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Biomedical subjects

C T Chen

Publications and source records attributed to C T Chen.

At least 55 records · Page 3Linked to original sources
PubMed2001

Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure.

Hepatic encephalopathy is a complex neuropsychiatric syndrome seen secondary to acute liver failure, chronic parenchymal liver disease, or portal-systemic anastomosis. Vasodilatation induced by nitric oxide (NO) may be involved in the development of hepatic coma. However, there are no comprehensive data concerning the effects of NO inhibition on the severity of hepatic encephalopathy. Male Sprague-Dawley rats weighing 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection of thioacetamide (TAA, 350 mg kg-1 day-1) for 3 days. Rats were divided into two groups to receive either NG-nitro-L-arginine methyl ester (L-NAME, 20 mg kg-1 day-1 via intragastric gavage) or normal saline (N/S) from 2 days prior to TAA administration for 5 days. Severity of encephalopathy was assessed by counts of motor activity and neurobehaviour test scores. Plasma levels of endotoxin, tumour necrosis factor-alpha and nitrate/nitrite were determined by the chromogenic Limulus assay, enzyme-linked immunosorbent assay and colorimetric assay, respectively. Compared with N/S-treated rats, the mortality rate was significantly higher in rats receiving L-NAME (59% vs. 18%, P < 0.01). Inhibition of NO had detrimental effects on the counts of motor activities (P < 0.05) and neurobehaviour score (P < 0.01). Rats treated with L-NAME had significantly higher plasma levels of endotoxin (26.7 +/- 3.8 pg mL-1) and tumour necrosis factor-alpha (29.4 +/- 6.5 pg mL-1) compared with rats treated with N/S (13.2 +/- 2.7 pg mL-1 and 11.2 +/- 2.6 pg mL-1, respectively, P < 0.01). Plasma levels of endotoxin and tumour necrosis factor-alpha, but not of nitrate/nitrite, were significantly correlated with the severity of hepatic encephalopathy (P < 0.05). Chronic L-NAME administration had detrimental effects on the severity of encephalopathy in TAA-treated rats, suggesting a protective role of NO in the development of fulminant hepatic failure.

Animals↗
PubMed2001

Dipyridamole inhibits TGF-beta-induced collagen gene expression in human peritoneal mesothelial cells.

BACKGROUND: Peritoneal matrix accumulation is characteristic of peritoneal fibrosis (PF). Continuous ambulatory peritoneal dialysis (CAPD) patients who had persistent transforming growth factor-beta (TGF-beta) in their drained effluent had an increased risk of PF. We previously reported that TGF-beta stimulates the expression of types I and III collagen mRNA in cultured human peritoneal mesangial cells (HPMCs), which may predispose them to develop PF. Pharmacological interventions to attenuate TGF-beta-stimulated matrix accumulation in HPMC may have therapeutic potential for the treatment of PF. The SMAD family and the extracellular signal-regulated protein kinase (ERK1/2, p44/p42) pathways have been shown to participate in TGF-beta signaling. Our current study identified these signal pathways in HPMCs and investigated the molecular mechanisms involved in the inhibitory effects of dipyridamole on TGF-beta-induced collagen gene expression in HPMCs. METHODS: HPMCs were cultured from human omentum by an enzyme digestion METHOD: Expression of collagen alpha1(I) mRNA was determined by Northern blotting. The SMAD proteins and the ERK1/2 activity were determined by Western blotting. RESULTS: TGF-beta-stimulated collagen alpha1(I) mRNA expression of HPMC was inhibited by dipyridamole in a dose-dependent manner. Smad2 and ERK1/2 were activated in response to TGF-beta; however, TGF-beta had little effect on the protein expression of Smad4. The addition of PD98059, which blocked activation of ERK1/2, suppressed TGF-beta-induced collagen alpha1(I) mRNA expression in a dose-dependent manner. At a concentration that inhibited collagen gene expression (17 microg/mL), dipyridamole suppressed ERK1/2 activation by TGF-beta. In contrast, the same concentration of dipyridamole had no effect on TGF-beta-induced activation of Smad2. CONCLUSION: Dipyridamole inhibits TGF-beta-induced collagen gene expression in HPMC through modulation of the ERK pathway. Our study of dipyridamole may provide therapeutic basis for clinical applications in the prevention of PF.

Cells, Cultured↗
PubMed2001

Dipyridamole inhibits PDGF-stimulated human peritoneal mesothelial cell proliferation.

BACKGROUND: It has been proposed that proliferation of human peritoneal mesothelial cells (HPMCs) accompanied by collagen synthesis may contribute to the development of peritoneal fibrosis (PF) in patients of long-term continuous ambulatory peritoneal dialysis (CAPD). However, the precise molecular mechanism regulating HPMC proliferation has never been reported. Dipyridamole has been reported to have potential as an antiproliferative and antifibrotic agent. We investigated the mechanism and effect of dipyridamole in regulation of HPMC proliferation. METHODS: HPMCs were cultured from human omentum by an enzyme digestion METHOD: Cell proliferation was measured by the methyltetrazolium assay and intracellular cAMP was measured using an enzyme immunoassay kit. Cell-cycle distribution of HPMC was analyzed by flow cytometry. Extracellular signal-regulated protein kinase (p44/p42 ERK) activity and expressions of cell-cycle proteins (cyclin D(1), CDK4, pRB and p27(Kip1)) were determined by Western blotting. RESULTS: The addition of DP suppressed PDGF-stimulated HPMC proliferation by cell-cycle arrest at the G1 phase. The antimitogenic effect of dipyridamole was mediated through the cAMP pathway. PDGF (25 ng/mL) increased the ERK1/2 activity of HPMC within 15 minutes, which maximized at 30 minutes, and the pretreatment with dipyridamole (17 microg/mL) substantially reduced the ERK response to PDGF by approximately 78.5%. PDGF induced elevated protein levels of cyclin D(1), but the CDK4 protein level did not change. Dipyridamole and DBcAMP had no effect on the levels of cyclin D(1) and CDK4 in PDGF-stimulated HPMC. PDGF decreased p27(Kip1) and induced pRB phosphorylation of HPMC. In contrast, dipyridamole prevented PDGF-induced p27(Kip1) degradation and attenuated PDGF-stimulated pRB phosphorylation. CONCLUSION: Dipyridamole appears to inhibit PDGF-stimulated HPMC proliferation through attenuated ERK activity, preservation of p27(Kip1), and decreased pRB phosphorylation. Thus, dipyridamole may have therapeutic efficacy to prevent or alleviate PF.

Bucladesine↗
PubMed2001

Endothelin-1 induces vasoconstriction on portal-systemic collaterals of portal hypertensive rats.

Portal hypertension is associated with increased hepatic and collateral resistance to an increased portal blood flow. Endothelin-1 (ET-1) can induce intrahepatic vasoconstriction and consequently increase portal pressure. It is unknown if ET-1 also modulates portal pressure by a direct vasoconstrictive effect on collaterals. This study investigated the collateral vascular responses to ET-1, the receptors in mediation, and the regulation of ET-1 action by nitric oxide and prostaglandin. The portal-systemic collaterals of partially portal vein-ligated rats were tested by in situ perfusion. The concentration-response curves of collaterals to graded concentrations of ET-1 (10(-10)-10(-7) mol/L) with or without BQ-123 (ET(A) receptor antagonist, 2 x 10(-6) mol/L), BQ-788 (ET(B) receptor antagonist, 10(-7) mol/L) or both were recorded. In addition, the collateral responses to ET-1 with preincubation of n(omega)-nitro-L-arginine (NNA; 100 mol/L), indomethacin (INDO; 10 mol/L), or in combination were performed. ET-1 increased the perfusion pressure of collaterals and its effect was significantly suppressed by BQ-123 alone and BQ-123 plus BQ-788, but not BQ-788 alone (P <.05). Incubation with NNA, INDO, or both significantly enhanced the response of collaterals to ET-1 (P < .05). These results show that ET-1 produces a direct vasoconstrictive effect on the collateral vessels of portal hypertensive rats. This effect is mediated by ET(A,) but not ET(B), receptors. Both nitric oxide and prostaglandin modulate the collateral vascular response to ET-1 and may therefore participate in the development and maintenance of portal hypertension.

Animals↗
PubMed2001

Intercellular signaling as a cause of cell death in cyclically impacted cartilage explants.

UNLABELLED: Recently, in vitro cartilage studies have shown that impact loading can produce structural damage and osteoarthritis-like changes, including tissue swelling, collagen denaturation, and cell death. OBJECTIVE: This study was to determine whether a signal for cell death moves through the cartilage matrix, resulting in the spread of cell death over time from impacted to unimpacted regions. DESIGN: Cyclic impacts were applied to the 2 mm core of 4 mm cartilage discs. Post-impact culturing extended for 3, 6 or 21 days and occurred in one of two ways. In one, discs were cultured intact. In the second, cores were removed immediately after cessation of impact and cores and rings cultured separately. Cells in apoptosis and later stage necrosis were monitored using the TUNEL assay. RESULTS: The extent of cell death in impacted samples increased with increased duration of post-impact culturing. At the early time, the majority of cell death was located in the regions of direct impact whereas after extended culture, the extent of cell death was similar in the surrounding unimpacted regions and in the impacted core region. However, the physical separation of the impacted core from the surrounding, non-impacted ring regions immediately after impact, and prior to independent culture, kept the level of cell death in the surrounding ring close to control levels, even after 21 days of incubation. DISCUSSION: These findings indicate that soluble intercellular signalling is involved in the spreading of cell death through the cartilage matrix, and that its effects can be prevented by physical isolation of the surrounding ring from the impacted core.

Analysis of Variance↗
PubMed2001

Microsurgical tissue transplantation or replantation in patients with psychoneurological impairment.

Sometimes patients with a psychoneurological impairment present with a traumatic injury that requires either microsurgical replantation or free-tissue transfer. We reviewed 38 patients undergoing 40 microvascular operations; the patients included 26 patients with psychological impairment (group 1), 3 with mental disability (group 2), and 9 with an acquired head injury and consciousness disturbance (Glasgow Coma Scale score < or =14) (group 3). Patients with a psychological impairment, especially those with a self-inflicted injury, are often uncooperative and do not recognize the necessity of restorative procedures. A multidisciplinary approach by the trauma surgeon, plastic surgeon, psychiatrist, and neurosurgeon, with coordinated assistance from the physician, nurse, therapist, and family, is required for treatment. In our study the success rate of replantation was 77.8 percent (14 of 18); for free tissue transfer the success rate was 95.5 percent (21 of 22). The overall success rate of microsurgical procedures (87.5 percent, 35 of 40) was similar to that in the population at large. Patients with psychological impairment tend to be lost during follow-up; therefore, their functional results may be poorer than expected. Nonetheless, patients with psychological impairment should not be deprived of the benefits of restorative surgery.

Adult↗
PubMed2001

Endoscopically assisted repair of orbital floor fractures.

Traditionally, orbital floor fractures are repaired with standard transcutaneous or transconjunctival approaches. Complications such as external scarring, eyelid edema, ectropion, entropion, and granuloma formation have been associated with these open lid techniques. The endoscope has been used to assist in orbital floor exploration, to reduce entrapped orbital tissue, and to identify the posterior shelf for implant placement. However, an open lid incision is inevitable when implant placement is necessary. We present our experiences in repairing orbital floor fractures using transantral endoscopy without open lid incision.A 0-degree, 4-mm endoscope was placed through a 2 x 1.5-cm2 maxillary antrostomy to dissect the sinus roof. The endoscope was used to assist in the reduction of the floor fractures and prolapsed orbital tissue into the orbital cavity, if present. The orbital floor defect was reconstructed with titanium mesh or Medpor through the antrostomy under endoscopic control. This technique was applied to nine patients who had orbital floor fractures. Two of the patients had zygomatico-orbital fractures, whereas the rest had isolated orbital floor fractures. Three patients received Medpor reconstruction and the remaining six underwent titanium mesh reconstruction. The patients were followed up for 10 months on average. The enophthalmos was corrected in all patients but one, who suffered from mild enophthalmos because of uncorrected orbital medial wall fractures. Diplopia occurred in three patients preoperatively, which was resolved in two of them and improved in the other postoperatively. There have been no complications apart from transient anesthesia in the dermatome of the infraorbital nerve. The technique successfully reconstructed the orbital floor defects, minimized ocular globe manipulation, and eliminated a lower eyelid incision.

Adult↗
PubMed2001

Time- and concentration-dependent penetration of doxorubicin in prostate tumors.

The penetration of paclitaxel into multilayered solid tumors is time- and concentration-dependent, a result of the drug-induced apoptosis and changes in tissue composition. This study evaluates whether this tissue penetration property applies to other highly protein-bound drugs capable of inducing apoptosis. The penetration of doxorubicin was studied in histocultures of prostate xenograft tumors and tumor specimens obtained from patients who underwent radical prostatectomy. The kinetics of drug uptake and efflux in whole tumor histocultures were studied by analyzing the average tumor drug concentration using high-pressure liquid chromatography. Spatial drug distribution in tumors and the drug concentration gradient across the tumors were studied using fluorescence microscopy. The results indicate that drug penetration was limited to the periphery for 12 hours in patient tumors and to 24 hours in the more densely packed xenograft tumors. Subsequently, the rate of drug penetration to the deeper tumor tissue increased abruptly in tumors treated with higher drug concentrations capable of inducing apoptosis (i.e., = 5 microm), but not in tumors treated with lower concentrations. These findings indicate a time- and concentration-dependent penetration of doxorubicin in solid tumors, similar to that of paclitaxel. We conclude that doxorubicin penetration in solid tumors is time- and concentration-dependent and is enhanced by drug-induced cell death.

Animals↗
PubMed2001

Hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of endotoxin and tumor necrosis factor-alpha.

BACKGROUND: Hepatic encephalopathy, a complex neuropsychiatric syndrome secondary to acute liver failure, chronic parenchymal liver disease or portal-systemic shunting, may possibly develop through mediators of endotoxin and tumor necrosis factor-alpha (TNF-alpha). However, there are no published data concerning the relationships between the severity of encephalopathy and the plasma levels of endotoxin and TNF-alpha. METHODS: Male Sprague-Dawley rats weighing about 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection ofthioacetamide (350 mg/kg/day) for 3 consecutive days. Severity of encephalopathy was assessed by measuring motor counts using an Opto-Varimex animal activity meter. Plasma levels of endotoxin and TNF-alpha were determined by chromogenic Limulus assay and ELISA method, respectively. RESULTS: Our study revealed that higher plasma levels of endotoxin (> 5.9 pg/ml) and TNF-alpha (> 18.8 pg/ml) were significantly associated with more blunted motor activities in rats with fulminant hepatic failure (p < 0.05). A significant correlation was observed between plasma concentrations of endotoxin and TNF-alpha (r = 0.59, p < 0.001). Plasma levels of endotoxin were weakly correlated with the total movements in an open field (r = -0.34, p = 0.032) and the counts of ambulatory (r = -0.38, p = 0.014) and vertical movements (r = -0.40, p = 0.010). There were no correlations between the motor counts and plasma levels of TNF-alpha (p > 0.05). CONCLUSIONS: In addition to endotoxin and TNF-alpha, other factors may participate in the pathogenesis of hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure.

Animals↗
PubMed2000

Orexins: a role in medullary sympathetic outflow.

Orexin A and B, also known as hypocretin 1 and 2, are two recently isolated hypothalamic peptides. As orexin-containing neurons are strategically located in the lateral hypothalamus, which has long been suspected to play an important role in feeding behaviors, initial studies were focused on the involvement of orexins in positive food intake and energy metabolism. Recent studies implicate a more diverse biological role of orexins, which can be manifested at different level of the neuraxis. For example, canine narcolepsy, a disorder with close phenotypic similarity to human narcolepsy, is caused by a mutation of hypocretin receptor 2 gene. Results from our immunohistochemical and functional studies, which will be summarized here, suggest that the peptide acting on neurons in the rostral ventrolateral medulla augment sympathoexcitatory outflow to the spinal cord. This finding is discussed in the context of increased sympathetic activity frequently associated with obesity.

Animals↗
PubMed2000

Antiangiogenic gene therapy for cancer via systemic administration of adenoviral vectors expressing secretable endostatin.

A growing number of antiangiogenesis strategies have been investigated for the treatment of cancer and other angiogenesis-dependent diseases. One of the most promising strategies is to systemically administer one or more antiangiogenic proteins frequently enough to achieve a sufficient long-term steady state level of the protein(s) to achieve the maximum beneficial effect. However, the utility of this strategy is limited because of many technical difficulties, including obtaining both the quantity and quality of the protein(s) necessary for optimal therapeutic benefit. To overcome these difficulties, we hypothesized that a single administration of a replication-defective adenoviral vector expressing a secretable antiangiogenic protein could achieve an optimal long-term systemic concentration. We constructed a recombinant adenoviral vector, Av3mEndo, which encodes a secretable form of murine endostatin. We demonstrated secretion of endostatin from several cell lines transduced with Av3mEndo. Partially purified endostatin secreted from Av3mEndo-transduced mammalian cells was shown to potently inhibit endothelial cell migration in vitro. A single intravenous administration of Av3mEndo in mice was shown to result in (1) prolonged and elevated levels of circulating endostatin, (2) partial inhibition of VEGF-induced angiogenesis in a VEGF implant angiogenesis model, and (3) prolonged survival and in 25% of mice the complete prevention of tumor growth in a prophylactic human colon/liver metastasis xenograft murine model. These results support our contention that adenoviral vector-mediated expression of an antiangiogenic protein(s) represents an attractive therapeutic approach to cancer and other angiogenesis-dependent diseases.

Adenoviridae↗
PubMed2000

Vibrio vulnificus infection complicated by acute respiratory distress syndrome in a child with nephrotic syndrome.

A 9-year-old girl with nephrotic syndrome visited a local hospital after developing fever, chills, and edematous changes and multiple hemorrhagic bullae on both legs over 2 days. Cultures of blood and an aspirate from the bullae yielded Vibrio vulnificus. The patient was transferred to our hospital because of persistent fever, generalized edema, acute renal failure, and disseminated intravascular coagulopathy. We treated this patient as a V. vulnificus infection complicated with necrotizing fasciitis. With minocycline and ceftazidime combination therapy was instituted. Emergency fasciotomy and continuous peritoneal dialysis were performed. The patient developed acute respiratory distress syndrome (ARDS) during the hospitalization, requiring intubation and mechanical ventilation. She eventually died. The histopathological findings showed diffuse alveolar damage with lobular pneumonitis. Hyaline membranes, composed of proteinaceous exudate and cellular debris, covered the alveolar surfaces. Microscopic examinations of lung could not distinguish the effects of cytolysin from other insults to lungs that occur in ARDS. This report highlights the postmortem pathological findings in V. vulnificus infection in a child with nephrotic syndrome complicated by ARDS.

Acute Disease↗
PubMed2000

Finite element analysis of brain contusion: an indirect impact study.

The mechanism of brain contusion has been investigated using a series of three-dimensional (3D) finite element analyses. A head injury model was used to simulate forward and backward rotation around the upper cervical vertebra. Intracranial pressure and shear stress responses were calculated and compared. The results obtained with this model support the predictions of cavitation theory that a pressure gradient develops in the brain during indirect impact. Contrecoup pressure-time histories in the parasagittal plane demonstrated that an indirect impact induced a smaller intracranial pressure (-53.7 kPa for backward rotation, and -65.5 kPa for forward rotation) than that caused by a direct impact. In addition, negative pressures induced by indirect impact to the head were not high enough to form cavitation bubbles, which can damage the brain tissue. Simulations predicted that a decrease in skull deformation had a large effect in reducing the intracranial pressure. However, the areas of high shear stress concentration were consistent with those of clinical observations. The findings of this study suggest that shear strain theory appears to better account for the clinical findings in head injury when the head is subjected to an indirect impact.

Brain Injuries↗
PubMed2000

Automated registration of frontal and lateral radionuclide lung scans with digital chest radiographs.

RATIONALE AND OBJECTIVES: The purpose of this study was to develop and evaluate a fully automated method that spatially registers anterior, posterior, and lateral ventilation/perfusion (V/Q) images with posteroanterior and lateral digital chest radiographs to retrospectively combine the physiologic information contained in the V/Q scans with the anatomic detail in the chest radiographs. MATERIALS AND METHODS: Gray-level thresholding techniques were used to segment the aerated lung regions in the radiographic images. A variable-thresholding technique combined with an analysis of image noise was used to segment the adequately perfused or ventilated lung regions in the scintigraphic images. The physical dimensions of the segmented lung regions in images from both modalities were used to properly scale the radiographic images relative to the radionuclide images. Computer-determined locations of anatomic landmarks were then used to rotate and translate the images to achieve registration. Pairs of corresponding radionuclide and radiographic images were enhanced with color and then merged to create superimposed images. RESULTS: Five observers used a five-point rating scale to subjectively evaluate four image combinations for each of 50 cases. Of these ratings, 95.5% reflected very good, good, or fair registration. CONCLUSION: The automated method for the registration of radionuclide lung scans with digital chest radiographs to produce images that combine functional and structural information should benefit nuclear medicine physicians and radiologists, who must visually correlate images that differ greatly in physical size, resolution properties, and information content.

Female↗
PubMed2000

Application of endoscope in zygomatic fracture repair.

The endoscope has been used to visualise the upper face and brow in aesthetic facial surgery which is performed without a coronal incision. We applied these principles to repair zygomatic fractures with the aid of a 4 mm, 30 degree telescope inserted through a small temporal incision. Fracture sites at the zygomatic arch and the zygomaticofrontal suture were exposed and fixed with miniplates under endoscopic control. This technique was used in 15 consecutive patients including 2 with isolated zygomatic arch comminuted fractures and 13 having displaced zygomatic fractures with segmental, displaced zygomatic arch fractures. Nine patients were men and six patients were women with a mean age of 35 years. Three patients had associated mandibular fractures. The periods of follow-up ranged from 3 to 22 months. Two patients developed transient frontal nerve palsy which recovered within 2 months. One patient had mild temporal hollowing on the side of the facial fracture. All patients achieved the adequate anatomic reduction and satisfactory malar symmetry. There has been no case of chewing problems, cheek numbness or progressive enophthalmos developing postoperatively. Application of the endoscope in zygomatic fracture repair minimises the scalp scar, avoids forehead numbness, provides a comfortable postoperative recovery and shortens hospital stay. Careful preoperative evaluation and proper surgical technique are mandatory for achieving optimal results in selected patients.

Accidents, Traffic↗
PubMed2000

Chronic inhibition of nitric oxide ameliorates splanchnic hyposensitivity to glypressin in a hemorrhage-transfused rat model of portal hypertension.

BACKGROUND: Vasopressin given during hemorrhage is less effective than when given during a stable state in experimental portal hypertension or patients with cirrhosis (the so-called hyposensitivity phenomenon). This study investigated whether chronic inhibition of nitric oxide (NO) synthesis by NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NO synthase inhibitor, could potentiate the portal-hypotensive effect of glypressin (a long-acting vasopressin analogue) in portal-hypertensive rats during acute bleeding status. METHODS: Portal hypertension was induced by partial portal vein ligation (PVL). Rats were divided to receive either L-NAME (approximately 25 mg/kg/day in tap water) or placebo (tap water) treatment orally from 2 days prior to until 14 days after the operation. At the end of treatment, L-NAME-and placebo-treated PVL rats were subdivided into without-bleeding and with-bleeding groups to assess the effects of glypressin (0.07 mg/kg) on systemic and portal hemodynamics. In rats with a hypotensive hemorrhage, 4.5 ml of blood was withdrawn and 50% of the withdrawn blood was reinfused before the administration of glypressin. RESULTS: As compared with placebo-treated rats, chronic treatment with L-NAME in PVL rats significantly increased mean arterial pressure (P < 0.001) without modulating portal pressure (P > 0.05). In placebo-treated PVL rats, glypressin resulted in a less decrease in portal pressure in rats with bleeding than in those without bleeding (P < 0.05). For PVL rats with bleeding, the portal-hypotensive effect of glypressin was significantly potentiated after chronic L-NAME treatment (P < 0.05). CONCLUSIONS: Chronic inhibition of NO alleviates the splanchnic hyposensitivity to glypressin observed in bleeding PVL rats, suggesting the pathophysiological role of nitric oxide in mediating this splanchnic hyposensitivity.

Animals↗
PubMed2000

Lateral-dorsal neurovascular island flaps for pulp reconstruction.

Finger pulp loss is often observed in daily practice. When the lateral and dorsal surfaces of the injured digit remain intact, a neurovascular island flap can be designed and raised from that part of the finger for pulp reconstruction. Two types of homodigital lateral-dorsal neurovascular island flaps were used in 17 patients (13 type I and 4 type II) for reconstruction of traumatic pulp loss on an emergent basis. The type I flap was used for the pulp defect less than 2.5 cm in length; the type II flap was designed for extensive pulp loss. The size of the pulp defect varied from 1.7 x 1.2 cm to 3.8 x 1.7 cm. All flaps survived completely without any partial loss. The mean follow-up was 17.7 months. The mean static two-point discrimination was 5.2 mm in type I flaps and 9.3 mm in type II flaps. All patients except five had full range of motion of the interphalangeal joint. These five patients (3 type I and 2 type II) had 10 to 20 deg reduction in flexion of the distal interphalangeal joints. The homodigital lateral-dorsal neurovascular island flap offers a durable, well-vascularized, sensate skin flap for one-stage pulp reconstruction in select patients. This technique is relatively simple, allows early postoperative mobilization, and has an acceptable surgical outcome.

Adult↗