SAI Takuji Gifu University School of Medicine, Research Associate, 医学部附属病院, 助手 (30242720)
UEDA Norio Gifu University School of Medicine, Research Associate, 医学部附属病院, 助手 (20223464)
DOHI Shuji Gifu University School of Medicine, Professor, 医学部, 教授 (40155627)
|Budget Amount *help
¥1,800,000 (Direct Cost : ¥1,800,000)
Fiscal Year 1997 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1996 : ¥1,100,000 (Direct Cost : ¥1,100,000)
It is well known that abrupt changes in heumodynamics can occur after aortic cross-clamping (XC) and unclamping (XU) during abdominal aortic aneurysmectomy (AAAectomy). Several reports indicate that XU induces a significant rise in pulmonary arterial pressure. The rationale for hemodynamic management during AAAectomy is controversial. Vasodilators would decrease not only pulmonary vascular resistance (PVR), but also systemic vascular resistance (SVR), resulting in a fall in arterial pressure. Nitric oxide (NO) has been identified as the powerful endothelium-derived relaxing factor (EDRF). Although inhaled NO decreases PVR,it has no or little effect on SVR.
Following approval of the IRB,29 mongrel dogs were used for animal models to validate the efficacy of inhaled NO on the cardiac performance following XU after XC.The dogs were anesthetized with pentobarbital, intubated and mechanically ventilated. Systemic arterial pressure was monitored via a brachial and femoral arterial cannula. Th
e pulmonary artery catheter was advanced to the main pulmonary artery, cardiac output was measured with thermodilution technique. Anesthesia was maintained with fentanyl, midazoram and inhalation of fifty percent nitrous oxide in oxygen. After thoracotomy, descending aorta was exposed for cross-clamping at just above the diaphragm.
In all dogs, descending aorta was cross-clamped for thirty minutes and was unclamped. Anesthetized dogs (n=29) were divided into four groups with respect to the treatment before XU.In seven dogs (Group1), descending aorta was simply unclamped without any treatment. Dogs in group 2 were given extra-volume loading of lactated Ringer's solution before XD.Dogs in group 3 inhaled NO in a concentration of 20 ppm from just after XD to the end of the study. Dogs in group 4 were treated with inhalation of NO at 40ppm from XD.Hemodynamic variables were recorded at the following six time-points : just before XC (pre-XC), just before XU (pre-XU), 5 min after XU (5 min), 15 min after XU (15 min), 30 min after XU (30 min), and 60 min after XU (60 min).
Although in group 1,2 and 3, mean pulmonary arterial pressure (MPAP) significantly increased at 5 min, MPAP did not significantly increase in group 4 compared with the value of pre XU.At 15 min, although the values in MPAP were restored in group 1,3 and 4, the value in group 2 was not restored. The values in mean arterial pressure, central venous pressure, pulmonary arterial wedge pressure, heart rate and cardiac output did not show significant changes throughout the study protocol. Peak velocities of early diastolic flow wave in transmitral flow assessed by transesophageal pulsed Doppler echocardiography decreased at 5 min in group 1 and 3.
These results indicate that volume loading before XU may not always prevent post-XU hypotension, and that may have adverse effect on pulmonary hypertension. Although inhalation of NO at 20 ppm may not prevent pulmonary hypertension following XU,inhalation at 40 ppm would prevent pulmonary hypertension without a fall in MAP. Less