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Jun Maki Last modified date：2023.06.12

Lecturer / Intensive Care Unit
Kyushu University Hospital


Other Organization
Intensive Care Unit


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Homepage
https://kyushu-u.pure.elsevier.com/en/persons/jun-maki
　Reseacher Profiling Tool　Kyushu University Pure
Phone
092-642-5871
Fax
092-642-5874
Academic Degree
M.D., Ph.D.
Country of degree conferring institution (Overseas)
No
Field of Specialization
Anesthesiology, Critical Care Medicine、Emergency　Medicine
Total Priod of education and research career in the foreign country
02years00months
Outline Activities
I have taught undergraduate medical students intensive care medicine and emergency medicine in two classes, "pathophysiology and treatment of shock" and "primary survey for critically ill patients". I have instructed them in bed side learning mechanical ventilation, cardiopulmonary resuscitation and trauma care. I have been involved in instruction and evaluation in OSCE.
My research interest is about risk management and the efficacy of Rapid Response System.
As an intensivist and emergency physician, I'm　engaged in treatment for patients in ICU and ER. I also supervise residents of department of Anesthesiology in OR.
I teach critical care medicine to medical students.
Research
Research Interests
  • Usefulness of Peripherally Inserted Central venous Catheter in rapid fluid infusion
    keyword : Peripherally Inserted Central venous Catheter, Rapid Fluid Infusion, Blood Transfusion, In-line Pressure
    2021.04～2023.03.
  • Factors to determine the indication of extracorporeal cardiopulmonary resuscitation
    keyword : ECPR, survival rate, Indication
    2020.06.
  • Nursing education in order improve the Rapid response system in our hospital
    keyword : Rapid response system, Nursing education
    2018.04.
  • Pathogenesis and treatment for pulmonary hypertension due to congenital heart diseases
    keyword : pulmonary hypertension, congenital heart disease, shear stress
    2015.04～2019.03.
Academic Activities
Reports
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Papers
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1. Jun Maki, Mayumi Hirano, Sumio Hoka, Hideo Kanaide, Katsuya Hirano, Involvement of reactive oxygen species in thrombin-induced pulmonary vasoconstriction., American journal of respiratory and critical care medicine, 10.1164/rccm.201002-0255OC, 182, 11, 1435-44, 2010.12, RATIONALE: Pulmonary vascular thrombosis and thrombotic arteriopathy are common pathological findings in pulmonary arterial hypertension. Thrombin may thus play an important role in the pathogenesis and pathophysiology of pulmonary arterial hypertension. OBJECTIVES: The present study aimed to elucidate the contractile effect of thrombin in the pulmonary artery and clarify its underlying mechanisms. METHODS: The changes in cytosolic Ca²(+) concentrations ([Ca²(+)](i)), 20-kD myosin light chain (MLC20) phosphorylation, and contraction were monitored in the isolated porcine pulmonary artery. The production of reactive oxygen species (ROS) was evaluated by fluorescence imaging. MEASUREMENTS AND MAIN RESULTS: In the presence of extracellular Ca²(+), thrombin induced a sustained contraction accompanied by an increase in [Ca²(+)](i) and the phosphorylation of MLC20. In the absence of extracellular Ca²(+), thrombin induced a contraction without either [Ca²(+)](i) elevation or MLC20 phosphorylation. This Ca²(+)- and MLC20 phosphorylation-independent contraction was mimicked by hydrogen peroxide and inhibited by N-acetyl cysteine. Fluorescence imaging revealed thrombin to induce the production of ROS. A Rho-kinase inhibitor, Y27632, inhibited not only the thrombin-induced Ca²(+)- and MLC20 phosphorylation-dependent contraction, but also the Ca²(+)- and MLC20 phosphorylation-independent contraction and the ROS production. These effects of thrombin were mimicked by a proteinase-activated receptor 1 (PAR₁)-activating peptide. CONCLUSIONS: This study elucidated the Ca²(+)- and MLC20 phosphorylation-independent ROS-mediated noncanonical mechanism as well as Ca²(+)- and MLC20 phosphorylation-dependent canonical mechanism that are involved in the thrombin-induced PAR₁-mediated pulmonary vasoconstriction. Rho-kinase was suggested to play multiple roles in the development of thrombin-induced pulmonary vasoconstriction..
2. Jun Maki, Mayumi Hirano, Sumio Hoka, Hideo Kanaide, Katsuya Hirano, Thrombin activation of proteinase-activated receptor 1 potentiates the myofilament Ca2+ sensitivity and induces vasoconstriction in porcine pulmonary arteries., British journal of pharmacology, 10.1111/j.1476-5381.2009.00591.x, 159, 4, 919-27, 2010.02, BACKGROUND AND PURPOSE: Thrombus formation is commonly associated with pulmonary arterial hypertension (PAH). Thrombin may thus play an important role in the pathogenesis and pathophysiology of PAH. Hence, we investigated the contractile effects of thrombin and its mechanism in pulmonary artery. EXPERIMENTAL APPROACH: The cytosolic Ca(2+) concentrations ([Ca(2+)](i)), 20 kDa myosin light chain (MLC20) phosphorylation and tension development were evaluated using the isolated porcine pulmonary artery. KEY RESULTS: Thrombin induced a sustained contraction in endothelium-denuded strips obtained from different sites of a pulmonary artery, ranging from the main pulmonary artery to the intrapulmonary artery. In the presence of endothelium, thrombin induced a transient relaxation. The contractile effect of thrombin was abolished by either a protease inhibitor or a proteinase-activated receptor 1 (PAR(1)) antagonist, while it was mimicked by PAR(1)-activating peptide (PAR(1)AP), but not PAR(4)AP. The thrombin-induced contraction was associated with a small elevation of [Ca(2+)](i) and an increase in MLC20 phosphorylation. Thrombin and PAR(1)AP induced a greater increase in tension for a given [Ca(2+)](i) elevation than that obtained with high K(+)-depolarization. They also induced a contraction at a fixed Ca(2+) concentration in alpha-toxin-permeabilized preparations. CONCLUSIONS AND IMPLICATIONS: The present study revealed a unique property of the pulmonary artery. In contrast to normal arteries of the systemic circulation, thrombin induces a sustained contraction in the normal pulmonary artery, by activating PAR(1) and thereby increasing the sensitivity of the myofilament to Ca(2+). This responsiveness of the pulmonary artery to thrombin may therefore contribute to the pathogenesis and pathophysiology of PAH..
Presentations
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1. Jun Maki, Asami Ikeda, Tsukasa Shimauchi, Kentaro Tokuda , Yuji Karashima, Posterior Reversible Encephalopathy Syndrome Diagnosed After Post Caesarian Section Atonic Hemorrhage, Anesthesiology 2018, 2018.10, A 39 years old primipara underwent a caesarian section because of arrested labor. After delivery, she suffered from atonic hemorrhage and needed massive blood transfusion. In the ICU, Nicardipine was administered to treat hypertension. After extubation, she complained of visual abnormality. MRI finding showed T2-FLAIR hyperintensities in bilateral occipital lobes, suggesting posterior reversible encephalopathy syndrome (PRES). Her blood pressure was tightly controlled, and visual abnormality was improved in a week.Although PRES associated with hypertensive disorder of pregnancy has been reported, PRES developed in perioperative period is rare and difficult to recognize..
Membership in Academic Society
  • American Society of Anesthesiologists
  • Society of Critical Care Medicine
  • Japanese Society of Anesthesiologists
  • Japanese Society of Intensive Care Medicine
  • Japanese Association for Acute Medicine


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