Although ischemia-reperfusion (I/R) strongly influences muscle flap survival in reconstructive surgery, there is limited knowledge about its relation to hemorheological parameters and oxidative stress markers in flaps. In the present study we investigated these changes during I/R of latissimus dorsi muscle (LDM) flaps in beagle dogs. In four animals LDM flaps were prepared bilaterally. The right side served as control, while the left side's vascular pedicle was clamped for 60 minutes, and a 60-minute reperfusion was allowed afterward. Blood samples (0.5 ml each) were taken from the pedicle's vein bilaterally before and after the ischemia, and at the 5th, 15th, 30th, 45th, and 60th minutes of the reperfusion, for hematological and erythrocyte aggregation tests. In muscle biopsies, taken before and after I/R, histological investigations and tests for measuring gluthation-peroxidase (GSH-PX) activity, glutathione (GSH) and carbonyl concentrations, and thiobarbituric acid reactive substances (TBARS) content were carried out. In I/R side leukocyte count increased during the reperfusion with a peak at the 30th minute. Hematocrit continuously increased from the 15th minute. In the first 5 minutes of the reperfusion, erythrocyte aggregation increased, than tented to be normalized. In muscle homogenates GSH-PX activity did not change markedly, GSH content slightly decreased, carbonyl and TBARS content increased during reperfusion. A 1-hour ischemia and reperfusion of LDM flaps caused local changes of leukocyte distribution and erythrocyte aggregation, supposedly due to the metabolic and inflammatory reactions. Oxidative damage during reperfusion was also demonstrated.

Introduction: We tested the hypothesis that asymmetric dimethylarginine (ADMA) interferes with other mechanisms in addition to inhibition of nitric oxide synthase (NOS). Thus, in skeletal muscle arterioles, in the presence of ADMA, we investigated the dilator effect of an NO donor and increases in flow and aimed to elucidate the underlying mechanisms, including the role of oxidative stress, which is known to reduce the bioavailability of NO. Methods and Results: In isolated rat gracilis skeletal muscle arterioles (∼160 µm at 80 mm Hg), ADMA (similarly to pyrogallol) reduced dilations to sodium nitroprusside (SNP), which was significantly prevented by the presence of superoxide dismutase (SOD) and catalase (CAT): SNP 10^–8M; control: 43.2 ± 3%, ADMA: 4.9 ± 1%, ADMA + SOD/CAT: 30.2 ± 9% (p < 0.05). Also, ADMA reduced basal diameter and flow-induced dilations, which were not restored by L-arginine, but prevented by SOD/CAT and by inhibition of NAD(P)H oxidase (but not xanthine oxidase) and by an angiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor blocker (ARB). ADMA increased the production of reactive oxygen species detected by lucigenin-enhanced chemiluminescence, which was significantly inhibited by SNP or ARB. Conclusion: We suggest that by activating the vascular renin-angiotensin-NAD(P)H oxidase pathway, ADMA elicits oxidative stress, which interferes with the bioavailability of NO and consequently reduces NO-mediated dilations.

We aimed to test two hypotheses: 1) isolated small veins develop substantial myogenic tone in response to elevation of intraluminal pressure, 2) H 2 O 2 contributes to the mediation of myogenic response via activation of arachidonic acid (AA) cascade and release constrictor prostaglandins. METHODS: Small veins were isolated from gracilis muscle of male rats, then cannulated. Changes of diameter to increases in intraluminal pressure, H 2 O 2 and arachidonic acid in the presence and absence of various inhibitors were measured by videomicroscope and microangiometer. At the end of experiments the passive diameter were obtained in Ca 2+ -free PSS solution. RESULTS: Isolated rat gracilis muscle small veins developed a substantial myogenic tone in response to increases in intraluminal pressure (1-12 mmHg). Calculated maximum myogenic tone was 70 ± 5% at 10 mmHg. Presence of catalase or indomethacin or SQ 29,548 reduced significantly the pressure-induced myogenic response. Also, H 2 O 2 (10 −9 −10 −5 M) and arachidonic acid (10 −7 −10 −4 M) elicited concentration dependent constrictions, which were inhibited by the presence of indomethacin or SQ 29,548. CONCLUSION: We propose that both myogenic response and pressure-induced release of H 2 O 2 play important roles in regulating the vasomotor function of venules both in physiological and pathological conditions. B. Debreczeni et al. / Mediation of myogenic response by H 2 O 2 and TP receptorsAlso, a correlation between diameter changes of arteries and flow changes in the adjacent capillaries has been published recently [36] and that postcapillary venules and small veins have important roles in the regulation of microcirculation as well [32,54,60] indicating that in the microvascular network all forms and sizes of vessles contribute to the fine regulation of blood flow [21,28,42,43,78].Historically, more attention has been paid to arterial vessels, but earlier and recent studies suggest that changes in the vasomotor tone of small venous vessels importantly contribute to the regulation of blood flow. Venous vessels are returning blood to the heart, but also by modulating capillary blood flow and pressure regulate filtration-reabsorption processes [32]. Thus diameter changes of small veins in response to changes in intraluminal pressure or can be important from many aspects, yet still there is insufficient amount of information regarding the characteristics of the myogenic responses and signaling mechanisms regulating the vasomotor tone of small veins.Constrictions of arterial vessels in response to increases in intraluminal pressure has been described and well studied in arterial vessel in vivo and in vitro since to original observation of Bayliss in 1902 [7, 19]. In contrast, earlier in vivo studies did not find appreciable myogenic tone in postcapillary venous vessels [9,73], whereas in vitro myogenic tone and response could be observed in these vessels. Recent studies suggest that myogenic response is present in small veins and venules of different organs [8,22,44] and s...

We hypothesized that isolated small veins (similarly arterioles) develop an appreciable myogenic tone in response to elevation of intraluminal pressure and aimed to elucidate the constrictor mechanism(s) involved. Thus small veins were isolated from gracilis muscle of male Wistar rats, then cannulated and incubated in the presence of 10 mmHg of intraluminal pressure at T = 37°C in a special pressure myograph chamber. Isolated small veins developed a substantial myogenic tone in response to increases in intraluminal pressure (from 1 to 12 mmHg). Calculated maximum myogenic tone was 70 ( 5 % of PD at 10 mmHg. Presence of indomethacin or catalase or SQ 29,548 reduced significantly the pressure‐induced myogenic tone. Also, H2O2 (10‐9‐10‐5 M) elicited concentration dependent constrictions, which were inhibited by the indomethacin or SQ 29,548. Arachidonic acid (10‐7–10‐4M) elicited concentration dependent constrictions, which were inhibited by indomethacin or SQ 29,548. In conclusion, in isolated small veins, 1) increases in pressure and H2O2 elicit substantial constrictons, both of which are inhibited by catalase, indomethacin or SQ 29,548 suggesting that the myogenic mechanism is mediated by H2O2 ‐induced arachidonic acid derived constrictor metabolite(s) such as prostaglandin H2/thromboxane A2 acting on TP receptors.Support: AHA Founders Aff. 0855910D and Hungarian Sci. Res. Funds, OTKA‐T48376.

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