Kunikazu Hisamochi

Hiroshima City Hospital, Hirosima, Hiroshima, Japan

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Publications (31)50.3 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: An 80-year-old woman underwent lower and middle lobe resections of right lung in 1990 and 1998 because of lung cancers. There was no recurrence. In 2009, she presented with exertional dyspnea, and echocardiography showed grade III mitral regurgitation (MR). We diagnosed with congestive heart failure caused by MR. Her chest CT showed her mediastinum was shifted to the right and her heart was in the right thoracic cavity. We performed mitral valve plasty via right 7th intercostal thoracotomy. Post-operative respiratory condition was stable and she was extubated on the first postoperative day. Post-operative UCG showed trivial MR. She was discharged on the 14th day.
    01/2015; 44(1):33-36. DOI:10.4326/jjcvs.44.33
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    ABSTRACT: We report a case of a 77-year-old man with a thoracic aortic aneurysm, combined with chronic myelomonocytic leukemia, polymyalgia rheumatica, and atial fibrillation. Open surgery was considered as high risk because he was severely ill. Instead, partial debranching and stent graft( TEVAR) were performed by chimney method. He had no major complication after surgery, and was discharged on foot on the 15th postoperative day. In high risk cases of thoracic aortic aneurysm, TEVAR with debranching and chimney methods is effective.
    Kyobu geka. The Japanese journal of thoracic surgery 08/2014; 67(9):827-30.
  • 01/2014; 43(2):49-52. DOI:10.4326/jjcvs.43.49
  • ANZ Journal of Surgery 10/2010; 80(10):745-6. DOI:10.1111/j.1445-2197.2010.05460.x · 1.12 Impact Factor
  • 01/2010; 39(3):129-132. DOI:10.4326/jjcvs.39.129
  • 01/2009; 38(5):340-343. DOI:10.4326/jjcvs.38.340
  • 01/2009; 38(3):212-215. DOI:10.4326/jjcvs.38.212
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    ABSTRACT: Hypoxic perfusion before arrest, an indeterminate period of warm ischemia, and subsequent reperfusion are major causes of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). The present study was undertaken to elucidate the cardioprotective effects of ET(A) receptor antagonist FR139317 for hearts obtained from asphyxiated NHBDs in a canine transplantation model. Hypoxic cardiac arrest was induced in 17 donor dogs. FR139317 (10 mg/kg) was given to 7 of the dogs over a period of 10 min before disconnecting the ventilator. The hearts were preserved with FR 139317-supplemented cardioplegic solution (FR group). The remaining 10 did not receive FR 139317 at any time during the experiment (control group). Orthotopic transplantation was performed after a mean myocardial ischemic time of 4h. During the agonal period, the highest systolic pulmonary artery pressure in the FR group was lower than that in the control group (47 +/- 14 vs. 58 +/- 27 mmHg). All animals in the FR group were weaned from cardiopulmonary bypass, whereas only five of the controls were weaned, two of which were identified to have dominant right ventricular failure. After transplantation, recovery rates of the left ventricular end-systolic pressure-volume ratio (E(max)) and the maximum first derivative of pressure measured over time (max dP/dt) were not significantly different between the groups, but recovery rates of the cardiac index, left ventricular minimum dP/dt and exponential time constant of LV relaxation (tau) in the FR group were higher than those in the control group. The ET(A) receptor antagonist FR 139317 reduced pressure overload on the right ventricle by decreasing the peak pulmonary artery pressure before donor arrest. Cardioprotective effects of this agent for heart transplantation from NHBDs are manifested by preserved diastolic properties of the left ventricle.
    The Japanese Journal of Thoracic and Cardiovascular Surgery 01/2007; 54(12):511-5. DOI:10.1007/s11748-006-0051-0
  • 01/2007; 36(2):85-87. DOI:10.4326/jjcvs.36.85
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    ABSTRACT: Noonan syndrome presents with dysmorphic facial features, short stature, and cardiac abnormalities (most commonly pulmonic stenosis and hypertrophic cardiomyopathy). This report describes a rare case accompanied by a secundum atrial septal defect (ASD) and a ventricular septal aneurysm causing right ventricular (RV) pressure gradient. A 29-year-old mentally retarded man was admitted to hospital with exertional dyspnea. His somatic features included short stature (148 cm), hypertelorism, a shield chest, and thoracic scoliosis. Echocardiogram showed a secundum ASD with bidirectional shunting and a ventricular septum bulging toward the left ventricle in diastole, and then toward the RV in systole causing obliteration of the RV. The peak pressure gradient measured across the RV outflow by continuous wave Doppler was 30 mmHg. Cardiac catheterization revealed an elevated RV pressure without pulmonary hypertension and confirmed the pressure gradient. Right ventriculography revealed the septal excursion toward the RV in systole, leaving only a small residual cavity in the inflow and outflow regions of the RV. The ASD was closed with an autologous pericardial patch. A thin, fibrous portion of the ventricular septum was resected and replaced with a Dacron patch. From the histological examination, the RV cavity obliteration turned out to be produced by the excursion of the infarcted ventricular septum.
    Circulation Journal 06/2006; 70(5):634-7. DOI:10.1253/circj.70.634 · 3.69 Impact Factor
  • 01/2005; 34(5):382-385. DOI:10.4326/jjcvs.34.382
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    ABSTRACT: EPC-K1, a hydroxyl radical scavenger synthesized by phosphate linkage of vitamin E and vitamin C, prevents myocardial reperfusion injury in vivo; however, the direct effects of EPC-K1 on coronary arteries are unknown. These experiments were undertaken to define possible mechanisms through which EPC-K1 imparts its protective action on the coronary vasculature. EPC-K1 (10(-5) to 10(-1) mg/ml) induced concentration-dependent relaxation in contracted canine coronary artery segments with endothelium, but no change in tension of arterial segments without endothelium (p<0.05, ANOVA). Endothelium-dependent relaxation to EPC-K1 was inhibited by N(G)-monomethyl-(L)-arginine ((L)-NMMA) (10(-5) mol/L). Inhibition of relaxation by (L)-NMMA was reversed by the addition of (L)-arginine (10(-4) mol/L), but not by (D)-arginine (10 (-4) mol/L). Subsequent exposure of canine coronary artery segments with intact endothelium to hydroxyl radicals for 30 min (generated by FeSO(4) [0.56 mmol/L] + H(2)O(2) [0.56 mmol/L]) impaired endothelium-dependent relaxation. However, pretreating the vascular segments with EPC-K1 (10(-4) mg/ml) prevented hydroxyl radical-mediated endothelial cell injury and maintained endothelium-dependent relaxation. These experiments indicate that EPC-K1 stimulates the release of endothelium-derived nitric oxide, an endogenous vasodilator and inhibitor of platelet and leukocyte activation and adhesion, from the coronary artery endothelium. Additionally, EPC-K1 scavenges hydroxyl radicals that mediate endothelial cell injury. These 2 independent and important actions are possible mechanisms by which EPC-K1 prevents reperfusion injury in the ischemic heart.
    Circulation Journal 12/2003; 67(12):1046-52. DOI:10.1253/circj.67.1046 · 3.69 Impact Factor
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    ABSTRACT: We attempted to predict the posttransplant cardiac function of nonbeating donor hearts. A total of 13 dogs were studied. Hearts were left in situ for 45 minutes after cardiac arrest caused by exsanguination. Hearts were then excised and reperfused in an ex vivo perfusion apparatus after 60 minutes of warm ischemia to test whether they could eject against an 80 mm Hg afterload from a preload of 10 mm Hg. Thereafter, all hearts were transplanted orthotopically. Four of 13 hearts were able to eject in the apparatus (group A). However, the other nine hearts could not eject under the defined conditions (group B). All four hearts in group A showed good posttransplant hemodynamics (systolic arterial pressure > 80 mm Hg with mean left atrial pressure < 10 mm Hg) without dopamine. However, none of nine hearts in group B could support the circulation without dopamine. Nonbeating donor heart function evaluated in the perfusion apparatus predicts posttransplant heart function. This method may be applicable for selection of transplantable hearts from nonbeating heart donors.
    The Annals of Thoracic Surgery 02/2001; 71(1):278-83. DOI:10.1016/S0003-4975(00)01939-1 · 3.63 Impact Factor
  • David G Cable, Kunikazu Hisamochi, Hartzell V Schaff
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    ABSTRACT: The deposition of complement components within grafts, complement consumption, and prolongation of graft function by complement inactivation imply a pivotal role for complement in xenograft hyperacute rejection. The current investigations examined the endothelial production of vasoactive substances in pulmonary arteries during simulated hyperacute rejection. Canine pulmonary arteries were suspended in organ chambers and exposed to either autologous canine serum for 90 minutes or heterologous porcine serum for 30, 60, or 90 minutes. Following serum exposure, the vessels were allowed a one-hour equilibration in buffered crystalloid solution. Dose-response curves were obtained with acetylcholine, sodium nitroprusside, and calcium ionophore A23187 following contraction with phenylephrine (10(-6) M) in the presence of indomethacin (10(-5) M). Receptor-dependent, endothelial-dependent relaxations to acetylcholine (10(-9)-10(-4) M) were impaired with 30-, 60-, or 90-minute porcine serum exposure when compared to vessels exposed to autologous canine serum (n = 10, 7, 9, respectively; p < .05; 2-way ANOVA). Receptor-independent, endothelial-dependent relaxations to calcium inophore (10(-9)-10(-6) M) were significantly impaired at 60- and 90-minute porcine exposures only (n = 7, 8; p < .05). Endothelial-independent relaxations to sodium nitroprusside (10(-9)-10(-4) M) were not impaired with either canine or porcine serum exposure. Oxyhemoglobin (10(-6) M) abolished acetylcholine-mediated relaxations, indicating that nitric oxide was the predominant mediator. Simulated hyperacute xenograft rejection impairs endothelium-dependent relaxation of canine pulmonary arteries. Both basal and stimulated production of nitric oxide is impaired by heterologous serum exposure and, subsequently, complement activation. Reduced production of nitric oxide may explain, in part, the vasospasm and thrombosis of xenografts during hyperacute rejection.
    The Journal of Heart and Lung Transplantation 04/1999; 18(3):177-84. DOI:10.1016/S1053-2498(98)00023-0 · 5.61 Impact Factor
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    ABSTRACT: This study was designed to verify the effect of reperfusion of donor hearts in a perfusion apparatus after 60 min of global ischemia prior to heart transplantation. Thirteen dogs were exsanguinated from the femoral artery and cardiac arrest was achieved. The hearts were left in situ at room temperature (25 degrees C) for 60 min. In group A (n = 7), the hearts were excised and reperfused 60 min after cardiac arrest in the perfusion apparatus with substrate-enriched warm blood cardioplegia (WBCP) containing a hydroxyl radical scavenger, EPC, followed by 45 min of blood perfusion. Next, the hearts were preserved in cold (4 degrees C) University of Wisconsin (UW) solution. In group B (n = 6), the hearts were perfused with cold (4 degrees C) St. Thomas' solution 60 min after cardiac arrest and preserved in cold UW solution. Thereafter, all hearts in both groups were transplanted orthotopically to recipient dogs. In group A, 6 of 7 dogs were weaned from cardiopulmonary bypass (CPB). In group B, only 2 of 6 dogs were weaned from CPB. Moreover, 3 of the 6 hearts in group B did not start beating after transplantation (stone heart). This study suggested reperfusion of the donor heart in the perfusion apparatus with WBCP to be a beneficial preconditioning method when utilizing 60-min arrested hearts for transplantation.
    Surgery Today 02/1999; 29(9):890-6. DOI:10.1007/BF02482781 · 1.21 Impact Factor
  • D G Cable, K Hisamochi, H V Schaff
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    ABSTRACT: Evidence for complement activation in xenograft hyperacute rejection includes prolongation of graft survival after complement inactivation as well as component deposition and consumption during hyperacute rejection. The current investigations examined the endothelial production of vasoactive substances during heterologous serum exposure. Segments of canine coronary artery were exposed to either autologous canine serum for 90 minutes or heterologous porcine serum for 30, 60, or 90 minutes. After replacement of the serum with buffered saline, segments were contracted with phenylephrine (10(-6) mol/L) in the presence of indomethacin (10(-5) mol/L). Compared with responses of vessels exposed to autologous canine serum, receptor-dependent relaxation to acetylcholine was impaired in arteries after 60 or 90 minutes of exposure to porcine serum. Receptor-independent relaxation to calcium ionophore A23187 was not significantly impaired at any length of porcine serum exposure. Endothelial-independent relaxation to sodium nitroprusside was not impaired with either canine or porcine serum exposure. Oxyhemoglobin (10(-6) mol/L) abolished acetylcholine-mediated relaxation, indicating that nitric oxide was the predominant mediator of the impaired pathway. Basal release of nitric oxide after a 60-minute porcine serum exposure was reduced by half compared with coronary arteries exposed to autologous canine serum. Serum pretreated by either heat inactivation of complement or immunoadsorption with anti-C3 antibodies failed to depress endothelial-dependent relaxation on 60 minutes of exposure to canine coronary arteries. Scanning electron microscopy revealed an intact endothelial layer in coronary arteries exposed to either porcine or canine serum for 60 minutes. Hyperacute xenograft rejection impairs receptor-dependent relaxation of canine coronary arteries at 60 and 90 minutes. These data strongly suggest that impairment of endothelial production of nitric oxide during acute xenograft rejection is mediated by complement activation.
    Circulation 12/1997; 96(9 Suppl):II-58-63; discussion II-63-4. · 14.95 Impact Factor
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    ABSTRACT: We experienced the case of a patient with d-TGA, small VSD who underwent arterial switch operation (ASO) at the age of 8 weeks. In pre-operative UCG, the LV posterior wall thickness was only 3.0 mm. LV systolic pressure had dropped to 29 mmHg at the time of operation. After arterial switch and VSD closure, myocardial contractility and coronary perfusion were good without any ST-T changes, however, the patient could not be weaned from cardiopulmonary bypass. Left ventricular assist device (LVAD) was then applied and LV training was performed with appropriate pre and after-load. On the 4th operative day, the patient was successfully weaned from LVAD. Training of the left ventricle with LVAD will be a useful life-saving method in the case of left ventricular failure after arterial switch operation.
    [Zasshi] [Journal]. Nihon Kyōbu Geka Gakkai 08/1997; 45(7):1015-9.
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    ABSTRACT: This study was performed to determine if an "arrested" heart, resuscitated with cardiopulmonary bypass (CPB) after the cessation of beating, can be successfully transplanted, and whether a hydroxyl radical scavenger EPC can reduce ischemic and reperfusion injury during resuscitation of the arrested heart and following orthotopic heart transplantation. A total of 16 pairs of canines were divided into a control group of eight pairs and an EPC-treated group of eight pairs. Cardiac arrest of the donor heart was induced by the discontinuation of respiratory support after the induction of brain death. The cadaver heart was then resuscitated and core-cooled to myocardial temperature of 15 degrees C using CPB. The donor heart was harvested using cold cardioplegia and orthotopically transplanted. All of the transplanted hearts in the EPC group were weaned from CPB without any inotropic support after 60 min of bypass support, whereas all the animals in the control group required 5 micrograms/kg/min dopamine (P = 0.001). Moreover, cardiac function (Emax) 1 h after orthotopic heart transplantation was better preserved in the EPC group than in the control group, at 110 +/- 36% vs. 70 +/- 21% of the post brain death values (P = 0.02) These findings demonstrate that EPC reduces posttransplant reperfusion injury, and thus it may prove to be a valuable adjunct in this challenging model.
    Surgery Today 02/1997; 27(10):930-5. DOI:10.1007/BF02388141 · 1.21 Impact Factor
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    ABSTRACT: A shortage of donor organs in clinical transplantation prompted us to study whether resuscitated "dead" hearts could be used for successful orthotopic heart transplantation. Donor hearts were resuscitated with cardiopulmonary bypass after 3 minutes (the control group; n = 8) or 60 minutes (the experimental group; n = 6) of hypoxic cardiac arrest after induction of brain death. All the animals of each group were successfully weaned from cardiopulmonary bypass with 5 micrograms/kg/min of dopamine 1 hour after transplantation, and cardiac function with or without dopamine was better preserved in the experimental group than the control group (with maximum slope of pressure-volume relationship with dopamine: 198.0% +/- 36.8% versus 121.2% +/- 47.2%; maximum slope of pressure-volume relationship without dopamine: 130.6% +/- 41.5% versus 70.8% +/- 21.5% [mean +/- standard deviation] as percentage of values after brain death, respectively; p < 0.01 by unpaired t test). These results indicate that cadaver hearts 60 minutes after anoxic arrest can be successfully reanimated and orthotopically engrafted with various methods and drugs.
    The Journal of Heart and Lung Transplantation 06/1996; 15(5):527-31. DOI:10.1016/0300-9572(96)89059-9 · 5.61 Impact Factor
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    ABSTRACT: Background: Protamine reversal of heparin anticoagulation often causes systemic hypotension, and in vitro studies suggest that this may be mediated by release of nitric oxide from the endothelium. The present investigations were designed to evaluate the direct myocardial effects of protamine and to determine in vivo whether nitric oxide inhibition can prevent hypotension during protamine infusion. Methods/Results: Protamine sulfate (50 microg/ml) was added to perfusate of eight isolated rabbit heart preparations; in six other preparations, a similar concentration of prolamine was added to heparinized (5 U/ml) Krebs perfusate. Left ventricular developed pressure, maximum rate of pressure rise, and heart rate declined significantly (p < 0.01) in hearts exposed to protamine only (65.0% +/- 6.6%, 55.5% +/- 6.0%, and 87.6% +/- 2.5% of baseline, respectively), whereas protamine added to heparinized perfusate caused little change in developed pressure, maximum rate of pressure rise, and heart rate (85.3% +/- 5.4%, 84.9% +/- 5.5%, and 98.8% +/- 1.6%). To study systemic effects of protamine, we measured hemodynamic parameters in 12 heparinized dogs (150 U/kg). During protamine infusion (1.5 mg/kg intravenously over 30 seconds), mean blood pressure decreased by 46% +/- 7% from baseline (P < 0.05), cardiac output decreased by 38% +/- 4% (p < 0.05), and systemic vascular resistance decreased bv by 14& +/- 9%. After hemodynamic stabilization, Ng-monomethyl-L-arginine (2 mg/kg), a competitive inhibitor of nitric oxide synthesis, was administered to six dogs, and methylene blue (2 mg/kg), an inhibitor of cyclic guanosine monophosphate synthesis, was administered to the remaining six dogs. After treatment with Ng-monomethyl-L-arginine and methylene blue, the second infusion of protamine sulfate caused no significant change in blood pressure or cardiac output. In an additional six dogs, Ng-monomethyl-L-arginine pretreatment (5 mg/kg) blocked the effects of the first dose of protamine. The effect of Ng-monomethyl-L-arginine could be reversed by the addition of (6 mg/kg) L-arginine but not D-arginine. Conclusions: Protamine-heparin complex does not cause direct myocardial depression but does lead to severe hypotension in vivo. The finding that hypotension can be blocked by inhibitors of the nitric oxide pathway confirms previous in vitro studies indicating that the effects of protamine are mediated, in part, by the vascular endothelium. Further, these studies suggest a novel approach to prevention of hemodynamic complications caused by heparin reversal after cardiopulmonary bypass.
    Journal of Thoracic and Cardiovascular Surgery 06/1996; 111(6):1240-6; discussion 1246-7. DOI:10.1016/S0022-5223(96)70227-1 · 3.99 Impact Factor

Publication Stats

110 Citations
50.30 Total Impact Points

Institutions

  • 2010
    • Hiroshima City Hospital
      Hirosima, Hiroshima, Japan
  • 1999–2001
    • Okayama University
      • Department of Cardiovascular Surgery
      Okayama, Okayama, Japan
  • 1996–1999
    • Mayo Clinic - Rochester
      Rochester, Minnesota, United States