RESUMO
Decreasing blood viscosity has been proposed since the advent of hemodilution as a means for increasing perfusion in many pathological conditions, and increased plasma viscosity is associated with the presence of pathological conditions. However, experimental studies show that microvascular functions as represented by functional capillary density in conditions of significantly decreased viscosity is impaired, a problem corrected by increasing plasma and blood viscosity. Blood viscosity, primarily dependent on hematocrit (Hct) is a determinant of peripheral vascular resistance, and therefore blood pressure. In the healthy population Hct presents a variability, which is not reflected by the variability of blood pressure. This is due to a regulatory process at the level of the endothelium, whereby the increase of Hct (and therefore blood viscosity) leads to increased shear stress and the production of the vasodilator nitric oxide (NO), a finding supported by experimental studies showing that the acute increase of Hct lowers blood pressure. Studies that in the healthy population show that blood pressure and Hct have a weak positive correlation. However, when the effect of blood viscosity is factored out, blood pressure and Hct are negatively and significantly correlated, indicating that as blood viscosity increases, the circulation dilates. Conversely, lower Hct and blood viscosity conditions lead to a constricted circulation, associated with a condition of decreased NO bioavailability, and therefore a pro-inflammatory condition.
Assuntos
Viscosidade Sanguínea/fisiologia , Hemodiluição/métodos , Microcirculação/fisiologia , Viscosidade Sanguínea/efeitos dos fármacos , Fenômenos Fisiológicos Cardiovasculares , Hematócrito , Humanos , Hipertensão/sangue , Óxido Nítrico/sangue , Óxido Nítrico/metabolismo , Resistência Vascular/efeitos dos fármacosRESUMO
Topological and geometrical characteristics of the anastomotic arteriolar network in cat sartorius muscle were studied. The vessels were dilated and filled with gelatin-ink solution and the muscle cleared with methylsalicylate. The analysis was done on 11 muscles and included 2297 vascular segments and 772 vascular loops classified according to their position within the network. On average, each muscle had 644 transverse arterioles arising from the anastomotic vessels. The length of vascular segments close to feeding arteries was greater than those located in the central region, while the number of transverse arterioles per unit length of arcade vessel showed an opposite tendency. Most vessel orders had similar diameters, except for the segments at the periphery of the muscle, which were significantly larger. No correlation was found between vessel length and diameter. Vascular loops located in the central part of the network were smaller, as assessed by area, perimeter, number of segments, segment length and number of branches. The variability of the parameters between muscles was smaller than variability within each muscle. We concluded that, in addition to the parameters previously reported, quantitative descriptions of anastomotic networks may be enhanced by considering certain topological aspects of microvessels. The separation of segments and loops according to the position in the network may reveal differences between muscles of different sizes and functions which would not be detected if the vessels were considered as a single group.
Assuntos
Gatos/anatomia & histologia , Músculo Esquelético/irrigação sanguínea , Animais , Arteríolas/anatomia & histologia , Arteríolas/fisiologia , Fluxo Sanguíneo RegionalRESUMO
BACKGROUND: Thromboembolic events may be related to thrombotic deposition on prosthetic valves. In a left ventricular assist device (LVAD) that contains two porcine pericardial bioprosthetic valves in addition to significant associated biomaterial placement, this may be particularly true. Thrombotic deposits on valves removed from LVADs at autopsy or heart transplantation were scored to determine (1) the nature and location of valvular deposition, (2) whether deposition was related to thromboembolic events, (3) correlations between deposition and patient hemodynamic and coagulation parameters, and (4) implant time dependency. METHODS AND RESULTS: Novacor LVADs were implanted in 23 patients as a bridge to transplantation for 1 to 303 days. Photographs of the concave (downstream) and convex (upstream) side of the inflow and outflow valve were made at explant and later scored for (1) total thrombus area (10 = equivalent of cusp area), (2) percent of cusp area occupied by solid thrombus, (3) thrombus color (10 = dark red, 0 = white), and (4) average percent of valve strut height involved with thrombus (from a side view). The inflow valve was shown to have heavier and redder deposition than the outflow valve. This was also true for the concave versus the convex side. Heaviest deposition was seen on the inflow valve concave side, which rests within the LVAD pumping sac and may be subject to poor convection. Patients with neurological thromboembolic events (8/23) during implantation had heavier deposition on the inflow valve concave side (5.7 +/- 2.7 versus 4.6 +/- 2.2, P < .05). Pump volumetric output was also found to negatively correlate with thrombus area on this valve and side (r = -.61, P = .002). Platelet release (platelet factor 4) was correlated with thrombus involvement on the upstream (convex) side of the inflow valve (r = .82, P = .002). No significant dependence of deposition on the implant time was found. CONCLUSIONS: Valve thrombus deposition was related to thromboembolic events. Pump volumetric output and platelet release were found to be related to deposition. These results may have implications for the role of hemodynamics and platelet activation in thromboembolism associated with prosthetic valve placement in general.
Assuntos
Bioprótese/efeitos adversos , Próteses Valvulares Cardíacas/efeitos adversos , Coração Auxiliar/efeitos adversos , Trombose/etiologia , Desenho de Equipamento , Hemodinâmica , Humanos , Tromboembolia/fisiopatologia , Trombose/fisiopatologiaRESUMO
Early thrombosis of artificial microvascular grafts (AMG, grafts < or = 2 mm internal diameter) prevents their reliable clinical use. The present studies were undertaken to examine the effect of hirudin, a thrombin-specific inhibitor, and of the F(ab')2 fragment of PG-1, a monoclonal antibody (MoAb) directed against guinea pig platelet membrane glycoprotein Ib (GPIb), on AMG patency in an animal model. One-centimeter long segments of expanded polytetrafluoroethylene (ePTFE), 0.88 mm internal diameter, were serially implanted as interposition grafts in the guinea pig femoral arterial systems bilaterally. A control group was treated with 0.5 mL saline intravenously (IV) 30 minutes before limb 1 and limb 2 graft implantation. Three experimental groups were treated with 0.5 mL saline IV before limb 1 graft implantation as an animal control and with either 0.5 mL saline containing 1.25 mg/kg IV PG-1 F(ab')2, (which inhibits ristocetin-induced platelet agglutination and von Willebrand factor binding), hirudin 1 mg/kg IV, or a combination of both agents before limb 2 graft implantation. GPIb inhibition, thrombin inhibition, and the combination resulted in a significant prolongation of AMG patency (P < .005). Whereas thrombin inhibition with hirudin prolonged AMG patency similar to that observed with GPIb inhibition, the combination of GPIb and thrombin inhibition provided the overall longest prolongation of AMG patency. These results indicate that both platelet membrane GPIb and thrombin play a role in AMG thrombosis.
Assuntos
Vasos Sanguíneos/transplante , Glicoproteínas da Membrana de Plaquetas/metabolismo , Trombose/etiologia , Trifosfato de Adenosina/farmacologia , Animais , Anticorpos Monoclonais , Cobaias , Hemostasia/efeitos dos fármacos , Hirudinas/farmacologia , Masculino , Microcirculação , Microscopia Eletrônica , Agregação Plaquetária/efeitos dos fármacos , Glicoproteínas da Membrana de Plaquetas/antagonistas & inibidores , Trombina/antagonistas & inibidoresRESUMO
Laser-assisted microvascular anastomoses can be performed more quickly than sutured anastomoses, yet manifest similar patency rates and tensile strength. This study was undertaken to determine if in vitro laser-assisted microvascular anastomoses could be created between human adult arteries (anterior tibial arteries), human placental arteries, and expanded polytetrafluoroethylene microconduits. A CO2 laser was applied in single or continuous bursts with a matrix of variables encompassing power P = 80 to 160 mW, spot size SS = 150 to 500 microns, and exposure time EXP = 1.0-second continuous exposure (n = 2 each composite setting). The endpoints measured to assess the ability to laser-weld vessels were morphologic appearance by scanning electron microscopy and bursting strength. Scanning electron microscopy revealed apparent fusion of human placental arteries and human adult arteries to expanded polytetrafluoroethylene microconduits at settings of P = 130 mW, SS = 300 microns, and EXP = 1.0 second, though bursting pressure at all settings was less than 10 mmHg. Laser-assisted microvascular anastomoses of human placental artery to human placental artery and human adult artery to human adult artery were successful at this setting, though bursting pressures of anastomoses incorporating placental vessels were significantly weaker than those created with adult tissue. The relative weakness of laser-assisted microvascular anastomoses incorporating placental arteries might be explained by qualitative or quantitative differences in vessel wall collagen, as seen in fetal tissue, and deserves further characterization.
Assuntos
Artérias/cirurgia , Prótese Vascular , Terapia a Laser , Microcirurgia/métodos , Politetrafluoretileno , Adulto , Anastomose Cirúrgica , Artérias/ultraestrutura , Fenômenos Biomecânicos , Humanos , Técnicas In Vitro , Microcirculação/cirurgia , Microscopia Eletrônica de Varredura , Placenta/irrigação sanguíneaRESUMO
The propensity for platelets to bind at a native vessel anastomosis is thought to be related to subendothelial exposure, the presence of suture material, and local flow disturbances. By using an artificial microvascular graft to artificial microvascular graft anastomosis model that mimics the geometry and topography of a native microvascular anastomosis but which eliminates the endothelial and subendothelial contributions, the influence of the normal anastomotic configuration alone on initial platelet deposition was measured. Anastomotic and immediate downstream platelet deposition was not augmented by the presence of the anastomotic configuration alone. This suggests that the enhanced initial platelet deposition in the region of a native vessel microanastomosis is primarily related to the presence of injured endothelium and exposed subendothelium rather than to flow disturbances.
Assuntos
Anastomose Cirúrgica/métodos , Prótese Vascular , Microcirurgia/métodos , Agregação Plaquetária/fisiologia , Politetrafluoretileno , Combinação de Medicamentos , Hemostáticos/química , Humanos , Radioisótopos de Índio , Microscopia Eletrônica de Varredura , Modelos Cardiovasculares , Palmitatos/química , Adesividade Plaquetária/fisiologia , Contagem de Plaquetas , Politetrafluoretileno/química , Reologia , Propriedades de Superfície , Ceras/químicaRESUMO
Initial platelet deposition (PD) in and around the region of a small-vessel anastomosis may set the stage for thrombosis and tissue loss. To study this problem, a human vessel model (human placental artery, HPA) has been designed to mimic the vascular injuries attendant on clinical microsurgery. To perform these studies, dissected lengths of human placental artery were treated to provide the following four types of injury: group I: control, dissected but otherwise uninjured (N = 5); group II: distal portion of vessel endothelium removed (N = 5); group III: central anastomosis, distal endothelium intact (N = 7); and group IV: central anastomosis, distal endothelium removed (N = 4). Vessels were perfused with 25 ml human whole blood for 17 +/- 5 s at an average shear rate of 536 s-1. Vessels in groups I to IV were segmented at 2-cm intervals, and the number of 111In-labeled platelets was measured. Data from the following groups of exposure zones were pooled and analyzed: endothelium intact, endothelium absent, anastomosis present, postanastomosis with endothelium intact, and postanastomosis with endothelium absent. Significant numbers of platelets were found to attach to intact endothelium, indicating that ischemia and microsurgical handling may augment platelet deposition to otherwise uninjured vessels. A similar degree of platelet deposition was measured after exposure of the subendothelium and perfusion, indicating that superficial subendothelial exposure in the absence of an additional prothrombotic stimulus may lead to no greater platelet deposition than occurs on slightly injured endothelium alone. Platelet deposition at anastomoses was strikingly elevated, although the anastomosis had no additive effect on platelet deposition to downstream endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)
Assuntos
Vasos Sanguíneos/fisiologia , Adesividade Plaquetária , Procedimentos Cirúrgicos Vasculares , Anastomose Cirúrgica , Vasos Sanguíneos/ultraestrutura , Endotélio Vascular/fisiologia , Humanos , Técnicas In Vitro , Microscopia Eletrônica de Varredura , Microcirurgia , Placenta/irrigação sanguínea , Fluxo Sanguíneo RegionalRESUMO
Vasodilation of small blood vessels is controlled in part by the endothelium-derived relaxing factor (EDRF), which also inhibits platelet adhesion. Methylene blue (MB), which is occasionally applied directly to blood vessels during microsurgery to provide orientation and prevent torsion, is an irreversible inhibitor of the effects of endothelium-derived relaxing factor and may thereby augment both vasospasm and platelet responses. We have investigated the effects of the extravascular adventitial application of methylene blue on platelet deposition to human placental arteries (HPA) in the presence and absence of surgically induced vasospasm. A trend toward increased platelet deposition to human placental arteries was seen in each group but did not reach significance. The degree of platelet deposition to control human placental arteries suggests that the effects of methylene blue on platelet deposition may be dwarfed by the effects of surgical trauma and ischemia.
Assuntos
Artérias/efeitos dos fármacos , Plaquetas/efeitos dos fármacos , Azul de Metileno/farmacologia , Óxido Nítrico/antagonistas & inibidores , Vasoconstrição/efeitos dos fármacos , Administração Tópica , Etidocaína/farmacologia , Feminino , Humanos , Técnicas In Vitro , Azul de Metileno/administração & dosagem , Placenta/irrigação sanguínea , GravidezRESUMO
The mechanism of platelet thrombus growth on an artificial surface is incompletely understood. While glycoprotein (GP)Ib and GPIIb/IIIa are required for normal attachment and thrombus formation on subendothelium, their roles in platelet deposition to artificial surfaces remain unclear. Using selected platelet inhibitors (aspirin [ASA], low molecular weight dextran, monoclonal antibodies 10E5 [v GPIIb/IIIa], and 6D1 [GPIb]) we examined the mechanism of platelet deposition to polyethylene (PE) surfaces under steady laminar and oscillatory flow conditions. Polyethylene-100 (PE-100) tubes (0.86 mm internal diameter) were perfused under steady laminar flow with citrated human whole blood reconstituted with 111indium-labeled platelets at 312 seconds-1 shear rate in the presence and absence of platelet inhibitors. The effect of oscillatory flow on platelet deposition was examined in a microwell system using 3/16-inch diameter discs of National Heart, Lung, and Blood Institute primary reference PE as the test surface. ASA and dextran did not significantly (P greater than .05) inhibit platelet deposition in laminar flow (not tested in oscillatory). Antibody 10E5 was a potent inhibitor (laminar less than 1%, P less than .0001, oscillatory less than 1.6%, P less than .01) of platelet deposition in both systems, and in this case, true adhesion (first attached layer) was blocked. Antibody 6D1 unexpectedly inhibited 70% of platelet deposition (P less than .01) in steady laminar flow and 56.5% in oscillatory flow (P less than .01). Scanning electron microscopy demonstrated platelets atop platelets in the controls, rare platelets in the 10E5 group, and a patchy monolayer of platelets in the 6D1 group. Transmission electron microscopy of cross-sections confirmed these observations. We conclude that the adhesion of the first platelet layer to an artificial surface requires GPIIb/IIIa. The data also suggest that GPIb is required for the development of the second layer in vertical platelet thrombus growth.
Assuntos
Anticorpos Monoclonais/farmacologia , Plaquetas/fisiologia , Adesividade Plaquetária , Inibidores da Agregação Plaquetária/farmacologia , Glicoproteínas da Membrana de Plaquetas/fisiologia , Difosfato de Adenosina/sangue , Trifosfato de Adenosina/sangue , Aspirina/farmacologia , Plaquetas/citologia , Plaquetas/efeitos dos fármacos , Humanos , Técnicas In Vitro , L-Lactato Desidrogenase/sangue , Perfusão/instrumentação , Perfusão/métodos , Adesividade Plaquetária/efeitos dos fármacos , Agregação Plaquetária/efeitos dos fármacos , Glicoproteínas da Membrana de Plaquetas/imunologiaRESUMO
Nine patients with extensive wounds of the hip joint due to chronic infection following total hip arthroplasty or internal fixation of fractures of the femoral head and neck have been treated by serial radical debridements to remove infected bone, contaminated remnants of bone cement, and the surrounding fibrotic soft tissues. The resultant deep cavity extending down to the acetabulum has then been obliterated with either pedicled muscle flaps or free muscle flaps. Subcutaneous or transpelvic transposition of rectus abdominis muscle flaps is preferred for smaller defects, but only the free latissimus dorsi muscle flap provides sufficient volume of tissue to obliterate the more extensive hip defects. Systemic antibiotics have been continued only for a short-term course of 14 days postoperatively. There has been no recurrence of infection, with follow-up ranging between 6 months and 3 1/4 years. One patient has undergone reimplantation of a second custom hip prosthesis into the vascularized bed of a free latissimus dorsi muscle flap.