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Biomedical subjects

Yoshihisa Tanoue

Publications and source records attributed to Yoshihisa Tanoue.

21 records · Page 2Linked to original sources

Acute volume reduction with aortic valve replacement immediately improves ventricular mechanics in patients with aortic regurgitation.

OBJECTIVES: Few data have been available regarding the immediate response in ventricular mechanics to acute volume reduction caused by aortic valve replacement for aortic regurgitation. METHODS: We studied 9 patients in the operating room immediately before and after the institution of cardiopulmonary bypass. Left ventricular pressure and cross-sectional area (a surrogate of left ventricular volume) were measured with a catheter-tip manometer and a transesophageal echocardiographic system equipped with automated border-detection technology. Left ventricular pressure-area loops were constructed, and the caval occlusion method was used to obtain the slope of the end-systolic pressure-area relationship and the end-systolic area associated with 100 mm Hg. From the steady-state beats, stroke area was obtained by subtracting the minimum area from the maximum area. Effective arterial elastance, a measure of ventricular afterload, was calculated from end-systolic pressure, and stroke area as follows: effective arterial elastance equals end-systolic pressure divided by stroke area. RESULTS: Reductions in maximum area (21.0 +/- 8.5 to 16.0 +/- 6.8 cm(2) [SD])and minimum area (15.3 +/- 8.4 to 12.0 +/- 6.1 m(2)) shifted the baseline pressure-area loops to the left. The slope of the end-systolic pressure-area relationship (11.6 +/- 4.8 to 16.0 +/- 7.5 mm Hg/cm(2)) and afterload (effective arterial elastance, 17.9 +/- 11.6 to 26.3 +/- 16.4 mm Hg/cm(2)) were increased, and the end-systolic area associated with 100 mm Hg was reduced (18.3 +/- 10.0 to 13.7 +/- 5.8 cm(2)). CONCLUSION: Correction of volume overload reduced preload (minimum area), shifted the end-systolic pressure-area relationship to the left (decreased end-systolic area), and improved ventricular contractility (increased slope of the end-systolic pressure-area relationship). The result indicated that acute volume reduction favorably influenced ventricular mechanical parameters immediately after the operation.

Adult↗

Ischemic preconditioning reduces unloaded myocardial oxygen consumption in an in-vivo sheep model.

OBJECTIVE: Ischemic preconditioning (IP) describes the adaptation of the myocardium to ischemic stress preceded by short periods of ischemia and reperfusion. However, its cardioprotective mechanisms are not completely understood. We assessed the effect of IP on ventricular energetics in an in-vivo sheep model. METHODS: IP was performed in six sheep by three 5 min aortic cross-clamping periods interspersed with 5 min of reperfusion during cardiopulmonary bypass and with six sheep as time-matched controls. Global myocardial ischemia was subsequently achieved by 30 min aortic cross-clamping with left ventricular unloading during normothermic cardiopulmonary bypass. Weaning from cardiopulmonary bypass was performed 40 min after reperfusion. At baseline, after treatment (IP or time-matched cardiopulmonary bypass), and up to 100 min after reperfusion, left ventricular pressure-volume loops were measured using a conductance catheter during a right heart bypass preparation. Contractility, diastolic function, and ventriculo-arterial coupling were evaluated. Ventricular energetics [the relation between myocardial oxygen consumption (MVO(2)) and systolic pressure-volume area (PVA)] was also evaluated. A right heart bypass was instituted to control the preload and to decompress the right ventricle completely, thereby eliminating parallel conductance variation and minimizing the contribution of the right ventricle to MVO(2). RESULTS: IP reduced unloaded MVO(2) (PVA-independent MVO(2)). Contractility, diastolic function, and ventriculo-arterial coupling in the IP group were better preserved than in the control group after ischemia-reperfusion. CONCLUSIONS: IP reduces unloaded MVO(2), and preserves contractility, diastolic function, and ventriculo-arterial coupling after 30 min global myocardial ischemia in an in-vivo sheep model.

Analysis of Variance↗

Cardioprotective effect of ischemic preconditioning on global myocardial ischemia in a sheep right heart bypass model.

OBJECTIVES: Ischemic preconditioning has been used to induce the myocardium to adapt to ischemic stress preceded by short periods of ischemia and reperfusion. We used a sheep right heart bypass model with a conductance catheter to assess the cardioprotective effect of ischemic preconditioning on 30-minute normothermic global myocardial ischemia. METHODS: Ischemic preconditioning was conducted in 6 sheep in 35-minute aortic cross-clampings interspersed with 5 minutes of reperfusion during cardiopulmonary bypass, with 6 sheep as time-matched controls. Global myocardial ischemia was subsequently achieved in 30-minute aortic cross-clamping with left ventricular unloading during normothermic cardiopulmonary bypass. Weaning from cardiopulmonary bypass was conducted 40 minutes after reperfusion. Before ischemia and 40, 70, and 100 minutes after reperfusion, left ventricular pressure-volume loops were measured using a conductance catheter during right heart bypass preparation. Left ventricular contractility, diastolic function, and mechanical efficiency were then evaluated. Right heart bypass was instituted to control the preload and to decompress the right ventricle completely, thereby eliminating parallel conductance variation. RESULTS: No differences in the studied parameters were seen between ischemic-preconditioning and control groups before ischemia. Left ventricular contractility, diastolic function, and mechanical efficiency in the ischemic-preconditioning group were significantly superior to those in the control group after reperfusion. CONCLUSIONS: Ischemic preconditioning attenuates postischemic myocardial dysfunction in a sheep model using 30-minute unloaded normothermic global myocardial ischemia. Ischemic preconditioning would thus be clinically significant when the ischemic damage is severe.

Animals↗