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1.
Eur J Vasc Endovasc Surg ; 58(4): 615-622, 2019 Oct.
Article in English | MEDLINE | ID: mdl-31500989

ABSTRACT

OBJECTIVES: The ProGlide® vascular closure device (Abbott Vascular, Redwood City, CA, USA) is approved for the closure of arterial punctures (typically 5-21 Fr sheath; maximum outer diameter, 26 Fr). However, a failure rate of about 2-8% is reported. This study was conducted to analyse factors predisposing to failure when the devices were used for the closure of large hole (16-26 Fr) arteriotomies, and to determine the predictive cut off values of predisposing factors. METHODS: In this retrospective study, the ProGlide® device was used to achieve vascular access site closure in 458 patients undergoing repair of abdominal aortic aneurysm, thoracic aortic aneurysm, type B aortic dissection, or transcatheter aortic valve implantation. The primary endpoint was device failure, defined as inability to achieve common femoral artery (CFA) closure; successful repair, development of acute lower limb ischaemia and haemodynamic compromise; or delayed pseudoaneurysm formation during the follow up period, requiring open repair. RESULTS: Overall, ProGlide® failure occurred in 7.6% of cases. Factors that predisposed to failure included a history of peripheral arterial disease (PAD) (p < .001), the presence of CFA calcification (p < .001), the depth of the skin puncture site ≥ 33 mm (p < .001), body mass index (BMI) of ≥28.7 kg/m2 (p < .001), and use of sheath size ≥ 19 Fr (p < .001). CONCLUSION: Factors such as BMI, history of PAD, the presence of CFA calcification, the depth of the skin puncture site, and sheath size are significantly associated with ProGlide® failure. Hence, careful patient and device selection and operating procedure are paramount to achieve successful outcomes.


Subject(s)
Catheterization, Peripheral/instrumentation , Endovascular Procedures/instrumentation , Equipment Failure , Femoral Artery , Hemorrhage/prevention & control , Hemostatic Techniques/instrumentation , Vascular Access Devices , Vascular Closure Devices , Aged , Aged, 80 and over , Catheterization, Peripheral/adverse effects , Clinical Decision-Making , Endovascular Procedures/adverse effects , Equipment Design , Female , Hemorrhage/etiology , Hemostatic Techniques/adverse effects , Humans , Male , Middle Aged , Patient Selection , Punctures , Retrospective Studies , Risk Assessment , Risk Factors , Treatment Outcome
2.
J Chin Med Assoc ; 76(6): 350-3, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23602211

ABSTRACT

Nutcracker syndrome (NCS) is a rare pathology manifested by pain or hematuria in males and females alike. It can be easily overlooked, and should be considered in young men or women with symptoms of extended duration. We present a case of a 54-year-old female with chronic lower abdominal pain radiating to the left thigh of 4 years in duration. Computed tomography (CT) eventually revealed engorged left renal, gonadal, and uterine veins due to compression between the superior mesenteric artery (SMA) and the abdominal aorta, consistent with NCS. After a successful endovascular stenting and a 6-month period of antiplatelet and anticoagulant therapy, the patient returned to stable health. NCS, while rare, should be suspected in patients of both sexes with persistent pain or hematuria.


Subject(s)
Renal Nutcracker Syndrome/therapy , Stents , Female , Humans , Middle Aged , Renal Nutcracker Syndrome/diagnosis , Tomography, X-Ray Computed
3.
J Chin Med Assoc ; 76(2): 83-7, 2013 Feb.
Article in English | MEDLINE | ID: mdl-23351418

ABSTRACT

BACKGROUND: Takayasu's arteritis (TA) is a chronic inflammatory disease that involves the aorta and its major branches; however, only limited data are available on TA in Taiwan. This study presents the clinical features, angiographic findings, and response to treatment of patients with TA at a single institute in Taiwan. METHODS: A search of the hospital database for ICD9 code 446.7 (Takayasu's disease) between 1990 and 2010 was performed. Seven cases fulfilled the 1990 American College of Rheumatology diagnostic criteria for Takayasu's disease. Angiographic classification was made according to the guidelines of the 1994 International TA Conference in Tokyo. RESULTS: All of our cases were female, and the median age at diagnosis was 27.5 years (range 14-36 years). Four patients had an angiographic classification of type I (57.1%), two were classified as type V (28.6%), and one was classified as type III (14.3%). The most common symptoms/signs were dizziness and vascular bruits. Two patients underwent bypass surgery, four endovascular stenting, and one hybrid bypass with stenting. After a mean follow-up period of 50.3 ± 68.2 months (range 12.3-199.6 months), both the procedure success and survival rates were 100%. There were four restenosis cases (57.1%), one in the surgical bypass group without symptoms (33.3%), and three in the endovascular group (60%), five restenosis in 14 stents (35.7%). Also, these three patients received secondary endovascular procedure for percutaneous transluminal angioplasty or restenting. CONCLUSION: There have not been any case series reports about treatments of Takayasu's disease in Taiwan to date, based on a search of the PubMed/MEDLINE and Cochrane Library databases. Although endovascular treatment is becoming more prevalent, the restenosis rate is still high, and long-term follow-up and further strategy for restenosis management are the main challenges.


Subject(s)
Takayasu Arteritis/therapy , Adolescent , Adult , Female , Humans , Radiography , Takayasu Arteritis/diagnostic imaging
4.
Acta Pharmacol Sin ; 27(4): 469-76, 2006 Apr.
Article in English | MEDLINE | ID: mdl-16539848

ABSTRACT

AIM: Liver fibrosis represents a process of healing and scarring in response to chronic liver injury. Effective therapies for liver fibrosis are lacking. Interleukin-10 (IL-10) is a cytokine that downregulates pro-inflammatory responses and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether electroporative IL-10 gene therapy has a hepatic fibrolytic effect on mice. METHODS: Hepatic fibrosis was induced by administering carbon tetrachloride (CCl4) for 10 weeks in mice. The human IL-10 expression plasmid was delivered via electroporation after hepatic fibrosis was established. Histopathology, reverse transcription polymerase chain reaction (RT-PCR), immunoblotting, and gelatin zymography were used to investigate the possible mechanisms of action of IL-10. RESULTS: Human IL-10 gene therapy reversed CCl4-induced liver fibrosis in mice. RT-PCR revealed that IL-10 gene therapy attenuated liver TGF-beta1, collagen alpha1, fibronectin, and cell adhesion molecule mRNA upregulation. Following gene transfer, both the activation of alpha-smooth muscle actin and cyclooxygenase-2 were significantly attenuated. Furthermore, IL-10 significantly inhibited matrix metalloproteinase-2 (MMP-2) and tissue inhibitors of matrix metalloproteinase (TIMP) activation after CCl4 intoxication. CONCLUSIONS: We demonstrated that IL-10 gene therapy attenuated CCl4-induced liver fibrosis in mice. IL-10 prevented upregulated fibrogenic and pro-inflammatory gene responses. Its collagenolytic effect may be attributed to MMP and TIMP modulation. IL-10 gene therapy may be an effective therapeutic modality against liver fibrosis with potential clinical use.


Subject(s)
Genetic Therapy , Interleukin-10/genetics , Liver Cirrhosis, Experimental , Actins/metabolism , Animals , Collagen Type I/metabolism , Cyclooxygenase 2/metabolism , Electroporation , Fibronectins/metabolism , Gene Transfer Techniques , Intercellular Adhesion Molecule-1/metabolism , Liver/metabolism , Liver/pathology , Liver Cirrhosis, Experimental/therapy , Male , Matrix Metalloproteinase 2/metabolism , Mice , Mice, Inbred ICR , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Tissue Inhibitor of Metalloproteinases/metabolism , Transforming Growth Factor beta/metabolism , Transforming Growth Factor beta1 , Tumor Necrosis Factor-alpha/metabolism , Vascular Cell Adhesion Molecule-1/biosynthesis , Vascular Cell Adhesion Molecule-1/genetics
5.
J Gene Med ; 8(6): 764-72, 2006 Jun.
Article in English | MEDLINE | ID: mdl-16508911

ABSTRACT

BACKGROUND: Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Effective therapies are lacking. We have previously demonstrated that alpha-melanocyte-stimulating hormone (alpha-MSH) gene therapy protects against thioacetamide-induced acute liver failure in mice. Recent reports showed that collagen metabolism is a novel target of alpha-MSH. Therefore, the aim of this study is to investigate whether alpha-MSH gene therapy possesses anti-hepatic fibrogenic effect in mice. METHODS: Liver fibrosis was induced in mice by administering carbon tetrachloride (CCl4) continuously for 10 weeks. Alpha-MSH expression plasmid was delivered via electroporation after liver fibrosis had been established. Histopathology, reverse-transcription polymerase chain reaction (RT-PCR), immunoblotting, and gelatin zymography were used to investigate its possible mechanisms of action. RESULTS: Alpha-MSH gene therapy reversed established liver fibrosis in CCl4-treated mice. RT-PCR revealed that alpha-MSH gene therapy attenuated the liver TGF-beta1, collagen alpha1, and cell adhesion molecule mRNA upregulation. Following gene transfer, both the activation of alpha-smooth muscle actin (alpha-SMA) and cyclooxygenase-2 (COX-2) was significantly attenuated. Further, alpha-MSH significantly increased matrix metalloproteinase (MMP) activity with tissue inhibitors of matrix metalloproteinase (TIMP) inactivation. CONCLUSIONS: We have demonstrated that alpha-MSH gene therapy reversed established liver fibrosis in mice. It also prevented the upregulated fibrogenic and proinflammatory gene response after CCl4 administration. Its collagenolytic effect may be attributed to MMP and TIMP modulation. In summary, alpha-MSH gene therapy may be an effective therapeutic modality against liver fibrosis with potential clinical use.


Subject(s)
Carbon Tetrachloride/toxicity , Genetic Therapy , Liver Cirrhosis/genetics , Liver Cirrhosis/pathology , alpha-MSH/genetics , alpha-MSH/metabolism , Actins/metabolism , Animals , Cell Adhesion Molecules/genetics , Cyclooxygenase 2/metabolism , Electroporation , Enzyme Activation , Gelatin/metabolism , Gene Expression Regulation , Gene Transfer Techniques , Inflammation/genetics , Liver/cytology , Liver/pathology , Liver Cirrhosis/chemically induced , Liver Cirrhosis/therapy , Male , Matrix Metalloproteinases/genetics , Mice , Mice, Inbred ICR , RNA, Messenger/genetics , RNA, Messenger/metabolism , Tissue Inhibitor of Metalloproteinase-1/genetics
6.
Biochem Biophys Res Commun ; 336(1): 324-31, 2005 Oct 14.
Article in English | MEDLINE | ID: mdl-16126171

ABSTRACT

Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Interleukin-10 (IL-10) is a cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether IL-10 gene therapy possesses anti-hepatic fibrogenesis in mice. Liver fibrosis was induced by long-term thioacetamide administration in mice. Human IL-10 expression plasmid was delivered via electroporation after liver fibrosis established. IL-10 gene therapy reversed hepatic fibrosis and prevented cell apoptosis in a thioacetamide-treated liver. RT-PCR revealed IL-10 gene therapy to reduce liver transforming growth factor-beta1, tumor necrosis factor-alpha, collagen alpha1, cell adhesion molecule, and tissue inhibitors of metalloproteinase mRNA upregulation. Following gene transfer, the activation of alpha-smooth muscle actin and cyclooxygenase-2 was significantly attenuated. In brief, IL-10 gene therapy might be an effective therapeutic reagent for liver fibrosis with potential future clinical applications.


Subject(s)
Genetic Therapy , Interleukin-10/genetics , Liver Cirrhosis/therapy , Thioacetamide/toxicity , Animals , Base Sequence , Blotting, Western , Cyclooxygenase 2 , DNA Primers , Immunohistochemistry , In Situ Nick-End Labeling , Liver Cirrhosis/chemically induced , Male , Mice , Mice, Inbred ICR , Prostaglandin-Endoperoxide Synthases/metabolism , Reverse Transcriptase Polymerase Chain Reaction
7.
J Neuropathol Exp Neurol ; 64(1): 15-26, 2005 Jan.
Article in English | MEDLINE | ID: mdl-15715081

ABSTRACT

Aberrant calpain activation is a key mediator of neuron death. We examined the cell-permeable calpain inhibitor MDL28170 in the pathophysiological processes after spinal cord injury (SCI) including p35-p25- cyclin-dependent kinase-5 (Cdk5) activation, tau hyperphosphorylation, neuron cell death, calpain I activation, astrogliosis, and microglia activation. Our study showed that intrathecal administration of MDL28170 improved neurologic dysfunction, prevented neuron loss, decreased the number of apoptotic cells, and abated astrogliosis and microglia activation 7 days after spinal cord hemisection in rats. Reverse transcription polymerase chain reaction demonstrated calpain inhibition significantly attenuated the ratio of proapoptotic Bax/anti-apoptotic Bcl-2 mRNA in the lesion and penumbra after SCI. Calpain, the calcium-activated proteolytic enzyme, was found to digest p35 to its truncated product, p25. Moreover, abnormal Cdk5 activation by p25 and subsequent tau hyperphosphorylation triggers pathologic events leading to neurodegeneration and neurofibrillary tangles. We found p35-p25-Cdk5 activation and tau hyperphosphorylation in SCI, and then we showed that intrathecal MDL28170 treatment could diminish p35 truncation, and abrogate aberrant tau phosphorylation. Double labeling of calpain I and phosphorylated tau (AT8) in the same cells of spinal cord lesion further implicated pathogenesis of SCI. In conclusion, MDL28170 abated calpain I activation, inhibited apoptosis and neuron loss, quenched microglia and astrocyte activation, and significantly improved neurologic deficit one week after spinal cord hemisection. The neuroprotective mechanisms of calpain inhibitor in SCI could be attenuating upregulation of Bax/Bcl-2 ratio, preventing p35 truncation in the lesion and penumbra, and abrogating tau hyperphosphorylation.


Subject(s)
Calpain/antagonists & inhibitors , Cysteine Proteinase Inhibitors/pharmacology , Dipeptides/pharmacology , Glycoproteins/pharmacology , Nerve Tissue Proteins/antagonists & inhibitors , Nerve Tissue Proteins/metabolism , Spinal Cord Injuries/metabolism , tau Proteins/antagonists & inhibitors , tau Proteins/metabolism , Animals , Dipeptides/therapeutic use , Male , Phosphorylation/drug effects , Rats , Rats, Sprague-Dawley , Spinal Cord Injuries/drug therapy , Thoracic Vertebrae/innervation
8.
Acta Pharmacol Sin ; 26(1): 46-50, 2005 Jan.
Article in English | MEDLINE | ID: mdl-15659113

ABSTRACT

AIM: To investigate effects of the cyclin-dependent kinase5 (Cdk5) inhibitor roscovitine on formalin-induced nociceptive responses in rats. METHODS: The flinch response as a methood of pain threshold measurement and intrathecal injection techniques were used. Cdk5 and phosphorylation of its downstream target, DARPP-32 (dopamine- and cAMP-regulated phosphoprotein of M(r) 32 kDa), were investigated by Western blot analysis. RESULTS: Rats demonstrated a typical flinch response after formalin injection. Intrathecal roscovitine injections significantly suppressed the flinch response in a dose-dependent manner. Western blot analysis showed that phosphorylated DARPP-32 at Thr75 increased in concentration after formalin hyperalgesia, with this effect reduced by roscovitine administration. This antinociception was partially attenuated by administration of naloxone before the formalin test. CONCLUSION: DARPP-32 phosphorylation is involved in acute inflammatory pain response. Intrathecal roscovitine administration attenuates formalin-induced nociceptive responses and there is potential for further application.


Subject(s)
Cyclin-Dependent Kinases/metabolism , Hyperalgesia/metabolism , Purines/pharmacology , Animals , Cyclin-Dependent Kinase 5 , Cyclin-Dependent Kinases/antagonists & inhibitors , Dopamine and cAMP-Regulated Phosphoprotein 32 , Formaldehyde/pharmacology , Hyperalgesia/chemically induced , Injections, Spinal , Male , Nerve Tissue Proteins/metabolism , Pain Measurement , Pain Threshold/drug effects , Phosphoproteins/metabolism , Phosphorylation , Purines/administration & dosage , Rats , Rats, Sprague-Dawley , Roscovitine
9.
Acta Pharmacol Sin ; 25(8): 1027-30, 2004 Aug.
Article in English | MEDLINE | ID: mdl-15301735

ABSTRACT

AIM: To investigate the effect of cyclin-dependent kinase 5 (Cdk5) inhibitor roscovitine on the morphine antinociceptive tolerance development in rats. METHODS: Tail-flick test as pain threshold measurement and intrathecal injection techniques were used. RESULTS: Intrathecal roscovitine infusion alone produced an antinociceptive effect. Tolerance was induced by continuous intrathecal infusion of morphine 5 microg/h for 5 d. Co-administration of intrathecal roscovitine 1 microg/h for 5 d enhanced the morphine antinociceptive effect in tolerant rats. It also caused a shift in the morphine antinociceptive dose-response curve to the left when co-administered with morphine during tolerance induction, and caused a 67 % reduction in the increase in the ED50 of morphine (dose producing 50 % of the maximum response). CONCLUSION: Cdk5 modulation is involved in the antinociceptive tolerance of morphine. Intrathecal roscovitine administration could attenuate this tolerance development.


Subject(s)
Analgesics, Opioid/pharmacology , Cyclin-Dependent Kinases/antagonists & inhibitors , Drug Tolerance , Morphine/pharmacology , Purines/pharmacology , Animals , Cyclin-Dependent Kinase 5 , Injections, Spinal , Male , Pain Measurement , Pain Threshold/drug effects , Purines/administration & dosage , Rats , Rats, Sprague-Dawley , Roscovitine
10.
J Biomed Sci ; 11(5): 571-8, 2004.
Article in English | MEDLINE | ID: mdl-15316131

ABSTRACT

Liver injury is known to often progress even after the hepatotoxicant is dissipated. The hydrolytic enzyme calpain, which is released from dying hepatocytes, destroys the surrounding cells and results in progression of injury. Therefore, control of calpain activation may be a suitable therapeutic intervention in cases of fulminant hepatic failure. This study evaluated the effects of a potent cell-permeable calpain inhibitor, MDL28170, and its mechanisms of action on thioacetamide (TAA)-induced hepatotoxicity in mice. We found that MDL28170 significantly decreased mortality and change in serum transaminase after TAA administration. The necroinflammatory response in the liver was also suppressed. Furthermore, a significant suppression of hepatocyte apoptosis could be found by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay. The upregulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-alpha), both of which are known to mediate the propagation of inflammation, was abolished. MDL2810 also effectively blocked hepatic stellate cell activation, which is assumed to be the early step in liver fibrosis. These results demonstrated that MDL28170 attenuated TAA-induced acute liver failure by inhibiting hepatocyte apoptosis, abrogating iNOS and TNF-alpha mRNA upregulation and blocking hepatic stellate cell activation.


Subject(s)
Cysteine Proteinase Inhibitors/pharmacology , Dipeptides/pharmacology , Liver Failure, Acute/chemically induced , Liver Failure, Acute/prevention & control , Liver/pathology , Thioacetamide/toxicity , Alanine Transaminase/blood , Animals , Apoptosis/drug effects , Liver/drug effects , Male , Mice , Mice, Inbred C57BL , Nitric Oxide Synthase/genetics , Nitric Oxide Synthase Type II , Reverse Transcriptase Polymerase Chain Reaction , Tumor Necrosis Factor-alpha/genetics
11.
Biochem Biophys Res Commun ; 322(1): 153-61, 2004 Sep 10.
Article in English | MEDLINE | ID: mdl-15313186

ABSTRACT

Oxidative stress has been implicated in the propagation of acute liver injury. The aim of our study was to investigate whether gene transfer of alpha-melanocyte-stimulating hormone (alpha-MSH), a potent anti-inflammatory peptide, could prevent fulminant hepatic failure in mice. Acute liver damage was induced by intraperitoneal administration of thioacetamide. Hydrodynamics-based gene transfection with alpha-MSH expression plasmid via rapid tail vein injection was initiated 1 day prior to intoxication. The mortality in the alpha-MSH-treated mice was significantly lower compared to the vehicle group 3 days after injury. Liver histology significantly improved and TUNEL-positive hepatocytes decreased in the treated mice. The degradation of IkappaBalpha, endogenous inhibitor of nuclear factor kappaB, and upregulation of inducible nitric oxide synthase and tumor necrosis factor-alpha mRNA levels were prevented in the alpha-MSH-treated group, indicating decreased oxidative stress and inflammation. These results suggest alpha-MSH gene therapy might protect against acute hepatic necroinflammatory damage with further potential applications.


Subject(s)
Genetic Therapy/methods , Liver Failure, Acute/genetics , Liver Failure, Acute/therapy , Plasmids/administration & dosage , Plasmids/genetics , alpha-MSH/blood , alpha-MSH/genetics , Animals , Injections, Intravenous , Liver Failure, Acute/chemically induced , Liver Failure, Acute/pathology , Male , Mice , Mice, Inbred C57BL , Survival Rate , Thioacetamide , Treatment Outcome
12.
Pain ; 104(1-2): 159-67, 2003 Jul.
Article in English | MEDLINE | ID: mdl-12855325

ABSTRACT

Opioids remain the most efficacious pharmacological agents for various clinical pain syndromes. Recently, various engineered cells capable of secreting opioidergic peptides have been applied to relieve pain in animal models. In vivo gene delivery by viruses encoding endogenous opioids has also been used with success. In this study, we attempted non-viral intrathecal in vivo gene delivery by electroporation to induce analgesia. Thirty Sprague-Dawley rats were used in this study, six in each of five groups. Rats were treated as follows: vehicle without electroporation (group A), vehicle with electroporation (group B), 100 microg of pCMV-hPOMC plasmid without electroporation (group C), or 100 microg of pCMV-hPOMC plasmid with electroporation (group D). Group E was treated with both pCMV-hPOMC plasmid and electroporation, and given naloxone (1mg/kg) 1h before the formalin test. The tail flick, paw withdrawal latency from radiant heat, and formalin test results for each groups were compared. Radioimmunoassay (RIA) and reverse transcription-polymerase chain reaction (RT-PCR) were used to determine the levels of expression of beta-endorphin in the spinal cord. beta-Endorphin expression was localized by immunohistochemistry. A significant decrease in the number of flinches in phase 2 of the formalin test was observed in the group treated with both plasmid and electroporation (group D), whereas the other measures of pain did not differ between groups. RIA and RT-PCR both showed increased expression of beta-endorphin in group D. The expression of beta-endorphin was highest in laminae I and II of the dorsal horn of the spinal cord. We conclude that electroporation successfully delivered intrathecally administered pCMV-hPOMC into the dorsal horn cells of the spinal cord, and induced analgesia in phase 2 of the formalin test in rats.


Subject(s)
Analgesia/methods , Disease Models, Animal , Electroporation/methods , Pain Measurement/drug effects , Pro-Opiomelanocortin/administration & dosage , Animals , DNA, Complementary/administration & dosage , Drug Delivery Systems/methods , Humans , Male , Pain/drug therapy , Pain Measurement/methods , Rats , Rats, Sprague-Dawley , Spinal Cord/chemistry , Spinal Cord/drug effects , beta-Endorphin/analysis
13.
Neurosci Lett ; 333(3): 155-8, 2002 Nov 29.
Article in English | MEDLINE | ID: mdl-12429371

ABSTRACT

Injury to the peripheral nervous system can lead to spontaneous pain, hyperalgesia and allodynia. Previous studies have shown sprouting of Abeta-fibres into lamina II of the spinal cord dorsal horn after nerve injury and the formation of new synapses by these sprouts. Synaptophysin is a presynaptic vesicle protein, useful in the identification of synaptogenesis. Here we investigated whether synaptogenesis as measured by the expression of synaptophysin protein correlates with symptoms of neuropathic pain in rats with a chronic constriction injury (CCI) of the sciatic nerve. We used immunohistochemistry, Western immunoblotting and densitometry to study the distribution of synaptophysin and to quantify relative protein. Synaptophysin was increased in the ipsilateral dorsal horn with a peak level on day 14 and returned to baseline on day 21 post-CCI. Synaptophysin levels temporally correlated with thermal hyperalgesia but not with tactile allodynia. Our results indicate that thermal hyperalgesia in CCI significantly correlates with synaptogenesis within the superficial layers of the dorsal horn.


Subject(s)
Sciatic Nerve/injuries , Spinal Cord/metabolism , Synaptophysin/metabolism , Animals , Antigens, Nuclear/metabolism , Blotting, Western/methods , Functional Laterality/physiology , Immunohistochemistry/methods , Ligation , Male , Neurons/metabolism , Rats , Rats, Sprague-Dawley , Spinal Cord/cytology , Thermosensing/physiology , Time Factors
14.
Life Sci ; 70(25): 3039-47, 2002 May 10.
Article in English | MEDLINE | ID: mdl-12138017

ABSTRACT

UNLABELLED: Intrathecal (IT) lamotrigine, a sodium channel blocker which suppresses neuronal release of glutamate, has been shown to produce a long-lasting antihyperalgesic effect in the neuropathic pain models. In the present study, we examined the anti-hyperalgesic effects of pre- versus post-treatment of IT lamotrigine in an animal inflammatory pain model, the inflamed knee joint model of the rat. Thermal and mechanical antinociception was assessed in rats using a modified Hargreaves box and von Frey hairs. Induction of tonic persistent inflammatory pain was induced by intra-articular injection (i.a.) of a carrageenan-kaolin mixture (CK) into the right knee-joint. Rats were randomly assigned to the groups receiving IT lamotrigine in distinct doses of 5, 50 or 100 ug either pre- (10 min before CK injection) or post-inflammation induction (4 h or 23 h). We observed that CK injection resulted in a significant thermal and mechanical hyperalgesia throughout a 24-h observation period. Pre-treatment with IT lamotrigine revealed a time and dose-dependent suppression of thermal and mechanical hyperalgesia, whereas the post-treatment with IT lamotrigine only showed an effect for mechanical nociception. CONCLUSION: IT Lamotrigine is antihyperalgesic at a dose larger than 50 ug in the early phase of inflammatory pain model. It reverses tactile allodynia but not thermal hyperalgesia when given after the inflammation induction.


Subject(s)
Analgesics/therapeutic use , Inflammation/drug therapy , Pain/drug therapy , Triazines/therapeutic use , Analgesics/administration & dosage , Animals , Arthritis, Experimental/drug therapy , Dose-Response Relationship, Drug , Inflammation/chemically induced , Injections, Spinal , Knee Joint/physiopathology , Lamotrigine , Pain Measurement , Random Allocation , Rats , Triazines/administration & dosage
15.
J Vasc Surg ; 35(4): 707-12, 2002 Apr.
Article in English | MEDLINE | ID: mdl-11932667

ABSTRACT

BACKGROUND: Deep vein thrombosis (DVT) remains a leading cause of postoperative morbidity and mortality in patients who undergo total knee arthroplasty (TKA). Although patients with previous thrombotic episodes are inherently at a higher risk for subsequent episodes of DVT, it remains difficult to predict such an occurrence and to make a diagnosis in early stages. One potentially useful assay that can be used in the determination of changes of coagulation among patients who undergo arthroplasty is platelet activation. The goal of this study was to establish a predictive value for DVT with measurement of P-selectin levels that could help in planning appropriate perioperative management strategies for patients at high risk for DVT. METHODS: A total of 52 patients who underwent TKA with general anesthesia underwent contrast venography on the 5th postoperative day. Platelet activation before and after operation was measured with platelet surface expression of P-selectin with flow cytometry in these two groups of patients for TKA. None of the patients underwent any anticoagulation therapy. RESULTS: Nineteen of the 52 patients for TKA showed radiologic evidence of DVT, whereas 33 patients for TKA had no radiologic signs of DVT. There was no difference in platelet activation at baseline, which was 1 hour before induction of anesthesia, between the two groups (P >.05) as measured with P-selectin assays. Differences were noted between the two groups on the 5th day after operation, wherein P-selectin was expressed in only 2.72% +/- 0.9% (mean +/- standard deviation) of platelets in patients for TKA with healthy venogram results. This differed significantly from platelets in patients for TKA with DVT, who had P-selectin expression of 6.56% +/- 3.1% (mean +/- standard deviation; P <.01). Sensitivity for the diagnosis of DVT with P-selectin assay was calculated to be 74%, and specificity was found to be 94%. CONCLUSION: The findings showed that radiologically confirmed DVT in patients for TKA surgery with general anesthesia is associated with an elevated number of activated platelets. Perioperative assessment of P-selectin may predict the early onset of DVT in patients who undergo high risk surgical procedures like TKA. This laboratory assay may help prevent the occurrence of the fatal events caused by DVT with use of early therapeutic intervention, such as heparinization.


Subject(s)
Arthroplasty, Replacement, Knee , P-Selectin/metabolism , Venous Thrombosis/diagnosis , Aged , Case-Control Studies , Female , Flow Cytometry , Humans , Middle Aged , Phlebography , Platelet Activation , Predictive Value of Tests , ROC Curve , Risk Factors , Sensitivity and Specificity , Venous Thrombosis/blood
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