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1.
Plast Reconstr Surg ; 125(5): 1544-1552, 2010 May.
Artigo em Inglês | MEDLINE | ID: mdl-20440173

RESUMO

BACKGROUND: Venous thromboembolism is a devastating complication representing one of the major causes of postoperative death in plastic surgery. Within the scope of plastic surgery, body-contouring procedures are often considered to carry a higher risk of venous thromboembolism. Hereditary thrombophilias comprise a group of conditions defined by a genetic predisposition to thrombosis development. Collectively, hereditary thrombophilias are present in at least 15 percent of Western populations and underlie approximately half of thromboembolic events. Although the topic of venous thromboembolism is discussed widely throughout the literature, there is little published on the diagnosis and management of hereditary thrombophilias in the plastic surgery literature. The goals of this study were to present a review of the major inherited thrombophilias, to delineate the risk of these disorders, and to recommend a practical algorithm for patient screening and management before major plastic surgery. METHODS: A MEDLINE search was performed from 1965 to the present to review the literature on inherited thrombophilia disorders. RESULTS: Based on the English language literature and clinical experience, the authors suggest practical guidelines for screening and management of hereditary thrombophilias. A thorough medical history and preoperative evaluation are key to reducing venous thromboembolism complications. CONCLUSIONS: Hereditary thrombophilias are present in a significant number of thromboembolic events. Preoperative vigilance on the part of the plastic surgeon may help to identify patients with undiagnosed hereditary thrombophilias and thereby decrease the incidence of venous thromboembolism.


Assuntos
Cirurgia Plástica , Tromboflebite/genética , Resistência à Proteína C Ativada/metabolismo , Algoritmos , Deficiência de Antitrombina III/diagnóstico , Fatores de Coagulação Sanguínea/análise , Fator V/genética , Humanos , Hiper-Homocisteinemia/diagnóstico , Mutação , Deficiência de Proteína C/diagnóstico , Deficiência de Proteína S/diagnóstico , Protrombina/genética , Tromboflebite/diagnóstico , Tromboflebite/prevenção & controle
2.
Med Sci Monit ; 14(9): BR175-82, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18758409

RESUMO

BACKGROUND: The ideal endpoint of resuscitation after severe hemorrhage should indicate not only that optimal oxygen delivery has been achieved, but also that oxygen utilization has been restored. A modified Foley catheter for simultaneous assessment of microcirculatory blood flow (TBF) and mitochondrial NADH in the urethral wall was used in the female swine. We hypothesized that changes in mitochondrial NADH and TBF are associated with impaired energy metabolism in the urethra and that these changes correlate with impaired tissue perfusion in the bladder during shock and resuscitation. MATERIAL/METHODS: Female swine n=5 underwent laparotomy. TBF was measured by a laser Doppler flowmeter. Mitochondrial function was evaluated by measuring NADH fluorescence in vivo. Multiparameter sensors (pH, pCO2 and pO2) were placed in the bladder mucosa (BM), and in the skeletal muscle (Sk). Animals underwent hemorrhage and their MAP was maintained at 40 mm Hg by appropriate infusing or withdrawing of blood for 10 min. Animals were resuscitated and observed for 20 min. RESULTS: Urethral NADH increased during shock and recovered during resuscitation, while TBF showed an opposite effect (r(2)=0.74). Skeletal muscle and bladder pO2 decreased during shock (p<0.01) and recovered after resuscitation. NADH increased significantly (p<0.05) during shock and decreased after resuscitation. CONCLUSIONS: Changes in TBF and NADH in the urethral mucosa represent novel markers for the energetic state of the tissue. They could be measured in vivo by a minimally invasive approach and thus could provide important information on the end-points of resuscitation in hemorrhagic shock.


Assuntos
Hemorragia/metabolismo , Mitocôndrias/metabolismo , NAD/metabolismo , Ressuscitação , Uretra , Animais , Dióxido de Carbono/metabolismo , Feminino , Hemodinâmica , Concentração de Íons de Hidrogênio , Microcirculação/fisiologia , Músculo Esquelético/metabolismo , Oxirredução , Oxigênio/metabolismo , Pressão Parcial , Fluxo Sanguíneo Regional , Suínos , Uretra/irrigação sanguínea , Uretra/metabolismo , Bexiga Urinária/anatomia & histologia , Bexiga Urinária/metabolismo
3.
Microsurgery ; 27(2): 105-11, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17290380

RESUMO

Composite tissue allografts (CTAs) contain their own reservoir of vascularized bone marrow, offering novel aspects for the induction of donor-specific tolerance. Additionally, the manipulation of recipient dendritic cells, pulsed with donor allopeptide, has been shown to engender solid organ allograft survival. To exploit these modalities, we have developed a protocol utilizing injection of recipient bone marrow-derived dendritic cells (BMDCs) pulsed with a donor-derived peptide for use in CTA transplantation. Six days prior to orthotopic hind-limb transplantation, Lewis rats received IV injection of donor allopeptide-pulsed, recipient BMDCs, in conjunction with a single dose of anti-lymphocyte serum. Control groups displayed signs of allograft rejection within 5 days postoperatively. Animals within the primary experimental cohort demonstrated prolongation of graft survival to an average of 8 days, and exhibited low numbers of donor T cells. The use of BMDCs in conjunction with transient immunosuppression has potential therapeutic application for induction of donor-antigen-specific tolerance to hind limb allografts.


Assuntos
Células Dendríticas/transplante , Fêmur/transplante , Sobrevivência de Enxerto , Condicionamento Pré-Transplante/métodos , Tolerância ao Transplante , Animais , Células da Medula Óssea , Células Dendríticas/imunologia , Rejeição de Enxerto/fisiopatologia , Masculino , Peptídeos/imunologia , Ratos , Ratos Endogâmicos Lew , Ratos Endogâmicos WF , Tolerância ao Transplante/imunologia , Transplante Homólogo
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