Effect of Enflurane on the Baroreflex Control of Heart Rate in Decerebrate Rats

Volatile anesthetics alter the arterial baroreflex (BRX) but its mechanisms are poorly understood. This study was designed to determine the effect of 1 and 2 minimal alveolar concentrations (MAC) of enflurane on the BRX parameters in unanesthetized brain stem-intact and decerebrate rats. Under enflurane anesthesia, the femoral artery and both femoral vein were catheterized for pressor (phenylephrine) and depressor (nitroprusside) drug delivery and continuous blood pressure measurements. Decerebration was performed at midcollicular level. BRX tests were performed in 3 time periods; before enflurane (conscious brain-intact), during 1 or 2 MAC enflurane exposure 1 hour after a sham operation or a decerebration operation, and 2 hours after the termination of enflurane (zero enflurane). Mean arterial pressure (MAP) and heart rate (HR) were fitted to a sigmoid logistic equation, the Boltzman equation. The curve of best fit was obtained with a computer program. 1 MAC and 2 MAC of enflurane shifted MAP-HR baroreflex curves to the left in the all groups and significantly attenuated the baroreflex range. The slope of conscious intact period and zero enflurane period of each group did not change significantly, but during the enflurane period the slope was significantly lowered. Enflurane depressed the baroreflex sensitivity (slope) and the HR range in a similar dose-dependant manner in both brain stem-intact and decerebrate rats. Such results draw into question whether the suprapontine sites contribute to enflurane's actions on cardiovascular autonomic regulation.

Does Phenylephrine Affect Hypoxic Pulmonary Vasoconstriction and Arterial Oxygenation during One Lung Ventilation? / 대한마취과학회지

BACKGROUND: Vasoconstricting drugs such as dopamine, phenylephrine (PE) and epinephrine constrict normoxic lung vessels preferentially, thereby disproportionately increasing normoxic lung pulmonary vascular resistance (PVR) and inhibit hypoxic pulmonary vasoconstriction (HPV). In this study, we evaluated the effect of PE on HPV and arterial oxygenation. METHODS: This study was performed on 21 patients undergoing thoracotomy. After induction of anesthesia, Swan-Ganz catheter was inserted. After one lung ventilation was started, systolic blood pressure (SBP) of the patient was reduced to 100 mmHg using inhalation anesthetic agent and then the blood pressure was raised up to 140 mmHg by PE infusion. Hemodynamic variables were measured and arterial blood gas was analyzed at the start of one lung ventilation (control), SBP of 100 mmHg and SBP of 140 mmHg. RESULTS: The mean dose of PE infused was 5.9 +/- 3.8 microgram/kg. Infusion of PE did not increase pulmonary vascular resistant index (PVRI) significantly and did not reduce arterial PO2. There was no statistically significant difference in intrapulmonary shunt fraction (Qs/Qt) between the time of low and high blood pressures. CONCLUSION: Pulmonary vasomotor changes induced by PE are minimal and so should not affect the distribution of blood flow during one lung ventilation. On the basis of this result, PE appears to a reasonable vasoconstrictor to be used in patients undergoing thoracotomy.

The Effect of Pneumonectomy on Right Ventricular Function / 대한마취과학회지

BACKGREOUND: The pneumonectomy may depress the right ventricular (RV) function transiently. The thermodilution ejection/volumetric catheter is known to be most useful method assessing the changes in RV performance during pulmonary resection. The purpose of this study was to examine the RV function during and immediately after pneumonectomy using thermodilution methods. METHODS: 16 patients undergoing pneumonectomy were studied. After induction of anesthesia, a multilumen thermodilution catheter mounted with a rapid response thermister was inserted. Using computer system, RV ejection fraction (RVEF), cardiac output, and RV end-diastolic volume (RVEDV) were measured when the patient was in lateral position (control), after one lung ventilation (OLV) and the main pulmonary artery ligated, and at the completion of resection. Arterial blood gases were analyzed and pulmonary vascular resistance (PVR) was calculated. RESULTS: Systolic pulmonary blood pressure (SPAP)(28.3 +/- 6.2 mmHg) increased compared to the control (24.6 +/- 5.9) without a significant change of PVR. No statistically significant difference was found in either RVEF or RVEDV at each times. CONCLUSIONS: Our study demonstrate the pneumonectomy do not depress the RV function immediately and RVEF do not show any correlation with PVR or RVEDV.