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Am J Physiol Regul Integr Comp Physiol. 2015 Dec 15;309(12):R1512-20. doi: 10.1152/ajpregu.00380.2015. Epub 2015 Oct 14.

Microvascular oxygen partial pressure during hyperbaric oxygen in diabetic rat skeletal muscle.

Author information

1
Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Tokyo, Japan;
2
Clinical Center for Sports Medicine and Sports Dentistry, Hyperbaric Medical Center/Sports Medicine Clinical Center, Medical Hospital of Tokyo Medical and Dental University, Tokyo, Japan;
3
Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan; and.
4
Departments of Anatomy & Physiology and Kinesiology, Kansas State University, Manhattan, Kansas.
5
Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Tokyo, Japan; kano@pc.uec.ac.jp.

Abstract

Hyperbaric oxygen (HBO) is a major therapeutic treatment for ischemic ulcerations that perforate skin and underlying muscle in diabetic patients. These lesions do not heal effectively, in part, because of the hypoxic microvascular O2 partial pressures (PmvO2 ) resulting from diabetes-induced cardiovascular dysfunction, which alters the dynamic balance between O2 delivery (Q̇o2) and utilization (V̇o2) rates. We tested the hypothesis that HBO in diabetic muscle would exacerbate the hyperoxic PmvO2 dynamics due, in part, to a reduction or slowing of the cardiovascular, sympathetic nervous, and respiratory system responses to acute HBO exposure. Adult male Wistar rats were divided randomly into diabetic (DIA: streptozotocin ip) and healthy (control) groups. A small animal hyperbaric chamber was pressurized with oxygen (100% O2) to 3.0 atmospheres absolute (ATA) at 0.2 ATA/min. Phosphorescence quenching techniques were used to measure PmvO2 in tibialis anterior muscle of anesthetized rats during HBO. Lumbar sympathetic nerve activity (LSNA), heart rate (HR), and respiratory rate (RR) were measured electrophysiologically. During the normobaric hyperoxia and HBO, DIA tibialis anterior PmvO2 increased faster (mean response time, CONT 78 ± 8, DIA 55 ± 8 s, P < 0.05) than CONT. Subsequently, PmvO2 remained elevated at similar levels in CONT and DIA muscles until normobaric normoxic recovery where the DIA PmvO2 retained its hyperoxic level longer than CONT. Sympathetic nervous system and cardiac and respiratory responses to HBO were slower in DIA vs. CONT. Specifically the mean response times for RR (CONT: 6 ± 1 s, DIA: 29 ± 4 s, P < 0.05), HR (CONT: 16 ± 1 s, DIA: 45 ± 5 s, P < 0.05), and LSNA (CONT: 140 ± 16 s, DIA: 247 ± 34 s, P < 0.05) were greater following HBO onset in DIA than CONT. HBO treatment increases tibialis anterior muscle PmvO2 more rapidly and for a longer duration in DIA than CONT, but not to a greater level. Whereas respiratory, cardiovascular, and LSNA responses to HBO are profoundly slowed in DIA, only the cardiovascular arm (via HR) may contribute to the muscle vascular incompetence and these faster PmvO2 kinetics.

KEYWORDS:

Type 1 diabetes; phosphorescence quenching; streptozotocin; tibialis anterior muscle

PMID:
26468263
DOI:
10.1152/ajpregu.00380.2015
[Indexed for MEDLINE]
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