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H Suchy

Publications and source records attributed to H Suchy.

At least 19 recordsLinked to original sources
PubMed2001

Effects of liposome-mediated gene transfer of VEGF in ischemic rat gracilis muscle.

The purpose of the current study was to determine the effects of vascular endothelial growth factor (VEGF) on muscle flap survival and vascularity in a rat gracilis ischemia-reperfusion model. A total of 12 adult male Wistar rats were divided into two groups (n = 6). The experimental group received the plasmid encoding VEGF(165) cDNA plus lipofectamine (cationic liposome) injected directly to the gracilis muscle following 4 h of ischemia. The control group received lipofectamine only. The viability and vascularity of the flaps were evaluated after 7 days of reperfusion. The data demonstrated that the VEGF plasmid- and lipofectamine-treated muscle flaps had significantly greater total survival and capillary count 7 days after reperfusion compared with the flaps treated only with lipofectamine. These results indicate that VEGF exerts a protective effect on ischemic skeletal muscle flaps.

Animals↗
PubMed2001

Inhibition of the initial wave of NF-kappaB activity in rat muscle reduces ischemia/reperfusion injury.

Nuclear factor kappaB (NF-kappaB) is thought to play an important role in the expression of genes expressed in response to ischemia/reperfusion (I/R) injury. In this report, the activation of NF-kappaB in rat skeletal muscle during reperfusion following a 4-h ischemic period was studied. NF-kappaB activation displayed a biphasic pattern, showing peak activities from 30 min to 3 h postperfusion and 6 h to 16 h postperfusion, with a decline to baseline binding activity levels between 3 h and 6 h. Inhibition of NF-kappaB activation was investigated using proline dithiocarbamate (Pro-DTC). NF-kappaB binding activity during reperfusion was significantly reduced by intravenous administration of Pro-DTC. Additionally, Pro-DTC resulted in decreased muscle edema and neutrophil activity, with an increased percentage of muscle survival compared with vehicle controls. These results demonstrate that NF-kappaB is activated during reperfusion in a biphasic manner and that the regulation of the initial phase of NF-kappaB activation affords physiological protection against a severe ischemic stress. Selective inhibition of NF-kappaB during early reperfusion may therefore be a therapeutic intervention for I/R injury.

Active Transport, Cell Nucleus↗
PubMed1999

Induction of heat-shock protein 72 in rat skeletal muscle does not increase tolerance to ischemia-reperfusion injury.

Ischemia-reperfusion injury is implicated in the failure of free flap and replant surgeries and is associated with the pathogenesis of a wide variety of clinical diseases including stroke, myocardial infarction, spinal injury, and compartment syndromes. We used a skeletal muscle flap model to test if the induction of heat-shock protein 72 (HSP72) by mild hyperthermia provides tolerance against ischemia-reperfusion injury. Immunocytochemistry and Western blot analysis verified increased production of HSP72 in the gracilis muscle of globally heated rats. Neutrophil accumulation in the microvasculature and postischemic muscle survival after ischemia-reperfusion were unaltered by preischemic hyperthermia, indicating HSP72 induction is not sufficient to provide resistance against severe injury in skeletal muscle.

Adaptation, Physiological↗
PubMed1999

Single-vessel arteriovenous revascularization of the amputated ear.

Successful single-vessel arteriovenous replantation of a completely amputated human ear is described. This result was followed by an experimental study using a rabbit model, to confirm that an amputated ear could survive replantation with only a single arteriovenous anastomosis. Fifteen animals were placed in one of two experimental groups: Group 1-arteriovenous replantation, no treatment (n = 6); and Group 2-arteriovenous replantation with medicinal leeching (n = 9). All ears demonstrated initial reperfusion of the replantation immediately following microanastomosis. Laser Doppler flow readings in the non-leeched replanted ears fell to zero by 8 hr and, by 12 hr, the non-leeched ears demonstrated signs of necrosis. All the leeched, replanted ears demonstrated perfusion and complete viability at the time of sacrifice. The case report, combined with the results from the experimental study, confirm that single-vessel arteriovenous replantation of an amputated ear is feasible.

Adult↗
PubMed1999

Augmentation of cAMP improves muscle-flap survival and tissue inflammation in response to ischemia/reperfusion injury.

The authors hypothesized that augmenting skeletal muscle adenosine 3',5'-cyclic monophosphate (cAMP) levels could reduce tissue inflammation and improve muscle survival in response to ischemia/ reperfusion (I/R) injury. Gracilis muscle flaps in male Wistar rats were subject to 4 hr of ischemia followed by 3 hr of reperfusion, to assess neutrophil accumulation and microvessel tone, or by 24 hr to evaluate percentage of muscle survival. Animals were grouped as follows: positive (saline) or negative (sham) control, or with infused cAMP elevating agents (8 Bromo-cAMP (8 Br-cAMP) or forskolin). Radioimmunoassay demonstrated significant increases in tissue cAMP levels throughout 3 hr of reperfusion with forskolin, while the 8 Br-cAMP-treated group showed only a temporary increase. Compared with vehicle-infused controls, forskolin administered 5 min prior to reperfusion and repeated as an infusion during the first 45 min of reperfusion, resulted in reduced neutrophil adherence and transmigration, and muscle edema with sustained vasodilatation. The percentage of muscle survival using nitro-blue tetrazolium staining demonstrated enhanced muscle-flap preservation with forskolin. There was no beneficial change in the presence of 8 Br-cAMP These observations suggested that sustained elevation of the cAMP pathway may reduce ischemia-reperfusion injury by decreasing neutrophil-mediated injury and improving vessel tone. Elucidation of the cAMP pathway may provide novel opportunities to modulate ischemia/ reperfusion injury.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

Role of the thromboxane A2 receptor in the vasoactive response to ischemia-reperfusion injury.

Neutrophil-endothelial adhesion in venules and progressive vasoconstriction in arterioles seem to be important microcirculatory events contributing to the low flow state associated with ischemia-reperfusion injury of skeletal muscle. Although the neutrophil CD-18 adherence function has been shown to be a prerequisite to the vasoconstrictive response, the vasoactive substances involved remain unknown. The purpose of this study was to evaluate the role of thromboxane A2 receptor in the arteriole vasoactive response to ischemia-reperfusion injury. An in vivo microscopy preparation of transilluminated gracilis muscle in male Wistar rats (175 +/- 9 g) (n = 12) was used for this experiment. Three experimental groups were evaluated in this study: (1) sham, flap raised, no ischemia (20 venules, 20 arterioles), (2) 4 hours of global ischemia only (19 venules, 22 arterioles), and (3) 4 hours of global ischemia + thromboxane A2 receptor antagonist (ONO-3708) (17 venules, 20 arterioles). ONO-3708 (5 mg/kg), a specific competitive antagonist of thromboxane A2 receptor, was infused at a rate of 0.04 ml/minute into the contralateral femoral vein 30 minutes before reperfusion. Mean arterial blood pressure was not changed at this dose of ONO-3708 (88 +/- 6 mmHg before infusion, 81 +/- 4 mmHg after infusion, n = 3). The number of leukocytes rolling and adherent to endothelium (15-sec observation) were counted in 100-microm venular segments, and arteriole diameters were measured at 5, 15, 30, 60, and 120 minutes of reperfusion. Leukocyte counts and arteriole diameters were analyzed with two-way factorial analysis of variance for repeated measures and Duncan's post hoc mean comparison. Statistical significance was indicated by a p < or = 0.05. The ischemia-reperfusion-induced vasoconstriction was significantly reduced by the thromboxane A2 receptor antagonist (ONO-3708). The mean arteriole diameters at 30, 60, and 120 minutes reperfusion were significantly greater in the treated animals than in the ischemia-reperfusion controls. Despite a significant increase in treated mean arteriole diameters, 30 percent of arterioles still demonstrated vasoconstriction. Neutrophil-endothelial adherence was not reduced by ONO-3708. Thromboxane A2 receptor blockade significantly reduces but does not eliminate ischemia-reperfusion-induced vasoconstriction in this model. This finding suggests that additional and perhaps more important vasoactive mediators contribute to vasoconstriction. Furthermore, thromboxane A2 receptor blockade has no effect on polymorphonuclear endothelial adherence.

Animals↗
PubMed1998

Effect of ketorolac tromethamine (Toradol) on ischemia-reperfusion injury in skeletal muscle.

The eicosanoids, leukotriene B4 (LTB4) and thromboxane A2 (TXA2), contribute to neutrophil adhesion and arteriole vasoconstriction, important microcirculatory events in ischemia-reperfusion (I-R) injury. The purpose of this study was to evaluate the effect of ketorolac on I-R injury of skeletal muscle. A videomicroscopic preparation of gracilis muscle in male Wistar rats (n=7) in two experimental groups was evaluated: Group 1-4 hr global ischemia only (19 arterioles, 19 venules), and Group 2-4 hr ischemia plus ketorolac (13 arterioles, 14 venules). Ketorolac (0.86 mg/kg, i.m.) was given 30 min prior to reperfusion. The number of neutrophils, rolling and adherent, was counted in 100-micron venular segments, and arteriole diameters were measured at 5, 15, 30, 60 and 120 min of reperfusion. The I-R-induced increase in neutrophil adhesion was significantly reduced by ketorolac, which significantly increased arteriolar vasodilation in the first 30 min of reperfusion and significantly reduced the I-R-induced vasoconstriction in arterioles at 30 min; this effect was lost at 1 hr of reperfusion. Although ketorolac augments immediate arteriole vasodilation and blocks subsequent vasoconstriction, this effect appears to be transient. These findings suggest that ketorolac may have potential as a treatment for I-R injury.

Animals↗
PubMed1998

Microcirculatory studies of frostbite injury.

Frostbite represents a spectrum of injury ranging from irreversible cellular destruction to reversible changes seen after rewarming. These changes include increases in tissue edema, circulatory stasis, and progressive thrombosis leading to further tissue necrosis. For this reason, it is often difficult at the time of surgical debridement to determine the extent of frostbite injury. This delayed tissue injury is similar to that seen in muscle during ischemia/reperfusion injury. Muscle that initially appears viable on reperfusion may subsequently necrose due to collapse of the microcirculation. Adherent neutrophils have been specifically cited as important components in ischemia/reperfusion injury and have also been suggested to play a role in frostbite injury. We have used an intravital microscopic muscle preparation to study microcirculatory changes carefully in frostbite injury during rewarming. The right gracilis muscle of male Wistar rats is dissected free from its primary vascular pedicle and the rat is positioned on a specially constructed microsurgical stage. Temperature changes of the muscle are recorded. The prepared axial pattern flap is transilluminated with a microscope and projected on a video screen, allowing measurement of arteriolar diameters and changes in the numbers of stuck and rolling neutrophils before frostbite, during rewarming, and for several hours later. Cold silicone oil is used to freeze the muscle to -5+/-2 degrees C in 2 to 3 minutes and to hold this temperature for 5 minutes. The muscle is rewarmed with 42 degrees C normal saline placed directly on the muscle surface. Baseline vessel diameter and leukocyte counts in 100-mm segments of the microvasculature are recorded as well as at 5, 15, and 30 minutes, and at 1, 2, and 3 hours postrewarming of frozen muscle. Observations from our initial 11 animals show that reperfusion of the muscle following freezing is varied temporally and spatially, with circulation to most vascular segments restored 5 to 10 minutes after rewarming. In 9 of 11 animals we observed the shedding of "white clots" in small arterioles and venules occurring as soon as 5 minutes after thawing. In some instances shedding continued for as long as 1 hour after rewarming. Microvascular hemorrhage was widespread 1 hour following the thaw, but there was no significant increase in neutrophil adherence observed until 3 hours following rewarming. The exact nature of the vascular injury and the composition of the "white clots" are now being determined from ultrastructural studies. Blood flow in microcirculation stops during freezing, but small-vessel perfusion returns immediately on thawing. This suggests that the vascular architecture is maintained during the freezing and thawing. Unlike ischemia/reperfusion injury, neutrophil adhesion plays a smaller role in the early response to frostbite injury. The early microcirculatory observations seen after rewarming suggest progressive and severe perturbations in platelet function and fibrin formation that are significantly different from ischemia/reperfusion injury.

Animals↗
PubMed1997

Ischemia-reperfusion injury in skeletal muscle: CD 18-dependent neutrophil-endothelial adhesion and arteriolar vasoconstriction.

The purpose of this study was to evaluate if the venular neutrophil-endothelial adhesion associated with ischemia-reperfusion of skeletal muscle is dependent on leukocyte adhesion glycoprotein CD18 function and to determine if this interaction influences the vasoactive response in nearby arterioles. An in vivo microscopy preparation of transilluminated gracilis muscle in 13 male Wistar rats was used for this experiment. Observations of nonischemic muscle (sham) demonstrated this preparation to be stable for 8 hours with negligible change in neutrophil adherence or arteriole diameter. Three groups were evaluated in this study: (1) sham, no ischemia, no treatment (n = 5, 20 arterioles. 20 venules), (2) 4 hours of global ischemia only (n = 4, 19 venules, 22 arterioles), and (3) 4 hours of ischemia plus monoclonal antibody against CD18 (n = 4, 12 venules, 9 arterioles). The murine monoclonal antibody (WT.3, Seikagaku America, Inc.), which binds the rat leukocyte function antigen I CD18 chain, was infused into the contralateral femoral vein 30 minutes prior to reperfusion. The number of leukocytes rolling and adherent to endothelium (15 seconds of observation) was counted in 100-microns venular segments, and arteriole diameters were measured at various times during reperfusion. All counts and measurements were normalized to baseline preischemic readings for each animal. Mean changes from baseline were compared between groups. The increase in ischemia-reperfusion-induced neutrophil-endothelial adherence in venules was blocked by monoclonal antibody, but rolling behavior was not changed. The ischemia-reperfusion-induced progressive vasoconstriction in arterioles was blocked by monoclonal antibody. These results suggest that (1) neutrophil-endothelial adherence function associated with ischemia-reperfusion in this model is CD18-dependent, (2) neutrophil rolling function does not appear to be dependent on CD18, and (3) neutrophil CD18 function is a prerequisite for ischemia-reperfusion-induced arteriolar vasoconstriction. These findings provide important mechanistic information that may help explain the deleterious microcirculatory events associated with ischemia-reperfusion injury skeletal muscle.

Animals↗
PubMed1996

The use of cultured Schwann cells in nerve repair in a rabbit hind-limb model.

A 3-cm peripheral nerve gap in a rabbit hind-limb model was repaired by using a polyglycolic acid (PGA) conduit filled with a gelatin/Schwann-cell suspension. Postoperative nerve function after 16 weeks, as measured by isometric twitch and tetanic muscle strengths, and nerve conduction velocities, failed to demonstrate a statistically significant difference, compared to a control group in which the nerve gap was reconstructed by using a PGA conduit filled with gelatin only. The 3-cm gap in the described model may not have been long enough to show a significant difference between the two groups. Alternatively, the transferred cultured Schwann cells may have been functionally inactive.

Animals↗
PubMed1996

The effects of chronic ketorolac tromethamine (toradol) on wound healing.

Intramuscular ketorolac is a commonly used nonsteroidal anti-inflammatory (NSAI) agent for analgesia in surgical patients. Increasing numbers of surgical patients are chronically taking some form of an NSAI drug. We examined the effects of "chronic" intramuscular ketorolac on the healing of a closed linear surgical wound in the rat. Wistar rats were pretreated with 4 mg per kilogram per day ketorolac intramuscularly prior to receiving dorsal incisional wounds. The ketorolac treatment was continued and after 2 weeks the wounds were excised and separated with a tensiometer to measure mechanical properties. Breaking strength was directly measured, tensile strength was calculated, and collagen concentrations at the wound site were determined. A significant decrease in the mean breaking strength was seen in the ketorolac-treated animals when compared to controls. The ketorolac-treated animals had a mean tensile strength less than the controls, although this difference did not reach statistical significance. The mean collagen concentration of the ketorolac-treated wounds was significantly less than the untreated wounds. Use of ketorolac for just 1 week prior to surgery in rats produced a significant decrease in the breaking strength of their wounds. With the increasing use of ketorolac in surgical patients as well as the increasing use of oral NSAI drugs, more study of this effect is warranted.

Animals↗
PubMed1995

A model for recording the microcirculatory changes associated with standardized electrical injury of skeletal muscle.

The rate of major limb amputation following high voltage electrical injury remains high despite a decrease in mortality rate. Several theories about the pathophysiology of electrical injury have been discussed in the literature and different clinical regimens have been attempted to decrease the high amputation rate. However, to date, the overall tissue response after electrical injury remains incompletely understood with nothing new to offer these unfortunate patients. We have developed a rat gracilis muscle intravital microscopy preparation in order to better understand the mechanisms of this injury. A standardized 40-V stimulation of 10-sec duration was applied to the anterior belly of the gracilis muscle which translated into a current load of 30 mA. The current density was 750 mA/cm2. Sequential intravital assessment of microcirculatory changes before injury, as well as 5, 15, 30, 60, 120, 180 and 240 min after injury was performed. Consistent findings included initial cessation of blood flow in many capillary beds, focal flow reversal, venous and arterial vascular spasm. Restitution of microvascular flow varied from several minutes to 1 hr and was preceded by vasodilation at 5-15 min following the injury (+16.9 microns from baseline at 15 min). Starting at 30 min progressive vasoconstriction was noted (-0.8 micron from baseline at 30 min, -31.3 microns from baseline at 4 hr). High resolution observation of neutrophil behavior showed an increase in the number of these cells adherent to venular endothelium in areas exhibiting circulatory disturbances (+11.4 cells at 5 min, +15 cells at 4 hr). The standardization of this model allows a quantitative method of evaluating the microcirculatory changes associated with electrical injury and of studying ways to prevent tissue damage. The microcirculatory changes induced by electrical injury were similar to those reported in ischemia-reperfusion injury of skeletal muscle.

Animals↗
PubMed1994

Vitamin A-soaked gelfoam sponges and wound healing in steroid-treated animals.

Previous work has shown improved wound healing after the administration of systemic vitamin A in patients on chronic steroids. In contrast there have been mixed reports on the effect of topical vitamin A on wound healing in steroid-treated patients. Previous laboratory work has suggested that the topical application of vitamin A may be beneficial to wound healing in a sutured wound in a steroid-treated rat. Due to some inconsistencies in previous studies and steroid animal models, we sought to develop a better wound-healing model in a steroid-treated rat and to assess the effect of topical vitamin A as part of the wound closure. With preliminary studies, we developed a consistent and reliable wound-healing model in a steroid-treated rat using dexamethasone in contrast to cortisone acetate, which had been used in previous studies. Next, rats were randomized into 8 groups, some of which received steroids. Wounds were treated with saline or vitamin A topically or via a soaked gelfoam sponge. Rats were wounded 1 week after the commencement of steroid administration. Wounds were repaired and allowed to heal for 2 weeks. Strips of the wounds were then harvested and tested for tensile strength and breaking strength using a tensiometer. Wound edges were then fixed and wound surface area was measured using digital planimetry. Steroid treatment resulted in consistent weight loss and failure to gain weight as well as decreased breaking strength. Tensile strength was not decreased. Vitamin A applied for 10 minutes before wound closure and a gelfoam sponge alone placed before wound closure both resulted in an increased breaking strength and tensile strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1993

Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen.

The morphologic events in the microcirculation that lead to reperfusion injury of ischemic skeletal muscle remain incompletely understood. The purpose of this experiment was to evaluate leukocyte endothelial adherence characteristics and dynamic changes in microvessel caliber during reperfusion of an in vivo skeletal muscle ischemia preparation. In addition, the effect of hyperbaric oxygen treatment on these microcirculatory changes also was studied. An intravital microscopy preparation of a transilluminated gracilis muscle in 27 rats was used to observe a total of 101 arterioles and 63 venules (13 to 73 microns diameter). Baseline hemodynamics were videotaped for 30 minutes following muscle isolation. The animals were divided into six groups: (1) sham, no ischemia, (2) 4 hours of global ischemia only, (3) no ischemia plus hyperbaric oxygen (one 2.5 ATA/1 hour of treatment with 100% oxygen), (4) 4 hours of ischemia plus hyperbaric oxygen during ischemia, (5) 4 hours of ischemia plus hyperbaric oxygen immediately on reperfusion, and (6) 4 hours of ischemia plus hyperbaric oxygen 1 hour after reperfusion. Changes in arteriolar and venular diameters at specific times during 3 hours of reperfusion were recorded, and the number of adherent and slow-rolling leukocytes in 100-microns venular segments were counted and compared with baseline measurements. The proximity of arterioles to venules was classified as adjacent (< 15 microns) or distant (> 15 microns). No significant changes in leukocyte endothelial adherence or arteriolar diameter were noted in group 1 sham or group 3 nonischemic hyperbaric oxygen-treated rats when compared with baseline measurements. A significant increase in adherent leukocytes was observed in group 2 ischemic venules (+14.9 +/- 2.5) within 5 minutes of reperfusion, which was maintained for 3 hours. Reperfusion measurements of arteriolar diameter in group 2 ischemic muscle preparations demonstrated an initial vasodilation that was followed at 1 hour by a progressive and severe vasoconstriction (-46.9 +/- 11.3 percent at 3 hours) in arterioles adjacent to venules that was not seen in distant arterioles. The increase in adherent leukocytes seen in group 2 ischemic venules was significantly reduced by hyperbaric oxygen treatment given during ischemia (group 4) or up to 1 hour during reperfusion (groups 5 and 6). In addition, the progressive ischemic arteriolar vasoconstriction was inhibited in all groups (4, 5, and 6) treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Detection of foreign bodies in the hand.

Fresh cadaver hands were used to compare the ability of routine x-ray, xeroradiography, computerized tomography, and magnetic resonance imaging to identify a variety of foreign bodies including glass, gravel, plastic, and wood in the soft tissue of the hand. All types of glass were easily seen by all imaging methods. Gravel foreign bodies were visible with all methods except magnetic resonance imaging where ferromagnetic streak artifacts obscured visualization. Plastic, although not seen by routine x-ray or xeroradiography, was faintly seen by computed tomography, and easily detected by magnetic resonance imaging. Wooden foreign bodies, especially when wet, were seen only by computed tomography and magnetic resonance imaging. Xeroradiography had no benefit over plain films in identifying foreign bodies and should be discarded in favor of computed tomography or magnetic resonance imaging when plain films are unrevealing. A practical guide for identifying foreign bodies in the soft tissues of the hand is presented.

Aged↗
PubMed1989

Experimental evaluation of oxygen free radical scavengers in the prevention of reperfusion injury to skeletal muscle.

A prolonged preoperative ischemic interval decreases the chances for successful replantation of an amputated limb. Skeletal muscle is especially sensitive to periods of prolonged ischemia. It is now hypothesized that significant tissue injury occurs during reperfusion, when oxygen-rich blood contacts anaerobic metabolites forming toxic oxygen free radicals. A replantation model, using the rabbit hind limb tibialis anterior muscle, was developed to assess muscle function and histological appearance following ischemic intervals of five and eight hours. Muscle strength five weeks after injury was used as a functional measurement of tissue damage. The effects of the superoxide free radical scavenger superoxide dismutase (SOD) and the hydroxyl radical scavenger dimethylsulfoxide (DMSO), administered systemically just before reperfusion, were studied. Muscle treated with SOD following five hours of ischemia had essentially normal strength and histological appearance; however, there was no protective effect after eight hours. DMSO treatment had no beneficial effects after five hours of ischemia, but after eight hours DMSO-treated muscle had significantly better function than untreated muscle. Histological examination confirmed the functional results. Clinical treatment of ischemic limbs with free radical scavengers before revascularization may aid in avoiding reperfusion injury and may improve survival and later muscle function.

Animals↗
PubMed1988

Experimental pretransfer expansion of free-flap donor sites: I. Flap viability and expansion characteristics.

Expansion of cutaneous and myocutaneous free-flap donor sites prior to elevation is possible in the pig model. There is no significant difference in survival between control and expanded cutaneous buttock and myocutaneous latissimus dorsi flaps after elevation solely on their axial pedicles. Axial-pattern flap expansion appears to augment capillary blood flow. The maximum amount of expansion occurs directly over the center of the expander and decreases toward the periphery. There is virtually no expansion of skin adjacent to the expander.

Animals↗