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Severe blunt muscle trauma in rats: only marginal hypoxia in the injured area.

Funk K, Scheerer N, Verhaegh R, Pütter C, Fandrey J, de Groot H - PLoS ONE (2014)

Bottom Line: Directly after trauma and until the end of experiment (480 minutes), microvascular blood flow and relative hemoglobin amount were clearly increased.In contrast to blood flow and relative hemoglobin amount, there was no immediate but a delayed increase of microvascular hemoglobin O2 saturation.This increased O2 supply is obviously sufficient to ensure normoxic (or even hyperoxic) conditions in the vast majority of the cells.

View Article: PubMed Central - PubMed

Affiliation: University of Duisburg-Essen, Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany.

ABSTRACT

Background: After severe muscle trauma, hypoxia due to microvascular perfusion failure is generally believed to further increase local injury and to impair healing. However, detailed analysis of hypoxia at the cellular level is missing. Therefore, in the present work, spectroscopic measurements of microvascular blood flow and O2 supply were combined with immunological detection of hypoxic cells to estimate O2 conditions within the injured muscle area.

Materials and methods: Severe blunt muscle trauma was induced in the right Musculus gastrocnemius of male Wistar rats by a standardized "weight-drop" device. Microvascular blood flow, relative hemoglobin amount, and hemoglobin O2 saturation were determined by laser Doppler and white-light spectroscopy. Hypoxic cells were detected by histologic evaluation of covalent binding of pimonidazole and expression of HIF-1α.

Results: Directly after trauma and until the end of experiment (480 minutes), microvascular blood flow and relative hemoglobin amount were clearly increased. In contrast to blood flow and relative hemoglobin amount, there was no immediate but a delayed increase of microvascular hemoglobin O2 saturation. Pimonidazole immunostaining revealed a hypoxic fraction (percentage area of pimonidazole-labelled muscle cells within the injured area) between 8 to 3%. There was almost no HIF-1α expression detectable in the muscle cells under each condition studied.

Conclusions: In the early phase (up to 8 hours) after severe blunt muscle trauma, the overall microvascular perfusion of the injured area and thus its O2 supply is clearly increased. This increased O2 supply is obviously sufficient to ensure normoxic (or even hyperoxic) conditions in the vast majority of the cells.

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Effect of local blunt muscle trauma on microvascular blood flow, relative hemoglobin amount and hemoglobin O2 saturation.Animals (n = 8) were ventilated with 100% O2. Parameters were determined immediately before trauma (base values, base), 1–2 minutes after trauma (0) and every 40 minutes until the end of the experimental period. flow, microvascular blood flow (A); rHb, relative hemoglobin amount, representing blood filling of microvessels (B); SO2, microvascular hemoglobin O2 saturation (C); AU, arbitrary unit; trauma, injured area of traumatized muscle; contralateral, respective area of the contralateral non-traumatized muscle. Values shown represent means ± SEM. *P<0.05 (versus base). #P<0.05 (versus contralateral; significant to all post trauma time points of flow and rHb except for flow at time point 160 minutes; not significant for SO2, but post-hoc t-tests reveal significant differences between the groups for the time points 200 and 240 minutes).
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pone-0111151-g002: Effect of local blunt muscle trauma on microvascular blood flow, relative hemoglobin amount and hemoglobin O2 saturation.Animals (n = 8) were ventilated with 100% O2. Parameters were determined immediately before trauma (base values, base), 1–2 minutes after trauma (0) and every 40 minutes until the end of the experimental period. flow, microvascular blood flow (A); rHb, relative hemoglobin amount, representing blood filling of microvessels (B); SO2, microvascular hemoglobin O2 saturation (C); AU, arbitrary unit; trauma, injured area of traumatized muscle; contralateral, respective area of the contralateral non-traumatized muscle. Values shown represent means ± SEM. *P<0.05 (versus base). #P<0.05 (versus contralateral; significant to all post trauma time points of flow and rHb except for flow at time point 160 minutes; not significant for SO2, but post-hoc t-tests reveal significant differences between the groups for the time points 200 and 240 minutes).

Mentions: Immediately after trauma, blood flow in the injured area significantly increased (compared to base) from 134 AU to 208 AU. It continued to rise slightly up to 255 AU at 240 minutes after trauma and remained elevated around this value until the end of the experiment at 480 minutes (shown for the first 240 minutes in Figure 2A). Parallel to the rise in blood flow, there was an immediate significant increase from 67 AU to 104 AU in the relative hemoglobin amount, which persisted at this level for the whole experimental period (shown for the first 240 minutes in Figure 2B). In contrast to both other microvascular parameters, directly after trauma the microvascular hemoglobin O2 saturation was similar to baseline values (approximately 80%). However, 200 minutes after trauma, the microvascular hemoglobin O2 saturation reached a significant increase (to 91%) and remained elevated until the end of experimental period (shown for the first 240 minutes in Figure 2C).


Severe blunt muscle trauma in rats: only marginal hypoxia in the injured area.

Funk K, Scheerer N, Verhaegh R, Pütter C, Fandrey J, de Groot H - PLoS ONE (2014)

Effect of local blunt muscle trauma on microvascular blood flow, relative hemoglobin amount and hemoglobin O2 saturation.Animals (n = 8) were ventilated with 100% O2. Parameters were determined immediately before trauma (base values, base), 1–2 minutes after trauma (0) and every 40 minutes until the end of the experimental period. flow, microvascular blood flow (A); rHb, relative hemoglobin amount, representing blood filling of microvessels (B); SO2, microvascular hemoglobin O2 saturation (C); AU, arbitrary unit; trauma, injured area of traumatized muscle; contralateral, respective area of the contralateral non-traumatized muscle. Values shown represent means ± SEM. *P<0.05 (versus base). #P<0.05 (versus contralateral; significant to all post trauma time points of flow and rHb except for flow at time point 160 minutes; not significant for SO2, but post-hoc t-tests reveal significant differences between the groups for the time points 200 and 240 minutes).
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4215885&req=5

pone-0111151-g002: Effect of local blunt muscle trauma on microvascular blood flow, relative hemoglobin amount and hemoglobin O2 saturation.Animals (n = 8) were ventilated with 100% O2. Parameters were determined immediately before trauma (base values, base), 1–2 minutes after trauma (0) and every 40 minutes until the end of the experimental period. flow, microvascular blood flow (A); rHb, relative hemoglobin amount, representing blood filling of microvessels (B); SO2, microvascular hemoglobin O2 saturation (C); AU, arbitrary unit; trauma, injured area of traumatized muscle; contralateral, respective area of the contralateral non-traumatized muscle. Values shown represent means ± SEM. *P<0.05 (versus base). #P<0.05 (versus contralateral; significant to all post trauma time points of flow and rHb except for flow at time point 160 minutes; not significant for SO2, but post-hoc t-tests reveal significant differences between the groups for the time points 200 and 240 minutes).
Mentions: Immediately after trauma, blood flow in the injured area significantly increased (compared to base) from 134 AU to 208 AU. It continued to rise slightly up to 255 AU at 240 minutes after trauma and remained elevated around this value until the end of the experiment at 480 minutes (shown for the first 240 minutes in Figure 2A). Parallel to the rise in blood flow, there was an immediate significant increase from 67 AU to 104 AU in the relative hemoglobin amount, which persisted at this level for the whole experimental period (shown for the first 240 minutes in Figure 2B). In contrast to both other microvascular parameters, directly after trauma the microvascular hemoglobin O2 saturation was similar to baseline values (approximately 80%). However, 200 minutes after trauma, the microvascular hemoglobin O2 saturation reached a significant increase (to 91%) and remained elevated until the end of experimental period (shown for the first 240 minutes in Figure 2C).

Bottom Line: Directly after trauma and until the end of experiment (480 minutes), microvascular blood flow and relative hemoglobin amount were clearly increased.In contrast to blood flow and relative hemoglobin amount, there was no immediate but a delayed increase of microvascular hemoglobin O2 saturation.This increased O2 supply is obviously sufficient to ensure normoxic (or even hyperoxic) conditions in the vast majority of the cells.

View Article: PubMed Central - PubMed

Affiliation: University of Duisburg-Essen, Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany.

ABSTRACT

Background: After severe muscle trauma, hypoxia due to microvascular perfusion failure is generally believed to further increase local injury and to impair healing. However, detailed analysis of hypoxia at the cellular level is missing. Therefore, in the present work, spectroscopic measurements of microvascular blood flow and O2 supply were combined with immunological detection of hypoxic cells to estimate O2 conditions within the injured muscle area.

Materials and methods: Severe blunt muscle trauma was induced in the right Musculus gastrocnemius of male Wistar rats by a standardized "weight-drop" device. Microvascular blood flow, relative hemoglobin amount, and hemoglobin O2 saturation were determined by laser Doppler and white-light spectroscopy. Hypoxic cells were detected by histologic evaluation of covalent binding of pimonidazole and expression of HIF-1α.

Results: Directly after trauma and until the end of experiment (480 minutes), microvascular blood flow and relative hemoglobin amount were clearly increased. In contrast to blood flow and relative hemoglobin amount, there was no immediate but a delayed increase of microvascular hemoglobin O2 saturation. Pimonidazole immunostaining revealed a hypoxic fraction (percentage area of pimonidazole-labelled muscle cells within the injured area) between 8 to 3%. There was almost no HIF-1α expression detectable in the muscle cells under each condition studied.

Conclusions: In the early phase (up to 8 hours) after severe blunt muscle trauma, the overall microvascular perfusion of the injured area and thus its O2 supply is clearly increased. This increased O2 supply is obviously sufficient to ensure normoxic (or even hyperoxic) conditions in the vast majority of the cells.

Show MeSH
Related in: MedlinePlus