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Biomedical subjects

William A Zamboni

Publications and source records attributed to William A Zamboni.

13 recordsLinked to original sources
PubMed2006

Melatonin reduces ischemia/reperfusion-induced superoxide generation in arterial wall and cell death in skeletal muscle.

The purpose of this study was to determine the effect of melatonin on superoxide generation in arterial wall at an early phase of reperfusion and on endothelial dysfunction of microvasculature and cell viability of cremaster muscle at late phase of reperfusion (24 hr) after prolonged ischemia. Bilateral vascular pedicles which supply blood flow to the cremaster muscle were exposed. After surgical preparation, microvascular clamps were applied on the right iliac, femoral and spermatic arteries to create 4 hr of ischemia in both feeding vessels and the unexposed cremaster muscle. The vascular clamping was omitted on the left iliac, femoral and spermatic arteries and served as an internal control. Melatonin or Vehicle was via by intravenous injection at 10 min prior to reperfusion and 10 min after reperfusion. In the first experiment, the vascular pedicle was harvested after reperfusion to measure superoxide generation in real time by lucigenin-derived chemiluminescence. In the second experiment, endothelial-dependent and -independent vasodilatation was examined in the terminal arteriole of cremaster muscle which was then harvested to examine cell viability by WST-1 assay on day 2. Superoxide generation in arterial wall peaked at first 5-min of reperfusion and declined to near baseline after 60 min of reperfusion. Melatonin treatment significantly reduced superoxide generation in arterial walls and improved cell viability in cremaster muscles. Melatonin treatment also significantly reduced microvascular endothelial dysfunction which was still observable in the microcirculation of cremaster muscle after 24 hr of reperfusion. Melatonin reduces superoxide generation in the early phase of reperfusion resulting in attenuating endothelial dysfunction and muscle cell death in the late phase of reperfusion.

Animals↗
PubMed2005

Acute microvascular action of vascular endothelial growth factor in skeletal muscle ischemia/reperfusion injury.

BACKGROUND: The purpose of this study was to investigate the acute action of vascular endothelial growth factor (VEGF) in the microcirculation of skeletal muscle subject to ischemia/reperfusion in vivo and to determine the role of nitric oxide synthase in VEGF-induced microvascular protection. METHODS: A vascular pedicle isolated rat cremaster muscle model coupled with local intraarterial infusion technique was used. Each muscle underwent 4 hours of zero-flow warm ischemia followed by 2 hours of reperfusion. Femoral artery cannulation was performed before reperfusion. The infusate was administered by continuous infusion into the arterial tree of the muscle beginning at 1 minute before reperfusion and at the rate of 0.1 ml/hour throughout the entire reperfusion period. Three groups were designed: (1) the ischemia/reperfusion group, with infusion normal saline; (2) the VEGF plus ische-mia/reperfusion group, with infusion of recombinant human VEGF165 protein; and (3) the L-NA plus VEGF plus ischemia/reperfusion group, with infusion of N-nitro-L-arginine (L-NA; a nonselective nitric oxide synthase antagonist) mixed with VEGF165 protein. After 2 hours of reperfusion, microcirculation measurements including arteriole diameter, capillary perfusion, and endothelium-dependent and endothelium-independent vasodilatation were performed. The muscle was harvested and processed for reverse-transcriptase polymerase chain reaction for measuring eNOS and endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) gene expression. RESULTS: Reperfusion caused significant microvascular alterations including vasoconstriction, poor capillary perfusion, and endothelial dysfunction in the skeletal muscle. These alterations were significantly attenuated by intraarterial infusion of VEGF during reperfusion, but the beneficial effect of VEGF was reduced significantly by coadministration of L-NA. Reverse-transcriptase polymerase chain reaction study revealed that ischemia/reperfusion depressed eNOS mRNA expression but enhanced iNOS mRNA expression. Intraarterial infusion of VEGF during reperfusion amplified mRNA expression of eNOS but not of iNOS. CONCLUSIONS: Local intraarterial infusion of VEGF produced significant microvascular protection from skeletal muscle ischemia/reperfusion injury. The VEGF-induced enhancement of eNOS may play an important mechanistic role.

Animals↗
PubMed2005

Nocardial septic arthritis of the wrist diagnosed and treated by arthroscopy.

This is the first case of Nocardial septic arthritis of the wrist that has been reported without any cutaneous presentation. It was successfully diagnosed and treated with wrist arthroscopy. Arthroscopy is less traumatic and done through smaller incisions than the traditional open technique.

Arthritis, Infectious↗
PubMed2005

Microcirculatory effects of melatonin in rat skeletal muscle after prolonged ischemia.

The purpose of this study was to determine microcirculatory effects and response of nitric oxide synthase (NOS) to melatonin in skeletal muscle after prolonged ischemia. A vascular pedicle isolated rat cremaster muscle model was used. Each muscle underwent 4 hr of zero-flow warm ischemia followed by 2 hr of reperfusion. Melatonin (10 mg/kg) or saline as a vehicle was given by intraperitoneal injection at 30 min prior to reperfusion and the same dose was given immediately after reperfusion. After reperfusion, microcirculation measurements including arteriole diameter, capillary perfusion and endothelial-dependent and -independent vasodilatation were performed. The cremaster muscle was then harvested to measure endothelial NOS (eNOS) and inducible NOS (iNOS) gene expression and enzyme activity. Three groups of rats were used: sham-ischemia/reperfusion (I/R), vehicle + I/R and melatonin + I/R. As compared with vehicle + I/R group, administration of melatonin significantly enhanced arteriole diameter, improved capillary perfusion, and attenuated endothelial dysfunction in the microcirculation of skeletal muscle after 4 hr warm ischemia. Prolonged warm ischemia followed by reperfusion significantly depressed eNOS gene expression and constitutive NOS activity and enhanced iNOS gene expression. Administration of melatonin did not significantly alter NOS gene expression or activity in skeletal muscle after prolonged ischemia and reperfusion. Melatonin provided a significant microvascular protection from reperfusion injury in skeletal muscle. This protection is probably attributable to the free radical scavenging effect of melatonin, but not to its anti-inflammatory effect.

Adjuvants, Immunologic↗
PubMed2004

Ischemic preconditioning-induced microvascular protection at a distance.

Ischemic preconditioning-induced microcirculatory protection appears to be a systemic rather than a local phenomenon. This protection induced by remote ischemic preconditioning (RIPC) may be attributed to a humoral rather than a neuronal mechanism. An innervated (Inn, Groups 1 and 4) or denervated (Den, Groups 2 and 3) and vascular isolated right cremaster of the rat was prepared. Left femoral vessels were clamped (Groups 1, 2, and 4) for 45 min or unclamped (Group 3) as a control. After 2 hr of reperfusion in the left lower extremity, 4 hr of ischemia in the right cremaster was applied in Groups 1, 2, and 3. However, in Group 4, 4 hr of ischemia in the cremaster muscle was instituted before reperfusion of the left femoral artery was begun. Microcirculatory responses, including terminal arteriole diameter, capillary perfusion, and endothelium function were evaluated. Four groups (six rats per group) were designed: Group 1: RIPC (Inn); Group 2: RIPC (Den); Group 3: sham RIPC (Den); and Group 4: fake RIPC (Inn). Ischemia of 45 min followed by 2 hr of reperfusion in the left lower extremity of the rat induced a significant microvascular protection against subsequent 4-hr ischemia in both innervated and denervated cremasters. This microvascular protection at a distance was lost in sham RIPC and in fake RIPC groups. The results demonstrated that remote protection induced by ischemic preconditioning is a systemic phenomenon and due to a humoral mechanism.

Animals↗
PubMed2004

Effect of L-arginine on leukocyte adhesion in ischemia-reperfusion injury.

Nitric oxide has been reported to be beneficial in preserving muscle viability following ischemia-reperfusion injury. The purpose of this study was to evaluate the influence of nitric oxide via L-arginine on leukocyte adhesion following ischemia-reperfusion injury. Intravital videomicroscopy of rat gracilis muscle was used to quantify changes in leukocyte adherence. The gracilis muscle was raised on its vascular pedicle in 48 male Wistar rats. The animals were assigned to one of five groups: (1) nonischemic control; (2) ischemia-reperfusion; (3) ischemia-reperfusion and L-arginine; (4) ischemia-reperfusion and Nomega-nitro-L-arginine methyl ester (L-NAME); and (5) ischemia-reperfusion, L-NAME, and L-arginine. All groups that included ischemia-reperfusion were subjected to 4 hours of global ischemia followed by 2 hours of reperfusion. L-Arginine (10 mg/kg) and L-NAME (10 mg/kg) were infused into the contralateral femoral vein beginning 5 minutes before reperfusion, for a total of 30 minutes. The number of adherent leukocytes was counted at baseline and at 5, 15, 30, 60, and 120 minutes after reperfusion (reported as mean change from baseline, +/- SEM). Groups were compared by repeated-measures analysis of variance (five groups, five times). P < or =0.05 was accepted as significant. L-Arginine significantly reduced leukocyte adherence to venular endothelium during reperfusion when compared with the ischemia-reperfusion group (1.39 +/- 0.92 versus 12.78 +/- 1.43 at 2 hours, p < 0.05). Administration of L-NAME with L-arginine showed no significant difference in adherent leukocytes when compared with the ischemia-reperfusion group (10.28 +/- 2.03 at 2 hours). The nitric oxide substrate L-arginine appears to reduce the deleterious neutrophil-endothelial adhesion associated with ischemia-reperfusion injury. L-NAME (nitric oxide synthesis inhibitor) given concomitantly with L-arginine reversed the beneficial effect of L-arginine alone, indicating that L-arginine may be acting via a nitric oxide synthase pathway. These results suggest an important role for nitric oxide in decreasing the neutrophil-endothelial interaction associated with ischemia-reperfusion injury.

Animals↗
PubMed2004

A quantitative method for determining polarization of neutrophil adhesion molecules associated with ischemia reperfusion.

Ischemia-reperfusion-induced neutrophil adhesion to endothelium is CD18-dependent, but information regarding polarity of CD18 adhesion molecules remains speculative. This study evaluated neutrophil adhesion using an in vitro cell adhesion assay and introduces a quantitative method of measuring CD18 membrane distribution using confocal microscopy. Neutrophils from normal animals were isolated from whole blood and incubated with plasma from rat gracilis muscle flaps with no ischemia and reperfusion (nonischemic control, n = 10) or 4 hours of ischemia and 90 minutes of reperfusion (ischemia/reperfusion, n = 10), on coverslips pretreated with and without (phosphate-buffered saline) soluble intercellular adhesion molecules. Coverslips without intercellular adhesion molecules represented a negative control (intercellular adhesion molecules were required for adhesion). Percent adherence to intercellular adhesion molecules was expressed as a ratio of adherent cells/total cells. CD18 polarization was assessed by staining neutrophils with fluorescein isothiocyanate-labeled anti-CD11b, followed by confocal microscopy and Z-stack analysis. Membrane-associated CD18 was expressed as fluorescence intensity units in three equal areas of the cell membrane. Capping was defined as twice as much fluorescence in 33 percent of the cell membrane as in the remaining 67 percent. Neutrophils exposed to ischemia and reperfusion plasma showed a significant increase in adhesion (0.8 +/- 0.1 percent versus 16.7 +/- 2.2 percent, p < 0.001) and CD18 polarization (6.2 +/- 1.7 percent versus 43.9 +/- 12.2 percent, p = 0.0206) compared with controls. This article describes an in vitro assay that reliably reproduces the neutrophil adhesion phenomenon associated with ischemia-reperfusion injury. Results from confocal microscopy allowed for quantitative estimation of membrane-associated receptor polarization.

Animals↗
PubMed2003

Hyperbaric oxygen and wound healing.

Problem wounds, which fail to respond to traditional medical and surgical therapy, can be challenging to the plastic surgeon. Surgical, outpatient, and inpatient wound care costs can be exorbitant. Indirect costs, such as those related to patient productivity, disability, and premature death, can also be significant. The underlying problem in failure of a wound to heal is usually hypoxia and infection. HBO treatments in selected patients can facilitate healing by increasing tissue oxygen tension, thus providing the wound with a more favorable environment for repair. Therefore, HBO therapy can be an important component to any comprehensive wound care program.

Blood Gas Monitoring, Transcutaneous↗
PubMed2002

Microvascular protection induced by late preconditioning was abolished in STZ-induced acute diabetic rats.

The authors attempted to determine whether ischemic preconditioning (IPC) can provide microvascular protection in skeletal muscle of diabetic rats against injury from a subsequent (24 hr later) prolonged period of ischemia and reperfusion. Male Sprague Dawley rats weighting 80 to 100 g were injected intraperitoneally with either streptozotocin (STZ, 65 mg/kg) or vehicle (sodium citrate, pH 4.5). Rats with a fasting blood glucose level over 300 mg/dl 1 week after injection of STZ were considered acute diabetic. The cremaster muscle of the rats underwent 45 min of IPC and 24 hr later, 4 hr of warm ischemia followed by reperfusion (I/R). Four groups were compared: IPC in normal rats (n=8); sham IPC in normal rats (n=8); IPC in diabetic rats (n=6); and sham IPC in diabetic rats (n=4). Microvascular responses in the cremaster muscle to IPC were determined by measuring the diameter of feeding, terminal arterioles and capillary perfusion using intravital microscopy, and by the evaluation of the endothelium-dependent nitric oxide system in the terminal arterioles. The average diameter of the feeding and terminal arterioles, as well as capillary perfusion, were significantly decreased in diabetic animals, compared to normal animals. There was a significant endothelial dysfunction detected in the terminal arterioles of diabetic rats. Ischemic preconditioning provided significant microvascular protection against prolonged ischemia/reperfusion in normal rats, but not in diabetic rats. IPC-induced microvascular protection in the normal skeletal muscle was abolished in STZ-induced acute diabetic rats.

Animals↗
PubMed2002

Effect of liposuction on skin perfusion.

Clinical reports of full-thickness skin necrosis have raised concern about the thermal and dermal ischemic effects of ultrasound-assisted liposuction. The purpose of this study was to evaluate skin perfusion in patients treated with ultrasound-assisted liposuction or suction-assisted liposuction. Patients (n = 75) were studied prospectively in the perioperative period surrounding their suction-assisted liposuction (31 patients) or ultrasound-assisted liposuction (64 patients). The laser Doppler flowmeter was used to monitor skin perfusion in the treated regions preoperatively, intraoperatively, and postoperatively at a series of time intervals. The effects of the anesthetic, wetting solution, and type of liposuction (suction-assisted liposuction or ultrasound-assisted liposuction) on skin perfusion were measured. Anesthetic induction significantly increased measured skin perfusion. Wetting solution infusion significantly decreased skin perfusion (-57.4 percent +/- 2.0) by 15 minutes postinfusion. Skin perfusion in the ultrasound-assisted liposuction group was significantly greater than that of the suction-assisted liposuction patients at 1 hour, 1 day, and 1 week postoperatively; however, by 2 to 5 weeks, no difference in skin perfusion was noted and skin perfusion had returned to preoperative levels in both groups. Although skin perfusion in the suction-assisted liposuction group was significantly lower than in the ultrasound-assisted liposuction group in the early postoperative period, no differences in skin perfusion between the groups were noted beyond 1 week postoperatively, suggesting that neither technique impairs perfusion.

Adolescent↗