Biomedical subjects

Haruo Aramoto

Publications and source records attributed to Haruo Aramoto.

4 recordsLinked to original sources

PubMed2005

Clinical implication of plasma level of soluble fibrin monomer-fibrinogen complex in patients with abdominal aortic aneurysm.

OBJECTIVE: We prospectively studied the clinical implication of plasma level of soluble fibrin monomer (FM)-fibrinogen complex, a recently established molecular marker reflecting thrombin activity, in patients with abdominal aortic aneurysm (AAA) undergoing elective aortic repair. METHODS: The study included 49 patients who underwent elective aneurysm repair using a gelatin-sealed or nonimpregnated Dacron prosthesis. Plasma level of soluble FM-fibrinogen complex was measured before surgery and on days 1, 3, 5, 7, and 10 postoperatively by latex agglutination assay utilizing monoclonal antibody IF-43. Plasma levels of thrombin-antithrombin complex (TAT), D-dimer, alpha2-plasmin inhibitor-plasmin complex (PIC), and fibrinogen were also evaluated. RESULTS: The preoperative level of soluble FM-fibrinogen complex showed variation in the degree of hemostatic activation, with fair correlations with TAT (r = 0.509, P < .001), D-dimer (r = 0.521, P < .001), and PIC (r = 0.579, P < .001). The patients with greater intraoperative blood loss (> or = 800 mL) showed a significantly elevated plasma level of soluble FM-fibrinogen complex preoperatively compared with those with less intraoperative blood loss (P = .009). Its postoperative fluctuation showed a similar pattern to that of TAT, reflecting the time course of coagulation activity. Gelatin impregnation of the Dacron vascular graft did not seem to influence the postoperative systemic coagulation mechanism. CONCLUSIONS: The results indicated that soluble FM-fibrinogen complex appears to be a useful diagnostic molecular marker to assess the activity of the coagulation system, and that its preoperative level may serve as a potential risk factor for intraoperative hemorrhagic diathesis in patients undergoing elective AAA repair.

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PubMed2005

Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.

OBJECTIVE: The authors tested the hypothesis that p42/44- (ERK-1/2) and/or p38-mitogen-activated protein kinases (MAPK) are in vivo regulatory elements in the platelet-activating factor (PAF) activated signaling cascade that stimulates microvascular hyperpermeability. METHODS: FITC-dextran 70 was used as the macromolecular tracer for microvascular permeability in the mouse mesenteric fat tissue. Interstitial integrated optical intensity (IOI) was used as an index of permeability. RESULTS: An application of 10(-7) M PAF increased IOI from 23.1 +/- 3.6 to 70.8 +/- 7.4 (mean +/- SEM). Inhibition of ERK-1/2 with 3 microM and 30 microM AG126 reduced IOI to 32.3 +/- 2.5. Similarly, inhibition of p38-MAPK with 6 nM, 60 nM and 600 nM SB203580 lowered IOI to 29.1 +/- 2.4. CONCLUSIONS: The results demonstrate that ERK-1/2 and p38MAPK participate in the signaling cascade that regulates PAF-induced microvascular hyperpermeability in vivo.

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PubMed2004

Vascular endothelial growth factor stimulates differential signaling pathways in in vivo microcirculation.

Vascular endothelial growth factor (VEGF) induces mild vasodilation and strong increases in microvascular permeability. Using intravital microscopy and digital integrated optical intensity image analysis, we tested, in the hamster cheek pouch microcirculation, the hypothesis that differential signaling pathways in arterioles and venules represent an in vivo regulatory mechanism in the control of vascular diameter and permeability. The experimental design involved blocking specific signaling molecules and simultaneously assessing VEGF-induced changes in arteriolar diameter and microvascular transport of FITC-Dextran 150. Inhibition of Akt [indirectly via phosphatidylinositol 3-kinase with LY-294002 or wortmannin] or PKC (with bisindolylmaleimide) reduced VEGF-induced hyperpermeability. However, phosphatidylinositol 3-kinase/Akt inhibition enhanced the early phase and attenuated the late phase of VEGF-induced vasodilation, whereas blocking PKC had no effect. Inhibition of extracellular signal-regulated kinase (ERK)-1/2 (with PD-98059 or AG-126) also reduced VEGF-induced hyperpermeability but did not block VEGF-induced vasodilation. Blockade of endothelial nitric oxide synthase (with N(omega)-monomethyl-l-arginine) inhibited VEGF-induced changes in both permeability and diameter. Furthermore, immunofluorescence studies with human umbilical vein endothelial cells revealed that bisindolylmaleimide, PD-98059, and l-NMMA attenuate VEGF-induced reorganization of vascular endothelial cadherin. Our data demonstrate that 1) endothelial nitric oxide synthase is a common convergence pathway for VEGF-induced changes in arteriolar diameter and microvascular permeability; 2) PKC and ERK-1/2 do not play a major role in VEGF-induced vasodilation in the hamster cheek pouch microcirculation; and 3) Akt, PKC, and ERK-1/2 are elements of the signaling cascade that regulates VEGF-stimulated microvascular hyperpermeability. Our data provide evidence for differential signaling as a regulatory step in VEGF-stimulated microvascular dynamics.

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PubMed2004

Ischemic preconditioning improves oxygenation of exercising muscle in vivo.

BACKGROUND: Ischemic preconditioning (IP) improves tissue tolerance to prolonged ischemia. In this study, we investigated the functional effect of IP on skeletal muscle of rat hind limb by means of near-infrared spectroscopy (NIRS) and by measuring myeloperoxidase (MPO) activity. MATERIALS AND METHODS: Adult male Sprague Dawley rats were divided into four separate protocol groups according to different preparations prior to 2 h of global ischemia: a group of ischemic reperfusion without any preparation (I/R), ischemic reperfusion with ischemic preconditioning (IP+IR), ischemic reperfusion with adenosine infusion (ADO+I/R), and sham operation. Ischemia and ischemic preconditioning were induced by clamping infrarenal abdominal aorta and left common iliac artery. For each rat, an exercise test of gastrocnemius muscles was performed by stimulating sciatic nerve before and after global ischemia while performing NIRS. MPO activity of ischemic muscles was also measured. RESULTS: Half-resaturation time after exercise and MPO activity were significantly improved in IP+IR and ADO+I/R groups. Difference of oxyhemoglobin during exercise was also improved in the IP+IR group. CONCLUSION: This study has demonstrated that IP provides the protective effect on in vivo skeletal muscle oxygenation during exercise.

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