Biomedical subjects

C R Forrest

Publications and source records attributed to C R Forrest.

At least 37 records · Page 2Linked to original sources

PubMed1999

Intraocular and intraorbital compartment pressure changes following orbital bone grafting: a clinical and laboratory study.

Visual loss is an uncommon but catastrophic complication after intraorbital bone grafting for the reconstruction of acute traumatic defects or long-standing enophthalmos. Increased intraocular or intraorbital compartment pressure may be pathogenic in this setting. A two-part study was designed to test the null hypothesis that intraocular and intraorbital compartment pressure values remain constant despite orbital volume reduction with graft material. Laboratory study: Intraocular and intraorbital compartment pressures were measured during sequential orbital volume reduction in New Zealand White rabbits that had been randomized to one of three groups: intact orbits (n = 10), acute orbital wall defects (n = 8), and chronic (3 months) orbital wall defects (n = 11). Intraocular pressure was significantly (p<0.05) elevated in all three groups of orbits undergoing orbital volume reduction compared with control, nonoperated orbits. Intraorbital compartment pressure values did not change significantly from control levels throughout the grafting sequence. Although no significant differences existed between groups in the maximum levels of intraocular pressure attained, the chronic group demonstrated a greater rate of rise and slower rate of decline. Clinical study: Using applanation tonometry, intraocular pressure was measured before and serially after orbital floor exploration and intraorbital placement of split calvarial bone grafts in 19 patients who presented with orbital-zygomatic complex fractures that required surgery. A separate group of 16 patients with orbital-zygomatic complex fractures that required exploration of the orbital floor but not bone grafting was used for comparison. A significant (p<0.05) elevation of intraocular pressure was observed immediately after bone grafting compared with nongrafted orbits, but values returned to normal within 30 minutes and remained stable through the third postoperative day. There were no cases of visual impairment in any patients in either group as the result of surgical treatment. These data indicate that orbital volume reduction with graft material results in significant, temporary elevation of intraocular pressure. No significant elevations of intraorbital compartment pressure were detected in the rabbit orbits. Data from this study may have direct relevance in defining guidelines for "tolerable" changes in orbital tissue and globe pressures after surgery.

Adult↗

PubMed1999

Application of endoscope-assisted minimal-access techniques in orbitozygomatic complex, orbital floor, and frontal sinus fractures.

BACKGROUND AND OBJECTIVES: Minimal-access endoscope-assisted techniques have been adapted for facial rejuvenation surgery over the past 5 years, allowing smaller incisions, limited dissection, and shorter recovery times. Their increasing popularity prompted the author to investigate their application in facial trauma patients. METHODS AND MATERIALS: Endoscope-assisted minimal-access surgical approaches were developed in cadavers and applied in the management of frontal sinus, orbital floor, and orbitozygomatic complex fractures over a 3-year period. At a Level 1 regional trauma center, these techniques were applied in 33 of 161 patients with facial fractures. Surgical techniques, applications of endoscope technology, and indications/contraindications are presented. A technique, known as the pulse test, was developed for assessing the integrity of the orbital floor. RESULTS AND/OR CONCLUSIONS: Endoscope-assisted minimal-access surgical techniques have a definite but perhaps limited application in the diagnosis, as well as in some aspects of the surgical treatment of fractures of the anterior table frontal sinus, orbitozygoma, and orbital floor. New indications for these techniques will depend upon the development of improved instrumentation.

Adolescent↗

PubMed1998

Role and mechanism of endothelin-B receptors in mediating ET-1-induced vasoconstriction in pig skin.

We investigated the functional importance and signal transduction pathways of endothelin (ET)-B receptors in mediating ET-1-induced vasoconstriction in pig skin. Skin vasoconstriction was studied by monitoring the perfusion pressure of isolated perfused pig skin flaps (6 x 16 cm) at a constant flow rate. Intra-arterial infusion of the ETA/B receptor agonist ET-1, the ETB receptor agonists sarafotoxin 6C (S6c) and BQ-3020, or the thromboxane A2 mimetic U-46619 (n = 4 or 5) caused a concentration-dependent skin vasoconstriction. The vasoconstrictor potency of ET-1 (EC50 3.1 x 10(-9) M) was lower (P < 0.05) than that of S6c (EC50 1.8 x 10(-9) M) and similar to that of BQ-3020 (EC50 2.6 x 10(-9) M). The vasoconstrictor potency of ET-1, S6c, and BQ-3020 was at least 300-fold higher than that of U-46619 (EC50 0.9 x 10(-6) M). The skin vasoconstrictor effect of ET-1 (10(-9)-10(-8) M) was partially inhibited by 10(-5) M BQ-123, an ETA receptor antagonist. Further inhibition was achieved with the combination of 10(-5) M BQ-123 and BQ-788 (an ETB receptor antagonist) or with an ETA/B receptor antagonist (10(-5) M bosentan or PD-145065) (n = 5; P < 0.05). In addition, the skin vasoconstrictor effect of the ETB receptor agonist BQ-3020 was completely blocked by 5 x 10(-6) M BQ-788 and partially inhibited by 5 x 10(-6) M of the phospholipase C (PLC) inhibitor 2-nitro-4-carboxyl-N,N-diphenylcarbamate (NCDC), an L-type Ca2+ channel antagonist (nifedipine), a protein kinase C (PKC) inhibitor (chelerythrine), or removal of Ca2+ from the perfusate (n = 4 or 5; P < 0.05). The vasoconstrictor effect of S6c was also partially blocked by 5 x 10(-6) M of NCDC, nifedipine, or chelerythrine or by removal of Ca2+ from the perfusate (n = 4; P < 0. 01). We conclude that ETB receptors play a central role in mediating ET-1-induced vasoconstriction in pig skin, and the mechanism probably involves L-type Ca2+ channels, PLC, and PKC.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1997

Acute adenosine treatment is effective in augmentation of ischemic tolerance in muscle flaps in the pig.

The objective of the present project was to investigate the efficacy and mechanism of acute (10-minute) adenosine treatment for augmentation of ischemic tolerance in muscle flaps in pigs. Varying doses of adenosine were infused into 28 latissimus dorsi muscle flaps through the axillary artery (0, 0.5, or 2.0 mg per flap) and 22 gracilis muscle flaps through the medial circumflex femoral artery (0, 10, or 20 mg per flap) over 10 minutes. Ten minutes after adenosine infusion, these muscle flaps were subjected to 4 hours of sustained warm global ischemia. In addition, one group of latissimus dorsi muscle flaps (n = 6) received a 10-minute intraarterial adenosine infusion (0.5 mg) at the beginning of reperfusion. Muscle biopsies (n = 4 or 5) for adenosine triphosphate (ATP) analysis were obtained before and after adenosine infusion and at the end of 4 hours of ischemia. The extent of muscle infarction was assessed at 48 hours of reperfusion by the tetrazolium dye staining technique. Muscle blood flow in latissimus dorsi muscle flaps was measured at the end of adenosine infusion (0 or 0.5 mg per flap, n = 8) by the radioactive microsphere (15-microns) technique. It was observed that adenosine, at all doses tested, significantly (p < 0.05) reduced the extent of muscle infarction in latissimus dorsi muscle flaps (control, 40.3 +/- 2.2 percent; 0.5 mg, 20.6 +/- 1.6 percent; 2.0 mg, 18.2 +/- 1 percent) and gracilis muscle flaps (control, 31.0 +/- 1.5 percent; 10 mg, 14.3 +/- 3 percent; 20 mg, 11.6 +/- 1.2 percent). Preischemic adenosine treatment (0.5 mg per flap) was associated with maintenance of a significantly (p < 0.05) higher muscle content of ATP in latissimus dorsi muscle flaps at the end of 4 hours of ischemia compared with saline-treated ischemic controls. Postischemic adenosine treatment did not protect latissimus dorsi muscle flaps against infarction. Furthermore, adenosine treatment did not have any significant effect on mean systemic arterial blood pressure or muscle blood flow in latissimus dorsi muscle flaps. It is concluded that acute (10-minute) preischemic adenosine treatment is effective in augmentation of ischemic tolerance in muscle flaps and that this protective effect of adenosine may be, at least in part, the result of slowing muscle ATP depletion during sustained ischemia. The possible mechanisms of this adenosine-induced energysparing effect are discussed.

Adenosine↗

PubMed1997

Role of ATP-sensitive K+ channels in ischemic preconditioning of skeletal muscle against infarction.

We studied the role and mechanism of ATP-sensitive K+ (KATP) channels in ischemic preconditioning (IPC) of skeletal muscle against infarction in vivo. Surgically denervated, noncontractile latissimus dorsi muscle flaps in pentobarbitone-anesthetized pigs were assigned to nine groups: control; IPC (3 cycles of 10-min ischemia/reperfusion); preischemic lemakalim (LMK, 0.18 mg/muscle); postischemic LMK; sodium 5-hydroxydecanoate (5-HD, 27 mg/muscle) before IPC; glibenclamide (Glib 0.3 mg/kg iv) before IPC; 5-HD before preischemic LMK; 5-HD before ischemia; and Glib before ischemia. Except for Glib, all drugs were delivered to each muscle by 10-min local intraarterial infusion to avoid systemic effects. All muscle flaps underwent 4 h of global ischemia. Infarction was assessed at 48 h of reperfusion. In a separate study, muscle biopsies were taken before, during, and after ischemia for assay of high-energy phosphate and lactate contents and myeloperoxidase (MPO) activity. It was observed that muscle infarction in the IPC (24 +/- 2%) and preischemic LMK (21 +/- 2%) groups were smaller (P < 0.05) than that in the control (42 +/- 2%). The anti-infarction effect of IPC and LMK was blocked by 5-HD or Glib. IPC and preischemic LMK caused a higher (P < 0.05) muscle content of ATP and energy charge potential, a lower (P < 0.05) muscle content of lactate during ischemia, and a lower (P < 0.05) muscle MPO activity throughout 16 h of reperfusion compared with the control. These observations indicated for the first time that KATP channels are also involved in the anti-infarction effect of IPC in noncontractile skeletal muscle in vivo. Presently, the cause and importance of energy-sparing and neutrophil-inhibitory effects of IPC and LMK are not known.

Adenosine Diphosphate↗

PubMed1997

Effector mechanism of adenosine in acute ischemic preconditioning of skeletal muscle against infarction.

We used adenosine A1 receptor agonist N6-1(phenyl-2R-isopropyl)-adenosine (PIA), A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and ATP-sensitive K+ (KATP) channel blockers sodium 5-hydroxydecanoate (5-HD) and glibenclamide (Glib), as probes to investigate the role and mechanism of adenosine in ischemic preconditioning (IPC) of noncontractile skeletal muscle against infarction, using the pig latissimus dorsi muscle flap model. Except for Glib, all drugs were delivered to each muscle flap by 10-min local intra-arterial infusion to avoid systemic effects. Muscle flaps that were subjected to 4 h of global ischemia and 48 h of reperfusion sustained 40 +/- 2% infarction. IPC with three cycles of 10 min ischemia and reperfusion, preischemic adenosine, or PIA treatment reduced (P < 0.05) muscle infarction to 24 +/- 2, 18 +/- 2, and 24 +/- 2%, respectively. The anti-infarction effect of IPC and adenosine was blocked by DPCPX, 5-HD, and Glib (P < 0.05). Preischemic adenosine treatment also maintained higher muscle contents of phosphocreatine, ATP, and energy charge potential and lower muscle contents of dephosphorylated metabolites and lactate during ischemia and a lower muscle myeloperoxidase (MPO) activity during reperfusion compared with the control (P < 0.05). Preischemic adenosine treatment did not increase muscle content of adenosine during ischemia or reperfusion. Furthermore, adenosine given at the onset of reperfusion was not effective in attenuating muscle MPO activity or infarction. Taken together, these observations indicate that adenosine, through A1 receptors, initiates the mechanism of IPC with postreceptor involvement of KATP channels in skeletal muscle. However, adenosine is unlikely to play a key role in the effector mechanism. Presently, the cause and role of energy sparing and neutrophil inhibitory effects associated with the anti-infarction effect of preischemic adenosine treatment are unknown.

Adenosine↗

PubMed1996

Anatomic and hemodynamic study of the vascularized pig fibula bone flap model.

Despite much interest in studying the pathophysiology of experimental skin and muscle flaps to better understand the pathobiology of flap failure, relatively little has been published in the investigation of vascularized bone flaps. The aim of this study was to develop a suitable vascularized bone flap model in the pig in the hope that this model may prove useful in studying the pathophysiology of vascularized bone tissue transfer. Yorkshire pigs (17-26 kg) were used for all experiments. Anatomic studies revealed that the fibula in the hindlimb was the most suitable bone for investigation as a flap model. Anatomic dissections, radiologic investigations (plain x-rays, angiograms), and morphometric analyses of the fibulae in both hindlimbs of five animals were carried out. In a separate group of pigs (n = 6), the fibula was elevated as a vascularized flap and then blood flow was measured using the 15-microns radioactive microsphere technique. The fibula in the pig is supplied by a branch of the cranial tibial artery, running along an intermuscular septum between the posterior and anterior compartments of the hindlimb accompanied by one or two vena commitans. The bone flap is raised with a cuff of flexor hallucis longus with a length of 9.2 +/- 0.2 cm (mean +/- SEM). Blood flow measurement confirmed that the entire fibula was well vascularized when elevated on its pedicle. Gradient blood flow showed a bimodal distribution, with regions of highest blood flow noted at the proximal and distal ends of the bone flap, in areas where there were greater percentages of cancellous bone. The results of these experiments suggest that the pig fibula may be a suitable model for the study of vascularized bone flap pathophysiology.

Animals↗

PubMed1995

Acute pharmacologic preconditioning as a new concept and alternative approach for prevention of skeletal muscle ischemic necrosis.

The phenomenon of ischemic preconditioning for augmentation of ischemic tolerance has been well documented in the myocardium of common laboratory animals and human cardiomyocytes. The cellular mechanism of ischemic preconditioning is unclear, but adenosine is most likely the mediator in the rabbit, dog, pig and human. We have demonstrated recently that the protective effect of ischemic preconditioning and adenosine against ischemic injury can also be induced in pig skeletal muscles [116]. We speculate that adenosine is a potential treatment modality for prevention of skeletal muscle ischemic injury in vascular and musculoskeletal reconstructive surgery and in muscle and limb procurement for transplantation in the future. It is hoped that this review will stimulate workers at other laboratories to join the adventure in exploring the cellular mechanism and clinical application of adenosine for augmentation of skeletal muscle ischemic tolerance.

Adenosine↗

PubMed1995

Cranioplasty: indications, technique, and early results of autogenous split skull cranial vault reconstruction.

Since 1990, fresh autogenous split skull cranioplasty has been the preferred method of reconstructing complicated cranial defects at the Sunnybrook Hospital. Eight cases of split skull cranioplasties were reviewed to illustrate the indications and technical considerations of the procedure. Clinical factors believed to be detrimental to the outcome of split skull cranioplasty were identified by: 1) a history of an infected, failed, previous cranial reconstruction, 2) inadequate scalp or skin to cover the external surface of an anticipated skeletal vault reconstruction, 3) the communication of adjacent paranasal sinuses with the epidural space, 4) the presence of an avascular dead space posterior to the reconstructed cranium. These potentially negative influences were systematically addressed as part of the surgical routine in autogenous split skull cranioplasty.

Adult↗

PubMed1995

Vascular effects and mechanism of action of endothelin-1 in isolated perfused pig skin.

We investigated the vascular effects and mechanism of action of endothelin-1 (ET-1) in the skin by intra-arterial infusion of ET-1 and its precursor Big ET-1 via a direct cutaneous artery in isolated perfused pig skin flaps (6 x 16 cm). The vascular contractivity was studied by monitoring the perfusion pressure in the skin flap. There was evidence to indicate local conversion of Big ET-1 to ET-1 in the pig skin. It was also observed that ET-1 was a potent long-lasting vasoconstrictor with a potency of approximately 10- and 300-fold higher than those of Big ET-1 and norepinephrine, respectively. The vasoconstrictor action of ET-1 was blocked (P < 0.01) by a selective ETA-receptor antagonist (BQ-123 or BQ-610; 10(-7) M) and enhanced (P < 0.05) by a nitric oxide synthase inhibitor (NG-monomethyl-L-arginine or N omega-nitro-L-arginine methyl ester; 10(-5) M). ET-1-induced increase in perfusion pressure was attenuated (P < 0.05) by an L-type Ca(2+)-channel antagonist (nitrendipine, verapamil, or nifedipine; 10(-5) M) and by removal of Ca2+ from the perfusate. ET-1-induced increase in perfusion pressure was also attenuated (P < 0.05) by a phospholipase C inhibitor (neomycin; 10(-2) M), a protein kinase C (PKC) inhibitor (chelerythrine or H-7; 10(-5) M), and an intracellular Ca2+ chelator [1,2-bis(2-aminophenoxy)]ethane-N,N,N',N'-tetraacetic acid (BAPTA); 10(-5) M]. Furthermore, it was observed that the concentration-dependent (5 x 10(-8) to 10(-5) M) increase in perfusion pressure induced by phorbol 12,13-dibutyrate, a PKC activator, was not affected by verapamil (10(-5) M) or removal of Ca2+ from the perfusate. Taken together, these observations suggest that the vasoconstrictor mechanism of ET-1 in the pig skin involved activation of ETA receptors, L-type Ca2+ channels, phospholipase C, and PKC and that the vasoconstrictor effect caused by activation of PKC was independent of L-type Ca2+ channels.

Animals↗

PubMed1995

Acute ischaemic preconditioning protects against skeletal muscle infarction in the pig.

OBJECTIVE: The aims were to investigate the efficacy of acute ischaemic preconditioning for protection of skeletal muscles against infarction and its effect on muscle blood flow and ischaemic muscle metabolism. METHODS: The efficacy of preconditioning was tested by subjecting pig latissimus dorsi and gracilis muscles to different numbers and durations of ischaemia/reperfusion cycles before 4 h of global ischaemia. Infarction was assessed at 48 h of reperfusion, using nitroblue tetrazolium dye. Blood flow in the latissimus dorsi was measured at the end of preconditioning and 1.5 and 3.0 h of reperfusion, using the radioactive microsphere (15 microns) technique. Muscle biopsies were taken from the latissimus dorsi before ischaemia, at the end of 2 and 4 h of ischaemia, and 1.5 h of reperfusion. RESULTS: At least three cycles of 10 min ischaemia and 10 min reperfusion were required for preconditioning of latissimus dorsi and gracilis muscles for protection against infarction. Preconditioning reduced the total infarct size by 44% and 62% in latissimus dorsi and gracilis muscles, respectively. Preconditioning did not affect preischaemia muscle blood flow but it reduced the muscle content (preischaemia reserve) of phosphocreatine and ATP and the muscle energy charge potential (ECP) by 13.5%*, 27.5%*, and 8%* (*P < 0.05), respectively. In spite of a lower preischaemia reserve of phosphocreatine and ATP, the muscle contents of phosphocreatine and ATP and muscle ECP were maintained higher and the lactate lower (*P < or = 0.05) in the preconditioned than in the non-preconditioned (control) muscles at the end of 4 h of ischaemia [phosphocreatine 8.0(SEM 0.4) v 3.2(0.3)*; ATP 9.8(0.7) v 7.8(0.3); ECP 0.72(0.02) v 0.66(0.01)*; lactate 115.4(8.6) v 160.5(11.8)* mumol.g-1 dry muscle]. The level of ATP and ECP also remained significantly higher and the level of lactate significantly lower in the preconditioned than in the non-preconditioned latissimus dorsi muscles at 1.5 h of reperfusion. Hyperaemia was seen in the preconditioned latissimus dorsi muscles at 1.5 h of reperfusion and it subsided by the end of 3h of reperfusion. CONCLUSIONS: The protective effect of preconditioning can be induced in pig skeletal muscle but at a higher threshold than reported previously in pig cardiac muscle (one cycle). Preconditioning of pig skeletal muscle is associated with a lower energy metabolism during sustained ischaemia. At the present time, it is not known if this energy sparing effect is a major mechanism of ischaemic preconditioning against infarction in skeletal muscles.

Acute Disease↗

PubMed1994

Evidence for nicotine-induced skin flap ischemic necrosis in the pig.

There is clinical and experimental evidence to indicate that cigarette smoking may increase the risk of skin ischemic necrosis in flap surgery but the pathogenic mechanism remains unclear. The objectives of this project were to investigate the potential deleterious effects and mechanism of action of nicotine, a major by-product of cigarette smoking, in skin flap surgery in the pig. It was observed that 4-5 weeks of intramuscular nicotine injections (4 mg/kg; twice daily) significantly (p < 0.05) decreased the skin flap capillary blood flow and the length and area of skin flap viability in the pig. This nicotine treatment also induced a 1.6-fold increase in skin flap tissue content of norepinephrine compared with the saline-treated control. The estimated mean wet skin tissue content of norepinephrine (5 x 10(-7) M) was much higher than the circulating level of norepinephrine (1.8 x 10(-9) M) in nicotine-treated pigs. This level of norepinephrine (5 x 10(-7) M) was seen to induce a significant vasoconstrictor effect (75% increase over basal perfusion pressure) in isolated perfused pig skin flaps. It was also observed that the vasoconstrictor effect of norepinephrine was significantly (p < 0.05) enhanced in the presence of 10(-4) M N omega-monomethyl-L-arginine or NG-nitro-L-arginine, an endothelium-derived relaxing factor--nitric oxide (EDRF/NO) synthesis inhibitor. This vasoconstrictor effect was further enhanced in the presence of NG-nitro-L-arginine and 10(-5) M indomethacin, a cyclooxygenase inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Pharmacologic intervention in ischemia-induced reperfusion injury in the skeletal muscle.

This article provides a concise review on the potential causes of ischemia-induced reperfusion (I/R) injury and pharmacologic intervention in the skeletal muscle. Special emphasis is placed on the recent observation of the acute ischemic preconditioning phenomenon for prevention of I/R injury in skeletal muscle. Finally, the mechanism of ischemic preconditioning and its clinical applications for augmentation of skeletal muscle tolerance to prolonged ischemic insult are discussed.

Animals↗

PubMed1993

The role of orbital ultrasound in the diagnosis of orbital fractures.

The role of CT scanning in the diagnosis and management of craniomaxillofacial injuries is well documented. However, coexistent injuries, limitations on patient positioning, CT availability, or financial constraints may prevent or delay the diagnosis of significant orbital wall defects. Real-time ultrasound represents a safe, inexpensive, noninvasive, portable, and readily available diagnostic modality which has had a limited application in the diagnosis of orbital pathology. The objectives of this study were to define the role of orbital ultrasound in the assessment of the traumatized orbit and to provide correlation of pathology with CT imaging. Eighteen patients (16 males, 2 females) having sustained trauma to the orbitozygomatic region were assessed at a regional trauma center over a 6-month period. Each patient underwent an ultrasound examination of both orbits. Confirmatory CT scans (5-mm axial and 1.5-mm coronal orbital cuts) were then obtained for comparative assessment. Patients with open globe injuries, alteration of visual acuity, or life-threatening conditions were excluded from the study. The results of the study revealed a positive correlation between the ultrasound and CT findings in 17 (94 percent) of the patients. Ultrasound demonstrated satisfactory sensitivity (92 percent) and specificity (100 percent) and positive predictive value (100 percent) when compared with CT scanning. Soft-tissue herniation, orbital emphysema, and muscle entrapment were well visualized by means of real-time ultrasound. It is concluded that orbital ultrasound is an accurate diagnostic modality in the investigation of orbital trauma and correlates well with CT findings. A cost analysis will be presented, and details of the limitations and efficacy of orbital ultrasound will be discussed.

Adult↗

PubMed1993

Assessment of ischemia-induced reperfusion injury in the pig latissimus dorsi myocutaneous flap model.

Experiments were conducted to assess ischemia-induced reperfusion injury in the pig latissimus dorsi myocutaneous flap model. Forty Yorkshire pigs (19.5 +/- 0.6 kg) were assigned to groups A, B, C, and D (n = 10 pigs). Bilateral 8 x 13 cm latissimus dorsi myocutaneous flaps were constructed in each pig, and one flap was assigned to ischemic treatment and the contralateral flap served as a nonischemic control. The treatment flaps in groups A, B, C, and D were subjected to 2, 4, 6, and 8 hours of warm global ischemia, respectively. Pigs in groups A, B, C, and D were divided into two subgroups (n = 5 pigs), and extents of skin and muscle necrosis in control and treatment flaps were assessed with the fluorescein and nitroblue tetrazolium dye stain tests, respectively, after 2 and 7 days of reperfusion. Significantly (p < 0.01) greater extents of skin and muscle necrosis were observed in latissimus dorsi myocutaneous flaps subjected to 4, 6, or 8 hours of ischemia compared with their contralateral controls. Extents of skin and muscle necrosis also increased significantly (p < 0.01) with increases in ischemia time in treatment flaps. Of particular importance was the observation that there was no significant difference in the extent of skin or muscle necrosis between 2 and 7 days of reperfusion in all control and treatment groups. This observation indicates that 2 days of reperfusion time is adequate to assess the maximum extent of skin and muscle ischemia-induced reperfusion injury in pig latissimus dorsi myocutaneous flaps. Furthermore, it was observed that 1-cm segments of latissimus dorsi muscle were not too thick to allow the use of the nitroblue tetrazolium dye stain test for assessment of muscle viability, as judged by the highly correlated (r = 0.98, n = 40) linear relationship between assessment of muscle viability from one transverse cut surface of muscle segments and by weighing total viable and nonviable muscles dissected from the flaps according to the nitroblue tetrazolium dye stain on both transverse cut surfaces. It is important to note that the maximum length of the latissimus dorsi myocutaneous flap model for ischemia-induced reperfusion injury research should not exceed the maximum length of skin viability in the nonischemic control in order to avoid the complication of skin necrosis due to excessive length of skin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Role of xanthine oxidase in reperfusion injury of ischemic skeletal muscles in the pig and human.

We investigated whether xanthine oxidase (XO) is a major source of oxygen-derived free radicals (oxy-radicals) in the pig and human skeletal muscles. It was observed that xanthine dehydrogenase and XO activities in nonischemic pig latissimus dorsi (LD) and gracilis muscles and human LD and rectus abdominis (RA) muscles were < 0.5 mU/g wet wt. The pig LD muscle hypoxanthine content increased significantly from 0.33 +/- 0.02 to 2.33 +/- 0.44 mumol/g dry wt after 5 h of warm ischemia, but the muscle uric acid content remained unchanged up to 2 h of reperfusion. Similarly, the hypoxanthine content in the human LD and RA muscles increased from 0.33 +/- 0.03 to 0.84 +/- 0.23 mumol/g dry wt after 2.0-3.5 h of warm ischemia, and the muscle uric acid content remained unchanged at the end of 15-90 min of reperfusion. Furthermore, 5 days of allopurinol treatment (25 mg/kg iv twice daily) starting 2 days before ischemia or 3 days of oxypurinol treatment (25 mg/kg iv twice daily) starting 15 min before reperfusion did not attenuate the extent of skeletal muscle necrosis in pig LD muscles subjected to 5 h of ischemia and 48 h of reperfusion. However, deferoxamine treatment (250 mg/kg iv twice daily) starting before or after ischemia, as described above, significantly reduced the extent of pig LD muscle necrosis. Finally, at 2 and 48 h of reperfusion significantly higher muscle neutrophil contents were seen in ischemic than in nonischemic control pig LD muscles. Neutrophil depletion with mechlorethamine (0.75 mg/kg iv) significantly reduced the extent of necrosis in pig LD muscles. These observations indicate that XO is not a major source of oxy-radicals in ischemia/reperfusion injury in the pig gracilis and LD muscles and human RA and LD muscles.

Adult↗

PubMed1993

Comparison of real-time ultrasonography and coronal computed tomography in the diagnosis of orbital fractures.

Real-time ultrasonography (US) was used to evaluate the bony orbit in 19 patients who had sustained orbital trauma. The ability of US to demonstrate clinically significant orbital fractures was compared with that of thin-section coronal computed tomography (CT); the latter method was treated as definitive. US had a sensitivity of 92%, a specificity of 100% and a positive predictive value of 100%. Quantification of the size of fragments by the two methods yielded similar results. Real-time US adequately displayed the anatomic features of the orbit and detected clinically significant fractures. This technique may have a role in post-traumatic imaging of the orbit when coronal CT is not possible.

Female↗

PubMed1992

Augmentation of acute random pattern skin flap viability in the pig.

Three experiments were conducted to study the effect of ketanserin and LY53857, S2-serotonergic receptor antagonists, on skin blood flow and viability in acute random pattern skin flaps (4 x 10 cm) in the pig. In experiment 1, the dose-response effect of intravenous ketanserin (0, 0.15, 0.25, 0.35, and 0.50 mg/kg) on skin flap capillary blood flow was studied 6 hr after skin flap surgery, using the radioactive microsphere (15 microns) technique and under pentobarbital anesthesia. Significant (P less than 0.05) increase in skin flap blood flow was seen at the dosages of 0.25 and 0.35 mg/kg compared with the saline-treated control. In experiment 2, the effect of five-day intramuscular ketanserin and LY53857 treatment (0.30 mg/kg/day; in divided doses) on skin flap viability was studied. The drug treatments were started two days preoperatively. It was observed that the length of skin flap viability in ketanserin (6.6 +/- 0.2 cm; n = 40 flaps) and LY53857 (6.8 +/- 0.3 cm; n = 40 flaps) treated flaps were significantly (P less than 0.05) higher than the saline-treated control (5.5 +/- 0.1 cm; n = 48 flaps). Ketanserin treatment started 30 min after flap surgery also significantly (P less than 0.05) increased the length of skin flap viability (6.1 +/- 0.1 cm) compared with the control. There was no significant difference in skin viability between ketanserin and LY53857 treated skin flaps. The preceding study on the effect of ketanserin treatment on random pattern skin flap viability was repeated in experiment 3. Again, it was observed that intramuscular ketanserin treatment significantly (P less than 0.05) increased the skin flap viability. It was concluded that ketanserin and LY53857 treatment resulted in significant augmentation of porcine acute random pattern skin flap viability. This is the first experimental evidence to indicate that S2-serotonergic receptors participate in the pathogenesis of skin flap ischemia.

Animals↗