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Biomedical subjects

M Siemionow

Publications and source records attributed to M Siemionow.

At least 19 recordsLinked to original sources
PubMed2000

Cranial defect repair using e-PTFE: part I. Evaluation of bone stiffness.

Autologous bone grafts are the preferred material for craniofacial reconstruction, but such procedures lead to increased operative time and bleeding, donor site morbidity, and graft resorption. The efficacy of expanded-polytetrafluoroethylene (e-PTFE) sheets to increase bone regeneration and remodeling in cranial defects using a rabbit model was evaluated by mechanical testing. New Zealand white rabbits were divided into 3 groups and sacrificed 6 months after surgery. In the Split Table group, (n = 16), a bilateral bone defect was created on the outer table of the parietal bones. In the Full Table group, (n = 16), a bilateral defect was created through both the inner and outer table of the cranium. The control group, (n = 10) was subjected to a sham operation. Indentation testing was performed to determine the stiffness of newly formed bone in and around the defect. Near the center of the defect, Split Table defects repaired with e-PTFE resulted in significantly stiffer bone than regenerated control bone. The Full Table defects repaired with e-PTFE also resulted in bone significantly stiffer than control regenerated bone around the central region of the defect. The data supports the hypothesis that e-PTFE improves the repair of cranial defects in a rabbit model. It is surmised that the porosity of the e-PTFE provides a stable scaffold for migration of tissue regenerating cells, which may be preferentially localized near the cranial suture lines. This porosity may also provide a barrier to fibrous tissue regenerating cells.

Animals↗
PubMed2000

Assessment of muscle flap sensibility by evoked potentials in the rat.

This study investigated whether the sensory-to-motor reinervation of the muscle flap provides a better sensory recovery of an overlying skin graft. Fifty-four animals were studied in three groups of 18 rats each: group I (control): 1 cm of the gastrocnemius muscle motor nerve was excised and no repair was performed; group II (motor-to-motor repair): the motor nerve of the gastrocnemius flap was transected and repaired; group III (sensory-to-motor repair): the motor nerve of the gastrocnemius muscle and sural nerve were transected and their distal and proximal ends, respectively, were repaired. At follow-up periods of 6, 12, and 24 weeks, evaluation of hair growth, muscle atrophy, and sensory evoked potentials was performed. Somatosensory evoked potentials (SSEP) at 6 weeks in the sensory-to-motor repair (group III) revealed a significant (P < 0. 05) increase (104.4% +/- 22.9) in the relative response of peak-to-peak potentials when compared with group I (46.6% +/- 19) and group II (51.8% +/- 14.0). Muscle flap stimulation was most prominent at 6 weeks in sensory-to-motor reinvervated flaps (group III 133.1% +/- 25.4; group I 84.9% +/- 20.2). In this study, sensory-to-motor nerve repair significantly improved the sensibility of skin flaps at 6 weeks. Denervated flaps presented with 3 months of sensory recovery delay.

Animals↗
PubMed2000

Microcirculatory window for early detection of allograft rejection.

The purpose of this study is to introduce a technical detail on a transplantation model for in vivo evaluation of microcirculatory changes during the acute phase of allograft rejection. The cremaster muscle is incorporated and transplanted along with the hind limb to detect and study ischemia/reperfusion injury and the acute phase of allograft rejection in rats. Thirty-six animals were studied in three experimental groups of 12 animals each. Each group was divided into subgroups and microcirculatory measurements were taken at two different time periods: 24 and 72 hours. In the ischemic control group (N = 12), cremaster muscles were denervated, prepared as a tube flap, and submitted to the same interval of ischemia as the other groups but without transplantation. In the isograft group (N = 12), rat hind limb-cremaster grafts were transplanted between genetically identical Lewis rats (RT11). In the allograft group (N = 12), 12 transplantations were performed across a major histocompatibility barrier between Lewis Brown-Norway (RT-11+/-n) and Lewis (RT 11) rats. The diameters of first-, second-, and third-order arterioles and venules; red blood cell velocities; and functional capillary density were recorded at 24 and 72 hours after transplantation. Daily follow-up observations were continued until 3 days after the first clinical signs of graft rejection. The mean number of perfused capillaries in the two transplantation groups was significantly lower than in the control group at both 24 hours and 72 hours (p < 0.05). Those results were as follows: 8.2 +/- 2.1 at 24 hours, 7.7 +/- 0.85 at 72 hours in the ischemic control group; 5.4 +/- 0.9 at 24 hours, 6 +/- 0.6 at 72 hours in the isograft group; and 5 +/- 0.9 at 24 hours, 5.5 +/- 0.3 at 72 hours in the allograft group. Red blood cell velocities and vessel diameters in the main arteries were also decreased in transplant groups at 24 hours (p < 0.05) but returned to normal 72 hours after the operation (p > 0.05). The composite rat hind limb-cremaster model presented in this study introduces a reproducible in vivo approach to monitor the differences in microcirculatory hemodynamics of ischemia/reperfusion injury and acute graft rejection. The model allows the study of the timing, sequence, and correlation between clinical and hemodynamic signs during the acute phase of allograft rejection.

Animals↗
PubMed1999

Arterial crush injury causes decrease in tissue perfusion at the level of the microcirculation in skeletal muscle flap.

This study was designed to evaluate the effects of crush injuries to the feeding arteries of a muscle flap on microcirculatory haemodynamics. Eighteen male Sprague-Dawley rats were divided into three experimental groups for intravital microscopy of the cremaster muscle flap. Group 1 served as control. In group 2 the common iliac artery and in group 3 additionally the lower abdominal aorta was crushed with a Kocher clamp (17.4 N) over 5 min. Microcirculatory parameters (red blood cell velocity, vessel diameter, and capillary perfusion) were monitored before and 2 h after crush. In the one-level crush group, red blood cell velocities significantly decreased by 39.17% (P=0.046) in first order arterioles and by 32. 91% (P=0.0106) in second order arterioles. In capillary perfusion, a drop of 48.02% (P=0.0039) was noted. In the two-level crush group, red blood cell velocities significantly dropped over 32.06% (P=0. 0250) in first order arterioles, 35.91% (P=0.0065) in second order arterioles, and 45.69% (P=0.0782) in first order venules. Capillary perfusion was reduced by 20.16% (P=0.374). Arterial crush injuries as possible thrombogenic insults may result in a significant decrease in skeletal muscle perfusion although the blood supply through the crushed supplying vessel is maintained.

Animals↗
PubMed1999

Failure in developing a model for complete vascular thrombosis in the common iliac artery in the rat.

The purpose of this study was to develop a model for complete arterial thrombosis proximal to the rat cremaster flap for subsequent fibrinolytic studies at the microcirculatory level. We divided 20 male Sprague-Dawley rats into four experimental groups of five animals each. We assigned each group to an established thrombosis model using crush and standard microsurgical anastomosis, crush and intimal abrasion, inverted arterial suture, and intravascular silk sutures combined with microsurgical anastomosis at the common iliac artery. Vessel patency was examined using the milking test 30, 60, 90, and 120 min after the thrombogenic insults. The model of perpendicular silk sutures and anastomosis caused complete arterial thrombosis in one animal over 120 min. The other models failed in all animals. In conclusion, the thrombogenic models used in this study are not capable of creating a reliable complete arterial thrombosis in the common iliac artery of the rat.

Animals↗
PubMed1999

Tissue-plasminogen activator restores muscle flap perfusion in the rat.

This study was designed to evaluate the effect of tissue-plasminogen activator on skeletal muscle flap perfusion after a thrombogenic insult. Twenty-four male Sprague-Dawley rats were divided into 4 experimental groups of 6 animals each. In group 1 (sham), the cremaster muscle was isolated as an end-organ flap. In group 2, after cremaster muscle isolation, a semicircular inverted suture as a thrombogenic insult was performed at the ipsilateral common iliac artery. In group 3, local tissue-plasminogen activator infusion followed the inverted suture. In group 4, vehicle was infused. After 24 hours, the cremaster muscle flap hemodynamics and leukocyte-endothelial interactions were measured using intravital microscopy. Capillary perfusion significantly decreased after the inverted suture from a median of 6.23 (group 1) to 1.50 (group 2) functional capillaries per visual field. Tissue-plasminogen activator significantly increased capillary perfusion after the thrombogenic insult from a median of 1.50 (group 2) and 2.50 (group 4) to 6.00 (group 3). Tissue-plasminogen activator restored capillary perfusion after a thrombogenic insult to the main feeding artery.

Animals↗
PubMed1999

[Applicability of the robot arm for microsurgical operations].

In this project, we evaluated a new robotic arm, RAMS (Robot Assisted Microsurgery) Workstation, for microsurgical procedures. We assigned seven microsurgical tasks to the robotic arm to investigate its capabilities and limitations during microsurgery. The robotic arm was able to function as the primary operating tool in removal of foreign bodies and thrombi as well as in intravascular positioning and holding of needles and catheters. The robot worked with great precision and without vibration. It served as an assisting tool in vessel dissection, ligation of side branches, and microsurgical anastomosis. The main drawbacks include a long warm-up period, the large size, poor rotation of the tip of the robotic arm, and frequent unintended shut-downs. The RAMS Workstation is a precise tool and can assist the surgeon as a "second" or "third hand". It cannot entirely replace the microsurgical instruments held by the surgeon.

Animals↗
PubMed1999

Determination of hindlimb transplantation-induced vascular albumin leakage and leukocyte activation during the acute phase of rejection.

Following transplantation, the microvascular endothelium and endothelial cells play a critical role in allograft rejection, as well as response to surgical trauma. In this study, endothelial-cell damage was assessed through microvascular permeability, and the role of surgical trauma was evaluated during the acute phase of limb allograft rejection. Eighteen isograft and 18 allograft composite-tissue transplantations were performed between 72 rats. At 24-hr, 72-hr, and 7-days follow-up, microvascular permeability, leukocyte activation, functional capillary perfusion, red-blood-cell velocity, vessel diameter, and an endothelial edema index were measured. The permeability index (PI) was statistically significantly greater in the allografts at all follow-up points, compared with the isograft controls (p <0.001). The number of rolling leukocytes was significantly greater in the allografts at 24 and 72 hr; the number of sticking and transmigrating leukocytes was greater at all three follow-up points; and the number of rolling lymphocytes was greater at 7 days (p <0.05). These findings demonstrate the increased rejection phenomenon in allografts, and the increased susceptibility to ischemia and reperfusion injury, compared with isograft transplants. Increased leukocyte activation and acute destruction of endothelial-cell barrier function were demonstrated during the acute rejection period following composite limb allotransplantation.

Acute Disease↗
PubMed1999

Dose-dependent response to IFN-gamma in muscle flap microcirculation.

In this study, the authors attempted to determine the effects of intraarterial administration of various doses of Interferon-gamma (IFN-gamma) on microcirculation in a rat muscle flap model. In Group 1 (control), 0.6 ml vehicle solution-PBS-BSA, in Group 2 0.6 ml IFN-gamma (25 ng/ml), in Group 3 0.6 ml IFN-gamma (50 g/ml), in Group 4 0.6 ml IFN-gamma (100 g/ml), were injected. The diameter of the cremaster arterioles and venules, red blood cell velocities, the number of rolling leukocytes and lymphocytes, sticking leukocytes and lymphocytes, capillary perfusion, and endothelial edema index were evaluated. Deterioration of flow hemodynamics was confirmed by a significant decrease in flow velocity in the main artery (A1) (47 percent in Group 3 and 65 percent in Group 4). All dosages of IFN-gamma caused a statistically significant decrease in rolling leukocytes, but this effect was more obvious in the 25 ng/ml group. Injury to the vascular endothelium was confirmed by a two-fold increase in transmigrating leukocytes in the 100 ng/ml group. This was accompanied by 60 percent and 75 percent drops in capillary perfusion, and by 12 percent and 24 percent drops in the endothelial edema index in Groups 3 and 4, respectively. The results indicate that direct intraarterial administration of IFN-gamma in doses higher than 25 ng/ml may be toxic to muscle flaps.

Animals↗
PubMed1999

Thrombogenic stimulus causes long-term decrease of muscle flap perfusion.

This study was designed to evaluate the effect of a continuous thrombogenic insult at the feeding artery on skeletal muscle flap perfusion over 24 hours. Twelve male Sprague-Dawley rats were divided into two experimental groups. In the control group (N = 6) and in the treatment group (N = 6) the right cremaster muscle was isolated on its neurovascular pedicle and the tubular muscle flap was preserved in the medial part of the hind limb over a 24-hour period for subsequent microcirculatory observation. In the treatment group, an inverting suture was applied over half of the circumference of the ipsilateral common iliac artery to create a continuous thrombogenic stimulus. Intravital microcirculatory measurements obtained were red blood cell velocities, vessel diameters, capillary perfusion, endothelial edema index, and leukocytic-endothelial interactions. There were no statistically significant differences seen in red blood cell velocities, vessel diameters, and leukocytic-endothelial interactions between the groups. However, the inverting suture caused a significant drop in capillary perfusion from 6.23 to 1.50 capillaries per visual field (median; p = 0.002). An arterial thrombogenic insult may result in a significant decrease in capillary perfusion in muscle flaps over 24 hours although the blood flow through the thrombogenic main feeding vessel is maintained.

Animals↗
PubMed1999

Microcirculatory response to halothane and isoflurane anesthesia.

Microcirculatory hemodynamics are often used to monitor tissue and organ survival. This study investigated the effect of halothane and isoflurane anesthesia on peripheral microcirculation using the cremaster muscle during intravital microscopy. Twenty-three Sprague-Dawley rats were studied in four groups. Two groups served as controls and did not undergo flap isolation but did receive halothane (N = 6) or isoflurane (N = 5). After induction with a single dose of intraperitoneal pentobarbital (40 mg per kilogram), rats were ventilated with either 2 minimum alveolar concentration (MAC) halothane or 2 MAC isoflurane. Esophageal temperature, electrocardiography, central venous pressure, mean arterial pressure, and blood gases were measured over 4 hours. In groups receiving surgery with either halothane (N = 6) or isoflurane (N = 6), the cremaster muscle was isolated on the neurovascular pedicle. Microcirculatory responses to both halothane and isoflurane anesthesia were evaluated by measuring red blood cell (RBC) velocity, vascular diameters in arterioles (A1, A2-1, A2-2, and A3) and the main venule (V1), functional capillary perfusion, and leukocytic endothelial interactions in postcapillary venules (rolling, adherent, and transmigrating leukocytes). Hemodynamic variables were compared among all four groups, and microcirculatory variables were compared between the two surgical groups. During isoflurane anesthesia in animals with flaps, significantly higher (p < 0.05) RBC velocities were recorded in arterioles A1 (24.4%), A2-2 (28.2%), and A3 (17.4%). Capillary perfusion was significantly higher in animals with flaps and halothane anesthesia (17.8%; p < 0.05). The number of rolling leukocytes (39.4%) was significantly higher during isoflurane anesthesia in animals with flaps (p < 0.05). Better flow hemodynamics in the peripheral microcirculation were seen during halothane anesthesia, and were confirmed by greater functional capillary perfusion and fewer activated leukocytes. In the isoflurane group, RBC velocity alone cannot serve as an indicator of microcirculatory function.

Anesthesia, General↗
PubMed1999

Interferon-gamma improves muscle flap microcirculation in double-strand RNA-induced inflammation.

Endothelial cell (EC) activation and subsequent expression of leukocyte adhesion molecules are initial events in multiple pathological processes. Viral double-strand ribonucleic acid (dsRNA) induces EC adhesion protein expression and leukocyte adhesion in vitro. Interferon-gamma (IFN-gamma) has been demonstrated to modulate the expression of certain adhesion proteins. The purpose of this study was to measure the inflammatory response to a viral mimetic--a synthetic dsRNA, polyinosinic-polycytidylic acid (poly-I:C)-on the microcirculation of a muscle flap in a rat model and to determine whether IFN-gamma attenuated the response. Two-stage surgery to create a cremaster muscle end-organ tube flap was performed on 18 male Sprague-Dawley rats in three groups. After intra-arterial injection into the abdominal aorta, the reagents (phosphate-buffered saline-bovine serum albumin [PBS-BSA] in groups I and II, and IFN-gamma in group III) were kept for 1 hour in this end-organ system. During the second stage at 16 hours, after injection into the penile vein (PBS-BSA in group I, poly-I:C in groups II and III), the flap was prepared for intravital microscopic measurement. The following parameters were measured: red blood cell velocity; vessel diameter; number of functional capillaries; and number of rolling, sticking, and transmigrating neutrophils and lymphocytes. Wilcoxon's rank sum test was used for statistical comparison. Poly-I:C caused a 70% increase in the main artery diameter and a 7% increase in velocity. But as a consequence of dynamic activation of leukocyte interaction, a 30% drop in functional capillary perfusion was observed. Injury to the entire vascular endothelium was confirmed by a 160% increase in transmigrating leukocytes. Treatment with IFN-gamma inhibited the poly-I:C-induced inflammation, as shown by 88%, 63%, and 85% decreases in rolling, sticking, and transmigrating leukocytes respectively, and by a 28% increase in capillary perfusion. Treating the system with IFN-gamma in advance, inhibited poly-I:C-induced inflammation, shown by marked decreases in rolling, adhering, and transmigrating leukocytes, and a notable increase in perfused capillaries. These observations reflect an inhibitory effect of IFN-gamma on leukocyte adhesion molecule expression in vascular endothelium in response to dsRNA in a muscle flap at the microcirculatory level.

Animals↗
PubMed1999

In vivo microscopic assessment of cremasteric microcirculation during hindlimb allograft rejection in rats.

Experimental and clinical studies of vascular allogenic extremity transplantation have yielded disappointing results and have not been clinically useful. With recent advances in transplantation immunology, considerable interest has focused on the understanding of leukocyte-endothelial interaction at the microcirculatory level. The objective of this study was to characterize the alterations in leukocyte-endothelial interaction in the early stages of rat hindlimb allograft rejection. To study the changes at the microcirculatory level, a new microsurgical model was developed; the cremaster muscle was incorporated into the transplanted hindlimb. The purpose of this study was to report on the microcirculatory changes during rat hindlimb allograft rejection. A total of 24 transplantations were performed among the four experimental groups. In a control group, 12 rat hindlimb-cremaster grafts were transplanted between genetically identical animals, Lewis to Lewis. Microcirculatory measurements of graft survival were taken at 24 hours (group 1A, n = 6) and at 72 hours (group 1B, n = 6). In the rejection control group, 12 transplantations were performed across a major histocompatibility barrier between Lewis-Brown Norway and Lewis rats. Microcirculatory measurements were taken at 24 (group 2A, n = 6) and 72 hours (group 2A, n = 6) as above. The following parameters were evaluated to discover the leukocyte-endothelial interaction: endothelial edema index and the number of rolling, adherent, and transmigrating leukocytes and lymphocytes in the postcapillary venule. Physical signs of limb rejection, such as edema, erythema, scaling, plaque formation on the skin, hair loss, and skin surface temperature, were monitored. Microcirculatory signs of rejection included the following. There was a significant increase in the number of adherent leukocytes in allograft transplants at both 24 hours (205 percent; 2.05 +/- 0.38) and 72 hours (431 percent; 9.11 +/- 3.41) when compared with isograft controls (1.00 +/- 0.89 at 24 hours; 2.11 +/- 0.34 at 72 hours) (p < 0.05). The activation of leukocyte transmigration increased more than 7-fold in muscle allografts at 24 hours (0.55 +/- 0.25 versus 4.16 +/- 1.89) and more than 6-fold at 72 hours (0.72 +/- 0.38 versus 4.38 +/- 1.28) after transplantation (p < 0.05). Endothelial edema index, a measure of endothelial swelling and cellular deposit accumulation, increased more than 119 percent in the allograft group 72 hours after transplantation (1.23 +/- 0.07 versus 1.46 +/- 0.09) (p < 0.05). The first clinical signs of limb rejection were scaling of the skin or hair loss; they were observed between the seventh and ninth postoperative days. The composite rat hindlimb-cremaster model presented in this study introduces a new in vivo approach to monitor acute graft rejection using the intravital microscopy system. This is a valuable model for defining the timing, sequence, and correlation between immunologic events and clinical signs during the acute phase of allograft rejection.

Abdominal Muscles↗
PubMed1999

Blockade of platelet endothelial cell adhesion molecule-1 (PECAM-1) protects against ischemia-reperfusion injury in muscle flaps at microcirculatory level.

Several lines of evidence show that platelet endothelial cell adhesion molecule-1 (PECAM-1), a component of endothelial cell junctions, is required for leukocyte transmigration through endothelial cell monolayers. Polymorphonuclear leukocytes play an important role in ischemia-reperfusion injury. We sought to determine whether administering an anti-PECAM-1 antibody would prevent or attenuate ischemia-reperfusion injury in a rat cremaster muscle flap injury model. Eighteen male Sprague-Dawley rats were divided into three groups. Group I (control): Cremaster muscle island flaps were dissected for baseline measurements of eight indicators: numbers of rolling, sticking, and transmigrating neutrophils, numbers of rolling and sticking lymphocytes, number of perfused capillaries, endothelial edema, and vessel permeability. Group II: The prepared cremaster flap was subjected to 4 hours of ischemia and 24 hours of reperfusion. Group III: The muscle flap was subjected to ischemia and reperfusion as in group II, and anti-PECAM-1 antibodies (1 mg/kg) were injected subcutaneously 15 minutes before reperfusion. Blood vessels were observed in vivo under an intravital microscopy system. Microvascular permeability was made visible with injected fluorescein isothiocyanate-labeled albumin and evaluated with Kontron Elektronik computer software. The ischemia-reperfusion-alone group (group II) presented a 225-percent increase in the activation of sticking leukocytes (2.4 +/- 0.4 to 7.8 +/- 0.8, p < 0.05) (p < 0.01). This leukocyte activation was reduced by 83 percent following anti-PECAM-1 monoclonal antibody treatment (1.3 +/- 0.5 per 100 microm) (p < 0.01). At 24 hours, endothelial injury in group II was confirmed by a 4-fold increase in the number of transmigrating leukocytes into the interstitial space (7.6 +/- 1.2 per field versus 1.9 +/- 0.4 per field in controls). This phenomenon was reduced by 85 percent following anti-PECAM-1 monoclonal antibody treatment (1.1 +/- 0.2 per field) (p < 0.01). Analysis showed that the number of flowing capillaries was 67 percent lower in group II (6.8 +/- 0.3 to 2.2 +/- 0.7, p < 0.01). Anti-PECAM-1 antibody treatment caused a 2.5-fold increase in this number (5.6 +/- 0.5, p < 0.01). Microcirculatory permeability index showed a 180-percent increase in group II (p < 0.05) when compared with baseline values. This increased albumin leakage was effectively attenuated by antibody treatment (p < 0.05). Blocking the action of PECAM-1 in vivo by administering monoclonal antibodies significantly attenuated ischemia-reperfusion injury, presumably by inhibiting transendothelial migration of neutrophils and by increasing capillary perfusion at a muscle flap microcirculatory level.

Animals↗
PubMed1999

Muscle flaps' triphasic microcirculatory response to sympathectomy and denervation.

Whether sympathectomy and somatic denervation in muscle flaps increased microcirculatory flow in the short or long term, thus producing an effect similar to the delay phenomenon, which increases survival in transferred skin flaps, was determined. The rat cremaster muscle flap model was used for in vivo microscopy. In the left cremasters of 30 Sprague-Dawley rats, the genitofemoral nerve was divided and the proximal vessels were stripped of their adventitia. The muscle was not elevated. In each rat, the contralateral cremaster served as the control. The rats were assigned to one of five groups: no delay before observation, a 24-hour delay, a 48-hour delay, a 7-day delay, or a 14-day delay. After the delay, red blood cell velocity, vessel diameters, number of functional capillaries, and leukocyte-endothelial interactions were measured. Microvessel response to topical vasoactive substances was measured. Immediately after denervation, red blood cell velocity increased transiently (71 percent; p = 0.006). Main arterioles dilated (20 percent; p = 0.02) at 24 hours, and capillary perfusion increased 36 percent (p = 0.001) at 2 weeks. The microvessels had hyperactive responses to all vasoactive agents 2 weeks after denervation. These findings indicate that proximal sympathectomy with somatic denervation leads to a triphasic, dynamic response in the peripheral microcirculation of the cremaster muscle flap. An initial acute hyperadrenergic phase was followed by a nonadrenergic phase, with significant vasodilatation, and a sensitized phase, with increased capillary perfusion and hyperresponsiveness to vasoactive substances. This study shows that with minimal access to the cremaster muscle flap neurovascular pedicle and without changing the blood supply to the flap, significant hemodynamic improvements can be made in the peripheral microcirculation.

Animals↗
PubMed1999

Effects of 8-Gy radiation on the microcirculation of muscle flaps in the rat.

Combination of radical excision and radiation has been used as a treatment modality for cancer patients. As a result, in reconstructive surgery there is often a need to harvest flaps in the vicinity of previously irradiated tissues. Radiation has been shown to cause progressive injury to the macrocirculation and microcirculation, often jeopardizing flap survival. The purpose of this study was to examine whether radiation significantly affects the sequence of leukocyte-endothelial interactions or the hemodynamics of the muscle flap in both acute and chronic situations. Male Sprague-Dawley rats (n = 42) were divided into seven groups of six rats each. Rats in group I were not irradiated. Groups II through VII received 8-Gy radiation to the right groin and scrotum. Groups II, III, and IV were examined at 4, 24 and 72 hours, respectively, and groups V, VI, and VII were examined at 1, 2 and 12 weeks. For intravital microscopy, the cremaster muscle was dissected on its neurovascular pedicle. Vessel diameters and red blood cell velocities were measured in the central cremasteric branches and branch arterioles. Capillary perfusion was evaluated in 27 visual fields of each flap. Leukocyte-endothelial interactions were evaluated by numbers of rolling, adhering, and transmigrating leukocytes in post-capillary venules. In the same postcapillary venule, we measured the endothelial edema index (constriction index). The hemodynamics of irradiated flaps did not differ significantly from those of controls. Diameter and red blood cell velocity were increased in the first- and second-order arterioles and were highest at 72 hours and 1 week. After irradiation, third-order arterioles were constricted. Radiation reduced capillary perfusion by 4.3, percent. None of the differences were statistically significant. Neither leukocyte behavior nor the constriction indices differed among the groups. In conclusion, low-dose radiation of 8 Gy does not affect hemodynamics or leukocyte-endothelial interactions of muscle flaps in the rat. Muscle tissue with intact microvasculature can be harvested for reconstructive procedures after low-dose radiation.

Animals↗