Experimental models to study microcirculatory dysfunction in muscle ischemia?reperfusion and osteomyocutaneous flap transfer

Menger, Michael D.; Laschke, Matthias W.; Amon, M.; Schramm, René; Thorlacius, Henrik; Rücker, Martin; Vollmar, Brigitte

doi:10.1007/s00423-003-0426-y

Cited by 23 publications

(17 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is likely that the application of heat caused endothelial cell damage at the vascular endothelium and induced an increased inflammatory tissue response [25]. This supports the findings reported by Menger et al, who detected an endothelin (ET)-1-mediated local inflammatory response after microvascular constriction following heat application [26]. This led to perfusion failures in microvessels [27].…”

Section: Discussionsupporting

confidence: 67%

Increase in periosteal angiogenesis through heat shock conditioning

et al. 2011

View full text Add to dashboard Cite

ObjectiveIt is widely known that stress conditioning can protect microcirculation and induce the release of vasoactive factors for a period of several hours. Little, however, is known about the long-term effects of stress conditioning on microcirculation, especially on the microcirculation of the periosteum of the calvaria. For this reason, we used intravital fluorescence microscopy to investigate the effects of heat shock priming on the microcirculation of the periosteum over a period of several days.MethodsFifty-two Lewis rats were randomized into eight groups. Six groups underwent heat shock priming of the periosteum of the calvaria at 42.5°C, two of them (n = 8) for 15 minutes, two (n = 8) for 25 minutes and two (n = 8) for 35 minutes. After 24 hours, a periosteal chamber was implanted into the heads of the animals of one of each of the two groups mentioned above. Microcirculation and inflammatory responses were studied repeatedly over a period of 14 days using intravital fluorescence microscopy. The expression of heat shock protein (HSP) 70 was examined by immunohistochemistry in three further groups 24 hours after a 15-minute (n = 5), a 25-minute (n = 5) or a 35-minute (n = 5) heat shock treatment. Two groups that did not undergo priming were used as controls. One control group (n = 8) was investigated by intravital microscopy and the other (n = 5) by immunohistochemistry.ResultsDuring the entire observation period of 14 days, the periosteal chambers revealed physiological microcirculation of the periosteum of the calvaria without perfusion failures. A significant (p < 0.05) and continuous increase in functional capillary density was noted from day 5 to day 14 after 25-minute heat shock priming. Whereas a 15-minute exposure did not lead to an increase in functional capillary density, 35-minute priming caused a significant but reversible perfusion failure in capillaries. Non-perfused capillaries in the 35-minute treatment group were reperfused by day 10. Immunohistochemistry demonstrated an increase in cytoprotective HSP70 expression in the periosteum after a 15-minute and a 35-minute heat shock pretreatment when compared with the control group. The level of HSP70 expression that was measured in the periosteum after 25 minutes of treatment was significantly higher than the levels observed after 15 or 35 minutes of heat shock exposure.ConclusionA few days after heat shock priming over an appropriate period of time, a continuous increase in functional capillary density is seen in the periosteum of the calvaria. This increase in perfusion appears to be the result of the induction of angiogenesis.

show abstract

Section: Discussionsupporting

confidence: 67%

Increase in periosteal angiogenesis through heat shock conditioning

et al. 2011

View full text Add to dashboard Cite

show abstract

“…We did consider perfusing each target tissue following sacrifice with the idea of flushing out leukocytes and identifying labeled cells. We decided against this because in our experience, and in the experience of other researchers (Durowicz and Olszewski, 2003; Menger et al, 2003), such procedures under the unphysiological condition of anesthesia introduce substantial additional sampling error, given the profound alterations in vascular resistance, adhesion molecule production by endothelium, and distribution that occur within individual tissue. Since the animals were passively exsanguinated, any labeled cells that we found within an organ would predominantly be those that were not freely circulating but likely marginated.…”

Section: Discussionmentioning

confidence: 99%

Exercise and leukocyte interchange among central circulation, lung, spleen, and muscle

Adams

Zaldivar

Nance

et al. 2011

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

Circulating leukocytes increase rapidly with exercise then quickly decrease when the exercise ends. We tested whether exercise acutely led to bidirectional interchange of leukocytes between the circulation and the lung, spleen, and active skeletal muscle. To accomplish this it was necessary to label a large number of immune cells (granulocytes, monocytes, and lymphocytes) in a way that resulted in minimal perturbation of cell function. Rats were injected intravenously with a single bolus of carboxyfluorescein diacetate succinamidyl ester (CFSE) dye which is rapidly and irreversibly taken up by circulating cells. The time course of the disappearance of labeled cells and their reappearance in the circulation following exercise was determined via flow cytometry. The majority of circulating leukocytes were labeled at 4 h. post-injection and this proportion slowly declined out to 120 h. At both 24 and 120 h, running resulted in an increase in the proportion of labeled leukocytes in the circulation. Analysis of the skeletal muscle, spleen and lung indicated that labeled leukocytes had accumulated in those tissues and were mobilized to the circulation in response to exercise. This indicates that there is an ongoing exchange of leukocytes between the circulation and tissues and that exercise can stimulate their redistribution. Exchange was slower with muscle than with spleen and lung, but in all cases, influenced by exercise. Exercise bouts redistribute leukocytes between the circulation and the lung, spleen and muscle. The modulatory effects of exercise on the immune system may be regulated in part by the systemic redistribution of immune cells.

show abstract

“…In brief, after intraperitoneal anesthesia and removal of the fur, a laterally based myocutaneous flap with a width-to-length ratio of 15 ϫ 11 mm, including the panniculus carnosus, was elevated perpendicularly to the spine, transsecting both the deep circumflex iliac artery (DCIA) and the lateral thoracic artery (LTA) (14). The flap and its neighboring skinfold tissue were then sutured into a skinfold chamber, which consisted of two symmetrical titanium frames (28). This was done in such a fashion that the observation window, incorporated in one of the frames, allowed direct view onto the muscle and subcutaneous tissue of the elevated flap.…”

Section: Methodsmentioning

confidence: 99%

Evolution of a “falx lunatica” in demarcation of critically ischemic myocutaneous tissue

Harder

Amon²,

Georgi³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

Using intravital microscopy in a chronic in vivo mouse model, we studied the demarcation of myocutaneous flaps and evaluated microvascular determinants for tissue survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the proximally normal from the distally necrotic tissue. Tissue survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density, and capillary remodeling, including dilation, hyperperfusion, and increased tortuosity. Angiogenesis and neovascularization were not observed over the 10-day observation period. The white rim distal to the red zone, appearing as "falx lunatica," showed a progressive decrease of functional capillary density similar to that of the necrotic distal area but without desiccation, and thus transparency, of the tissue. Development of the distinct zones of the critically ischemic tissue could be predicted by partial tissue oxygen tension (Pt(O(2))) analysis by the time of flap elevation. The falx lunatica evolved at a Pt(O(2)) between 6.2 +/- 1.3 and 3.8 +/- 0.7 mmHg, whereas tissue necrosis developed at <3.8 +/- 0.7 mmHg. Histological analysis within the falx lunatica revealed interstitial edema formation and muscle fiber nuclear rarefaction but an absence of necrosis. We have thus demonstrated that ischemia-induced necrosis does not demarcate sharply from normal tissue but develops beside a fringe of tissue with capillary remodeling an adjacent falx lunatica that survives despite nutritive capillary perfusion failure, probably by direct oxygen diffusion.

show abstract

Experimental models to study microcirculatory dysfunction in muscle ischemia?reperfusion and osteomyocutaneous flap transfer

Cited by 23 publications

References 84 publications

Increase in periosteal angiogenesis through heat shock conditioning

Increase in periosteal angiogenesis through heat shock conditioning

Exercise and leukocyte interchange among central circulation, lung, spleen, and muscle

Evolution of a “falx lunatica” in demarcation of critically ischemic myocutaneous tissue

Contact Info

Product

Resources

About