|Tetsuhiro Fujiyoshi||Last modified date：2021.04.05|
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Reseacher Profiling Tool Kyushu University Pure
Country of degree conferring institution (Overseas)
Field of Specialization
Anesthesiology and critical care medicine
Total Priod of education and research career in the foreign country
Research InterestsMembership in Academic Society
- Prediction model for intraoperative complication
keyword : preoperative evaluation, intra-operative complication, predictive model
- Epidemiological survey of perioperative anaphylaxis
keyword : perioperative anaphylaxis
- Neuron damage after cardiac arrest and cardio-pulmonary resuscitation
keyword : Neuron damage, ischemic-reperfusion neuron injury,
- Non-invasive hemodynamic monitoring for cesarean section
keyword : Delivery safety, cesarean section, hemodynamic stability
|1.||藤吉 哲宏、平野 勝也、平野 真弓、西村 淳二、高橋 成輔、金出 英夫, Plasmin Induces Endothelium-Dependent Nitric Oxide-Mediated Relaxation in the Porcine Coronary Artery, Arteriosclerosis, Thrombosis, and Vascular Biology, 2007.04, [URL].|
|1.||Tetsuhiro Fujiyoshi, Erico Shinjo, Kaoru Umehara, Kengo Hayamizu, Kentaro Tokuda and Yuji Karashima, A case of transient increased central venous pressure during kidney transplantation, American Society of Anesthesiologist, 2018.10.|
|2.||Tetsuhiro Fujiyoshi, Shoko Taguchi, Jun Maki, Yoshimasa Motoyama, Kozaburo Akiyoshi, Sumio Hoka, A Case Of Severe Peripartum Cardiomyopathy , Amerian Society of Anesthesiologist, 2017.10, Peripartum cardiomyopathy (PPCM) is a severe heart failure that is developed in a healthy woman without any history of cardiac disease. The pathology is similar to dilated cardiomyopathy. PPCM was informed in 1971 by Dr. Demakis, has no prognostic factors nor diagnosis criteria, although the mortality of severe case is high. We show a case of severe PPCM in our hospital.
A case is a Japanese 36-year-old female, 157 cm of height and 70 kg of body weight (50 kg before pregnancy). She has healthy 6 kids and there is no abnormal data of perioperative findings, except for moderate pregnancy-induced hypertension (PH). Cesarean section for Full-term delivery was planned by combined spinal and epidural anesthesia.
She came to an operation room on foot with no complain. When she laid down on the bed, she felt moderate dyspnea. She was hard to keep lateral position for spinal anesthesia and general anesthesia was performed. Her baby was perfectly delivered in a 10 minutes after general anesthesia induction. After delivery, percutaneous saturation of oxygen decreased below 90 % and airway pressure increased. Crackles was pointed out by auscultation and foamy sputum was suctioned from the tracheal tube. Ejection fraction of left ventricular (LVEF) was 40 % by ultrasound echography. She was unexpectedly transferred to intensive care unit. Cardiac output was decreasing and it was hard to improve hypotension, even using circulation support drugs, and intra-aortic balloon pumping device (IABP) was inserted. Cardiac function did not improve and we discussed about percutaneous cardio-pulmonary support and left ventricular assist device, include heart transplantation and we informed to her family. Fortunately, cardiac output was improving on POD1. Blood pressure improved without any drug and IABP, although LVEF was low. Severe lung edema was improved and mechanical ventilation was removed. She discharged on POD10 and she didn’t have any symptom of cardiac failure, although LVEF didn’t full-recovered.
This case recovered with intensive circulation support from unexpected PPCM. PPCM is rare, but it causes severe and refractory cardiac dysfunction. Although some risk factors of PPCM, PH, human race and obesity, were defined, it is hard to predict PPCM before pregnancy and delivery. We should consider that Healthy and no-risk expectant mother potentially become PPCM. .
|3.||Fujiyoshi Tetsuhiro, Inhibition of pro-inflammatory enzyme soluble epoxide
hydrolase exerts a neuro-protective effect after cardiac
arrest and cardio-pulmonary resuscitation in mice, European society of Anesthesia, 2013.06, Many survivors have neurologic deficits after cardiac arrest and cardio-pulmonary resuscitation (CA/CPR). Memory deficit is one of the biggest problems to be solved
for them. Inflammation damages neurons and exacerbates outcome following partial brain ischemia. Activation of microglia, the brain resident immune cells,
contributes to brain injury in brain stroke mice model. However, the role of microglial activation for neuronal damage after global ischemia during CA/CPR is not well
defined. Inhibition of pro-inflammatory soluble epoxide hydrolase (sEH) reduces infarct size after stroke. We tested whether therapeutic inhibition of sEH after CA/CPR
can reduce microglial activation and neuronal death, and improve memory function.
CA/CPR causes microglia activation and neuron death in hippocampus CA1 area. sEH-inhibitor accelerates microglia activation and suppresses
neuron death. Hippocampus-dependent memory dysfunction after CA/CPR is partially protected by sEH-inhibitor administration. We indicate that sEH-inhibition is a
promising new therapeutic approach to reduce neuronal death and improve memory function after global ischemia
|4.||The Mechanism Of Plasmin-induced Endothelium-dependent Relaxation In The Porcine Coronary Artery, [URL].|
- European society of Anesthesiology
- European society of intensive care medicine
- Japanese association for acute medicine
- The Japanese society of intensive care medicine
- The Japan society for clinical anesthesia
- Japanese Society of Anesthesiologists