL-MUSCLE;
HEART-FAILURE;
RODENT MODEL;
BLOOD-FLOW;
PRESSURE;
HYPOXIA;
IMPACT;
AGE;
HEMOGLOBIN;
RESPONSES;
D O I:
10.1007/s10522-024-10180-0
中图分类号:
R592 [老年病学];
C [社会科学总论];
学科分类号:
03 ;
0303 ;
100203 ;
摘要:
Human populations are experiencing unprecedented growth and longevity with lingering knowledge gaps of the characteristics, mechanisms, and pathologies of senescence. Invasive measurements and long-term control conditions for longitudinal studies are infeasible, necessitating the need for surrogate animal models. Rats have short lifespans (2-3 years) with translatable cardiovascular systems, and Sprague Dawley microcirculatory preparations are key to studying the oxygen transport mechanisms critical to the loss of skeletal muscle function in aging. Here we present baseline physiological data of 61 male, Sprague Dawley rats at 3, 6, 12, 18, and 24 months of age. Anesthetized animals were surgically prepared for femoral arterial and venous cannulations, tracheal intubation, and exteriorization of the spinotrapezius muscle. Measurements included cardiovascular function, blood gases, and peripheral tissue interstitial oxygen tension (PISFO2) using phosphorescence quenching microscopy. Intrinsic heart rates decreased with age without significant changes to blood pressure. Arterial oxygen tension declined 17% by 18 and 24 Months (p < 0.05) while p(A)CO(2) and PISFO2 were unchanged. Lactate was elevated at 12 and 18 Months along with an alkaline shift in blood pH. Heart rate and decreased p(A)O(2) decoupled from p(A)CO(2) are conserved phenomena in human aging. The continuity of resting PISFO2 despite an anaerobic shift in metabolism may be due to declining mitochondrial function and dysregulation of the vascular response to hypoxemia, which are also present in aged humans. These physiological and microcirculatory data offer a useful experimental model for investigating the detailed changes in oxygen supply and demand that affect senescing skeletal muscles in rats and humans.
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