学位論文内容の要旨

博士の専攻分野の名称

博士（医学）

氏 名飯島誠学 位 論 文 題 名

A Novel Percutaneous Cardiopulmonary Bypass Support System
Combined with a Closed-chamber Type Venous Blood Reservoirfor Cardiac unloading during Circulatory Assist.

（閉鎖チャンバー式静脈血リザーバを併用した経皮的心肺補助装置の左室前負荷軽減に関する研究）

Objective: The use of percutaneous cardiopulmonary bypass support (PCPS) is a
device that allows the percutaneous establishment of an extracorporeal circulationfrom the peripheral arteries and veins without thoracotomy. However, PCPS has
several disadvantages in terms of cardiac loading conditions. PCPS does not allow
reduction of left ventricular loading, preload and afterload. The reduction of preload orafterload considerably affects myocardial oxygen consumption. We have newly
designed a PCPS circuit combined with a closed-chamber type venous blood reservoir
which can control the venous blood removal volume for preventing left ventriculardistension during circulatory assist for relatively long time. Using this simple circuit,
we examined whether we can control the left ventricular preload both at base line andafter left ventricular ischemia in 5 pigs.
Methods: The use of animals, 5 cloned Landrace large White Duroc class pigs thatwere 3.5 months of age was consistent with the US National Institute of Health (NIHPublication No.85-23, revised 1996). PCPS was established by insertion of a perfusion
cannula in the thoracic descending aorta and a drainage cannula in the right atrium.
These cannulas were connected to a centrifugal pump and a membrane oxygenator. The
venous blood reservoir was placed in the middle of the venous blood drainage line. In
protocol 1, 15 minutes after introduction of general anesthesia, the venous blood of100, 200, 400 mL was sequentially removed into the venous blood reservoir. All theblood volume in the venous blood reservoir was then returned to the PCPS circuit, andthe left ventricular venting was started. The hemodynamic parameters were recorded at
the each time point after the procedures: systolic arterial pressure, mean arterialpressure, left ventricular end-diastolic pressure (LVEDP), left atrial pressure (LAP),and right atrial pressure. In protocol 2, acute left ventricular ischemia was induced byligation of the left anterior descending coronary artery (LAD). The protocol thereafter
was the same as protocol 1.

Results: Compared with the base line, LVEDP and LAP significantly increased after
acute left ventricular ischemia by LAD ligation due to reduced left ventricular
contractile function. In protocol 1, the effects of the venous blood removal procedureson hemodynamic parameters were not evident. In protocol 2(after acute ischemia),
LVEDP (5.1±1.2 v.s.10.4±1.2 mmHg) and LAP (5.6±1.8 v.s.11.4±1.5 mmHg)
significantly decreased when the maximum venous blood volume was removed into thevenous blood reservoir compared with those after PCPS introduction. All the blood
volume in the venous blood reservoir was then returned to the PCPS circuit, and theventing from the left ventricular apex was started at the maximum rate. Fifteen minutes
after the left ventricular venting was started, LVEDP and LAP also significantly
decreased compared with those after PCPS introduction. No significant difference wasfound in LVEDP and LAP values between maximum removal of venous blood and left
ventricular venting alone.
Conclusions: By adjusting blood removal volume using the venous blood reservoir, we
can achieve a significant decrease in left ventricular preload similar to the degree byleft ventricular venting alone, which might prevent over-distension of the failed heart.