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Results for “Microcirculation”

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At least 559 records · Page 31Linked to original sources

PubMed2004

He-Ne laser effects on blood microcirculation during wound healing: a method of in vivo study through laser Doppler flowmetry.

BACKGROUND AND OBJECTIVES: Low-intensity laser therapy (LILT) is widely used for wound healing promotion and its mechanism of action may be due to an enhancement of blood supply. The aim of this study was to evaluate blood flow alterations in a wound healing model, using laser Doppler flowmetry (LDF) associated with a normalized perfusion parameter. STUDY DESIGN/MATERIALS AND METHODS: An injury was provoked in 15 rats and blood flow was measured periodically over a period of 21 days. Control groups were established to evaluate LDF and He-Ne laser effects on microcirculation. A 1 J/cm(2) dose was utilized, with 6 mW/cm(2) irradiance. RESULTS: The results demonstrated flow alterations provoked by lesion, and inflammatory response (P < 0.05). There were no statistical differences between groups. CONCLUSIONS: The results did not show a significant sustained effect on microcirculation with this He-Ne dose.

Animals↗

PubMed2004

Ischemic preconditioning and intermittent clamping improve murine hepatic microcirculation and Kupffer cell function after ischemic injury.

The aim of this study was to evaluate whether the protective effect of intermittent clamping and ischemic preconditioning is related to an improved hepatic microcirculation after ischemia/reperfusion injury. Male C57BL/6 mice were subjected to 75 or 120 min of hepatic ischemia and 1 or 3 hours of reperfusion. The effects of continuous ischemia, intermittent clamping, and ischemic preconditioning before prolonged ischemia on sinusoidal perfusion, leukocyte-endothelial interactions, and Kupffer cell phagocytic activity were analyzed by intravital fluorescence microscopy. Kupffer cell activation was measured by tissue levels of tumor necrosis factor (TNF)-alpha, and the integrity of sinusoidal endothelial cells and Kupffer cells were evaluated by electron microscopy. Continuous ischemia resulted in decreased sinusoidal perfusion rate and phagocytic activity of Kupffer cell, increased leukocyte-endothelial interactions and TNF-alpha levels. Both protective strategies improved sinusoidal perfusion, leukocyte-endothelial interactions and phagocytic activity of Kupffer cells after 75-minutes of ischemia, and intermittent clamping also after 120 minutes ischemia. TNF-alpha release was significantly reduced and sinusoidal wall integrity was preserved by both protective procedures. In conclusion, both strategies are protective against ischemia/reperfusion injury by maintaining hepatic microcirculation and decreasing Kupffer cell activation for clinically relevant ischemic periods, and intermittent clamping appears superior for prolonged ischemia.

Animals↗

PubMed2005

Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation.

Microcirculatory disturbances are an initial causative determinant in hepatic ischemia/reperfusion injury. The aim of this study was to assess sinusoidal perfusion during human liver transplantation using orthogonal polarization spectral imaging and to evaluate the significance of intraoperative microcirculation for early postoperative graft function. Hepatic microcirculation was measured in 27 recipients undergoing full-size liver transplantation and compared to a group of 32 healthy living-related liver donors. The microvascular parameters were correlated with postoperative aspartate aminotransferase and bilirubin levels. Hepatic perfusion following liver transplantation was found to be significantly decreased when compared with the control group. Volumetric blood flow within the individual sinusoids increased due to sinusoidal dilatation and enhanced flow velocity. Regression analysis of postoperative aspartate aminotransferase and bilirubin with microvascular parameters revealed significant correlations. The extent of volumetric blood flow increased within the first 30 minutes after reperfusion and showed a significant correlation with postoperative aspartate aminotransferase release and bilirubin elimination. In conclusion, postischemic hepatic microvascular perfusion was analyzed in vivo, demonstrating significant microvascular impairment during liver transplantation. Sinusoidal hyperperfusion appears to confer protection against postischemic liver injury, as given by the correlation with aspartate aminotransferase and bilirubin levels. Thus, these findings may have therapeutic importance with respect to mechanisms mediating postischemic reactive hyperemia.

Adolescent↗

PubMed1998

In vivo demonstration of impaired microcirculation in steatotic human liver grafts.

The perfusion of human donor livers was studied during organ retrieval using laser Doppler flowmetry to assess the microcirculatory alteration caused by fatty infiltration (steatosis). Using a multichannel laser Doppler flowmeter, we measured the hepatic perfusion as flux units in 21 liver donors, eight of which were macroscopically fatty. Perfusion was recorded continuously for 2 minutes from two sites on each lobe at the beginning of organ retrieval, after the vascular dissection, and during sequential occlusion of the hepatic artery and portal vein. Mean flux value and SEM were calculated, and paired Student's t test was used for comparison between stages of perfusion. Multiple ANOVA was used to determine whether factors other than the normal or fatty parenchyma influenced the perfusion measurements. Mobilization of the graft did not affect parenchymal perfusion. Perfusion was significantly (P < 0.001) and rapidly reduced with hepatic artery or portal vein occlusion in both groups. Macroscopically steatotic livers (n = 8) had diminished microcirculation compared with normal livers (n = 13) (125 +/- 18 v 252 +/- 24 flux units; P = 0.002). Donors receiving inotropes (n = 10) had a lower mean perfusion rate (150 +/- 20 v 252 +/- 29 flux units; P = 0.026), but this effect was found in both the normal and steatotic groups with no interaction (ANOVA; P = 0.658). Steatosis diminishes the tissue perfusion in human liver grafts. Laser Doppler flowmetry may help identify grafts with a compromised microcirculation.

Adolescent↗

PubMed2001

Liver microcirculation after selective denervation.

Microcirculatory disturbances have been related to a decrease in survival after liver transplant. Because innervation is involved in liver hemodynamics regulation, we decided to evaluate microcirculatory hepatic perfusion. Thirty rats were divided into three groups: denervated (DG), hepatic microsurgical denervation; manipulated (MG), hepatic manipulation; control (CG), laparotomy. Hepatic microcirculation was assessed in the median lobe using laser Doppler flowmetry in the following moments: T(0), after laparotomy and T(1), after denervation; and in the following moments after denervation: T(2), 10 minutes, T(3), 20 minutes, T(4), 30 minutes, T(5), 1 hour, T(6), 1.5 hours, and T(7), 2 hours for DG, and in same moments for MG and CG. DG showed a decrease in hepatic perfusion for 20 minutes after denervation, different from MG and CG. After that, there was recovery in hepatic perfusion in MG and DG (Kruskal-Wallis and Friedman tests). Therefore, denervation and manipulation alter hepatic microcirculation, but denervation promotes a more severe decrease than manipulation.

Animals↗

PubMed2005

Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion.

Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyte-endothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22 degrees C did not affect the assessed microcirculation variables, whereas HTK at 4 degrees C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation.

Animals↗

PubMed2005

Dose response of enoxaparin at the cremaster muscle flap microcirculation.

The effects of different dosages of enoxaparin (Lovenox), a low molecular-weight heparin, on microcirculation were investigated. The cremaster muscle model for intravital microscopy was used. Four groups were studied: in group I (n = 6), the controls no agent was given; in group II (n = 6), enoxaparin (2 mg/kg s.c.), in group III, (n = 6), enoxaparin (4 mg/kg s.c.); and in group IV, (n = 6), exoxaparin (8 mg/kg s.c.). These agents were injected before muscle dissection. All animals were observed under intravital microscopy, and measurements of capillary density and red blood cell velocity were taken at 2, 3, 5, and 7 h following subcutaneous enoxaparin injection. Statistical analysis revealed that the capillary density significantly increased in group II and group III, respectively, (by 33% (P < 0.0001) and 25% (P < 0.01) when compared to group I at the fifth hour. Group IV was not significantly different from group I in capillary density. There was no significant difference in red blood cell velocity in any of the groups. Propensity for bleeding was not observed in any of the groups during the dissections and observation periods except in group IV. In conclusion subcutaneous administration of 2 mg/kg enoxaparin improves (by 33%) capillary density without any bleeding complications at the cremaster muscle flap microcirculation at the fifth hour following injection (P < 0.0001). (c) 2005 Wiley-Liss, Inc. Microsurgery 25:147-151, 2005.

Animals↗

PubMed2002

Lipid hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation.

Leukocyte dynamics were evaluatyed in vivo in rat retinal microcirculation following exposure to lipid hydroperoxide (LHP) in the vitreous.Various amounts (1, 5, 10 or 100 microg) of LHP (18:2) dissolved in 5 microl of sodium borate buffer (SBB, 0.02M) were injected into the vitreous of Brown-Norway rats. As a comparative study, 10 microg of linoleic acid (LA) dissolved in 5 microl of SBB was injected in the same way. Rats that did not undergo injection were evaluated as un-treated. At 2 to 48 hr after LHP exposure, the following were examined: (1) the flux of rolling leukocytes along the major retinal veins, (2) the number of leukocytes that accumulated in the retinal microvasculature using acridine orange digital fluorography and (3) the diameter of major retinal vessels. In the LHP-treated eyes, leukocyte rolling along the major retinal veins was observed and the number increased in a dose-dependent manner ( 1 to 10 microg). The flux of rolling leukocytes peaked at 6 hr after LHP (10-100 microg) injection. No rolling leukocytes were observed in LA-treated or un-treated eyes. The number of accumulated leukocytes started to increase at 4 hr and peaked at 24 hr after LHP (10 microg) injection. This number was significantly higher than that in LA-treated and un-treated eyes. Venous dilation was seen from 4 hr after LHP (10 microg) injection and became significant at 6 and 24 hr as compared with LA-treated and un-treated eyes. The results indicate that increased LHP levels in the vitreous due to oxidative stress enhance leukocyte-enothelium interaction in the retinal microcirculation.

Animals↗

PubMed1993

In vivo effects of endothelin on the renal microcirculation.

Endothelin-1 (ET) is a recently discovered vasoconstrictor peptide which is released by renal vascular endothelial cells in response to a number of pathologic insults including ischemia, endotoxemia, bacteremia, and cyclosporine nephrotoxicity. Because microvascular vasoconstriction is an integral component of the acute renal dysfunction associated with these conditions, this study was undertaken to determine the in vivo effects of ET on the renal microcirculation. We used the split hydronephrotic kidney model in decerebrate Sprague-Dawley rats to study vessel diameter and red cell velocity responses to ET using intravital videomicroscopy and doppler velocimetry. Topical administration of increasing concentrations of ET caused a dose-dependent constriction of interlobular arteries which reached a maximum of 27 +/- 5% at an ET concentration of 10(-8) M. A corresponding decrease of 64 +/- 8% in interlobular arterial blood flow was observed. Afferent and efferent arteriole diameters were reduced by 39 +/- 2% and 27 +/- 5%, respectively. These vascular effects were completely prevented by the systemic preinfusion of anti-endothelin antiserum. Infusion of antiserum alone had no effect on systemic hemodynamics or renal microvascular variables, suggesting that ET has little or no role in maintaining basal vascular tone in the kidney. We conclude that ET is a potent in vivo constrictor of the renal microcirculation and may be involved in mediating pathologic vasoconstriction.

Animals↗

PubMed1994

A new model for the study of pulmonary microcirculation: determination of pulmonary edema in rats.

Traditional studies of the lung microcirculation and pulmonary edema commonly employ indirect measurements of vascular hemodynamics or the examination of isolated lung segments. We have developed a new model which allows the direct investigation of the microcirculation at the surface of the lung in rats. A pulmonary window chamber of novel design was implanted into the chest wall of Sprague-Dawley rats to allow both short- and long-term observation of the pulmonary microvasculature in living animals. Pulmonary edema was induced by i.v. injection of either oleic acid or compound 48/80. The progression of pulmonary edema and alveolar flooding was assessed by monitoring the leakage of fluorescein-labeled albumin and rhodamine dye from the pulmonary capillaries into the alveoli. Animals given oleic acid or compound 48/80 showed progressive leakage of both fluorescein-labeled albumin and rhodamine. The greatest leakage occurred over the first 30 min of observation. No changes in pulmonary capillary permeability were observed in control animals over the period of observation.

Animals↗

PubMed1995

The interaction between endothelium-derived relaxing factor (EDRF) and eicosanoids in the regulation of the mesenteric microcirculation.

Locally produced eicosanoids and endothelium-derived factors are believed to be the mediators of vascular tone of various vascular beds including the mesentery. Using a small vessel isometric myograph which allows direct measurement of microvascular reactivity, the interaction of eicosanoids and endothelium-derived relaxing factor (EDRF) in regulating vascular tone of mesenteric microcirculation of the rat was characterized. The microvascular response to various vasoactive agents before and after inhibition of prostacyclin production with indomethacin (INDO, 5 microM) and inhibition of EDRF synthesis with N omega-nitro-L-arginine methyl ester (L-NAME, 50 microM) was compared. Analysis of dose-response curves for prostaglandin F2 alpha (PGF2 alpha), U46619, a stable thromboxane analog, and norepinephrine (NE) after pretreatment with INDO demonstrated that inhibition of endogenous eicosanoids significantly attenuated the vasoconstrictor response to PGF2 alpha and U46619 but not to NE. Inhibition of EDRF synthesis with L-NAME potentiated the vasoconstrictor response to PGF2 alpha, U46619, and NE. These results suggest that EDRF acts as the primary mediator of vasodilator tone in the mesenteric microcirculation rather than vasodilator cyclooxygenase products such as prostacyclin. It also appears that the vasoconstrictor action of PGF2 alpha and U46619 may be mediated by a release of an endogenous indomethacin-sensitive factor.

Animals↗

PubMed1998

Amrinone, a selective phosphodiesterase III inhibitor, improves microcirculation and flap survival: a comparative study with prostaglandin E1.

BACKGROUND: Amrinone, a selective phosphodiesterase (PDE) III inhibitor, is a newly developed agent that possesses a combination of positive inotropic and vasodilating properties as a result of preventing the degradation of cAMP and it has recently been licensed for treatment of heart failure alone. Amrinone is expected to be useful for the treatment not only of heart failure but also of peripheral circulatory disorders, including vascular disease, and for ischemic flaps, because it improves microcirculatory hemodynamics. To investigate potential therapeutic applications of amrinone, we evaluated its ability to improve microcirculatory hemodynamics and flap survival. MATERIALS AND METHODS: The rat skinfold chamber technique was employed to quantify microcirculation directly in vivo. The improved survival area of random flaps in rats treated with amrinone was examined to assess therapeutic efficacy of this drug. Its effects were compared with those of prostaglandin E1 (PGE1), which has been widely approved as an agent for improving hemodynamics. RESULTS: Microcirculatory blood flow and flap survival area were significantly increased in both amrinone- and PGE1-treated animals, compared to the saline-treated controls. The ameliorating effects of amrinone were comparable to those of PGE1. CONCLUSIONS: The results of this study suggest amrinone to be a potentially useful drug not only for treating heart failure but also for improving microcirculation in patients with vascular diseases and for postoperative care after reconstructive surgery.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1995

Mediator-induced changes in macromolecular permeability in the rat mesenteric microcirculation.

An intravital fluorescence microscopic method for measurement of changes in macromolecular permeability has been established in the mesenterial microcirculation of the rat. After exteriorization of the fat-free distal part of the ileal mesentery, a 1-hr period of stabilization was followed by the injection of FITC-labeled macromolecules. Five minutes later, histamine, leukotriene B4, or leukotriene C4 was topically applied to the tissue by means of a micromanipulator. Areas of 1 mm2 were videotaped with a SIT camera. The fluorescence intensity of these areas was measured by an analogous video image processing system and displayed as gray value histograms. The shift of the frequency of gray levels from lower to upper regions could be attributed to an increase in light intensity in the mesentery, indicating an increase in vessel wall permeability. The sites of action of histamine and leukotriene C4 were very similar. Both mediators affected mainly the larger collecting venules. In contrast, leukotriene B4 exerted its effect at postcapillary venules. Moreover, leukotriene B4-induced extravasation was inhibited by superoxide dismutase, suggesting an involvement of oxygen radicals. The studies with histamine alone and with H1- and H2-antagonists demonstrated that histamine-induced extravasation in the rat mesentery was mediated by H1-histamine receptors. The present study introduces an experimental model for the measurement of changes in macromolecular permeability, which is useful for studying mediator effects and their pharmacological inhibition in the microcirculation of the rat mesentery.

Animals↗

PubMed1995

Effects of monoionic and nonionic radiographic contrast media on cutaneous microcirculation in patients with peripheral arterial occlusive disease.

The purpose of the study was to compare the in vivo effects of two low-osmolar radiographic contrast media, a monoionic (sodium/-meglumine ioxaglate, Hexabrix) and a non-ionic one (iopromide, Ultravist 300) on the cutaneous microcirculation in patients with peripheral arterial occlusive disease in a prospective randomised double-blind study. In 20 patients with peripheral arterial occlusive disease scheduled for percutaneous transluminal angioplasty skin microcirculation was assessed by laser Doppler fluxmetry and transcutaneous oxygen tension measurements at the foot dorsum for continuous recordings of the cutaneous microvascular perfusion and skin oxygenation. Before angioplasty 10 ml nondiluted contrast medium was injected intraarterially and the acute effect on transcutaneous oxygen tension and laser Doppler flux was registered. Mean laser Doppler flux and oxygen tension were evaluated initially, after arterial puncture and after contrast medium injection. In addition, flux motion was analysed with respect to frequency and amplitudes changes. No significant changes in laser Doppler flux and fluxmotion patterns were found between both groups after contrast medium injection. However, mean transcutaneous oxygen tension of the patients receiving monoionic ioxaglate dropped significantly (P = 0.01). The differences of both contrast media on red blood cell aggregation shown in vitro do not correlate to intravital microcirculatory measurements in patients with arterial occlusive disease of the lower limb. Microvascular skin blood flow and flux motion at the foot in these patients do not change significantly after intraarterial injection of ioxaglate and iopromide. However, oxygen supply of the skin is transient impaired after interarterial injection of the anionic contrast agent ioxaglate, which was not associated with clinical symptoms.

Aged↗

PubMed1995

Energy optimization and bifurcation angles in the microcirculation.

Our purpose was to examine the relationship between bifurcation angle and energy optimization in the arteriolar microcirculation. We measured bifurcation angles and diameters for sequential branches along a third-order feed arteriole (25 microns) in the superfused cremaster muscle of anesthetized (pentobarbital, 70 mg/kg) Golden hamsters (N = 51). Predicted bifurcation angles were calculated using the diameter data in a model designed to minimize total energy or using four different models each designed to minimize a specific energy cost (vessel wall surface area, vascular volume, wall shear stress, power losses), these models each assuming constant viscosity and that branching occurs with perfect space filling (i.e. junction exponent, x, = 3). The range of the predicted bifurcation angles for any model was small (+/- 10 degrees), and they were not different for the sequential junctions along the feed arteriole, where the observed angles significantly decreased in angle along the feed (first junction, 115 +/- 4.4 degrees; second, 88 +/- 5.2 degrees; third, 76 +/- 4.8 degrees; and last, 57 +/- 3.4 degrees). We next corrected for a nonconstant viscosity by using our in vivo tube hematocrit data and a published relationship among diameter, tube hematocrit, and apparent viscosity. Again assuming that x = 3, the total energy minimization model now predicted that the bifurcation angle was always obtuse and not different for the sequential branches along the feed arteriole (first, 125 +/- 3.3 degrees; second, 124 +/- 3.4 degrees; third, 120 +/- 6.6 degrees; and last, 132 +/- 2.7 degrees); the predicted angles were not correlated with the observed angles (r = 0.25). Using the geometric resistance (diameters) and the angles measured in vivo, and assuming constant viscosity, we next calculated the value of chi for each of the bifurcation junctions for each of the four models described above. The average value of x was not equal to 3 for any of the four models. The value of x decreased along the feed arteriole (first to last branch) from 2.7 +/- 0.26 to 1.6 +/- 0.22 (surface) and from 4.2 +/- 0.36 to 2.9 +/- 0.23 (volume), and x increased along the feed from 3.0 +/- 0.35 to 15.5 +/- 2.6 (shear stress) and from 40 +/- 31 to 82 +/- 49 (power loss). These calculations suggest that both changing viscosity and a changing value for the junction exponent are likely important when examining the energy optimization within the arteriolar microcirculation.

Animals↗

PubMed1997

Novel neuropeptide Y receptor antagonists block vasoconstriction in the hamster cheek pouch microcirculation.

We investigated the efficacy of novel neuropeptide Y (NPY) antagonists to inhibit the microcirculatory dynamics of NPY in the hamster cheek pouch microcirculation using intravital microscopy and computer-assisted image analysis. Changes in arteriolar diameter served as an index of vasomotor alterations. Fluorescein isothiocyanate-labeled Dextran 150 served as a tracer for measurements of macromolecular transport. GW 383 and GW 1229, two novel NPY receptor antagonists, were applied topically in separate experiments. Pretreatment with 10(-5), 10(-6) and 10(-7) M GW 383 and with 10(-6) and 10(-8) M GW 1229 attenuated the vasoconstriction induced by 10(-7) M NPY in a dose-dependent manner. Furthermore, pretreatment with 10(-7) and 10(-8) M GW 1229 significantly inhibited the 10(-9) M NPY-induced vasoconstriction. At these doses, the NPY antagonists did not alter microvascular permeability. Our results demonstrate that the novel NPY antagonists inhibit the vasoconstriction induced by NPY in the hamster check pouch microcirculation. We suggest that the inhibition is due to binding of antagonists to Y1-type NPY receptors.

Animals↗

PubMed2001

Microcirculation is similar in ischemic and venous ulcers.

Microcirculation of 15 ischemic and 15 venous ulcers, their scars, and intact surrounding skin were examined in order to demonstrate their similarities in the development and healing process. Subpapillary and nutritive perfusion of four areas were investigated by a laser Doppler perfusion imager (arbitrary units) and capillary microscopy (capillaries/mm2): one ulcer area without granulation tissue (no wound healing) and one with granulation tissue (ulcer healing); one skin area adjacent to the ulcer (1-8 mm) (scar developed from ulcer areas) and one distant (12-25 mm; intact skin). Areas without granulation tissue in ischemic and venous ulcers were similar, demonstrating a lack of capillaries (0.13 +/- 0.52; 0.93 +/- 2.09) and low laser Doppler flux (0.81 +/- 0.69; 1.47 +/- 1.17; P > 0.05 for each). In granulation tissue of both ulcers there was a tendency to a higher capillary density (0.67 +/- 1.40; 5.60 +/- 2.32; P < 0.0001 for venous ulcers) and a higher laser Doppler flux (1.15 +/- 0.67; 4.04 +/- 1.62; P < 0.0001 for venous ulcers) than in areas without granulation tissue. In scars of ischemic and venous ulcers capillary density (8.18 +/- 8.84; 13.60 +/- 5.45) and laser Doppler flux (1.72 +/- 1.00; 1.94 +/- 1.45) were similar (P > 0.05). In skin distant from ischemic ulcers very high capillary density (24.63 +/- 1.89) was associated with low laser Doppler flux (0.99 +/- 0.59); distant from venous ulcer capillary density was moderate (10.47 +/- 3.42) while laser Doppler flux was high (3.77 +/- 1.62; P < 0.0001 between both groups). The development and healing process of ischemic and venous ulcers is similar. Nutritive and subpapillary perfusion are involved in ulcer healing. In intact skin surrounding ischemic and venous ulcers, microcirculation is different due to the underlying pathophysiology.

Aged↗

PubMed2005

Microcirculation and reperfusion injury in organ transplantation.

There are many interesting aspects regarding hemorheology and tissue oxygenation in organ transplantation (such as liver, kidney, heart, etc.). The ischemia-reperfusion injury syndrome is a very important problem. Much damage in organs appears to be induced by reperfusion injury syndrome. In fact, not only immunological etiopathogenesis but also biochemically-mediated microcirculation alterations can modulate the organ damage induced by ischemia-reperfusion injury during organ transplantation. During ischemia-reperfusion injury, xanthine oxidase activity, the increase in oxygen free-radicals, and the activation of neuthrophils are all very important. Platelet activating factor (PAT) and LTB4 (promoting neuthrophils adhesiveness), activated by the xanthine oxidase-derived oxidants during reperfusion, activates the final post-ischemia injury. Much research is necessary in order to gain a fuller knowledge of the microcirculation conditions and oxygenation during organ transplantation.

Adult↗