Effects of Inotropic Drugs on Mechanical Function and Oxygen Balance in Postischemic Canine Myocardium: Comparison of Dobutamine, Epinephrine, Amrinone, and Calcium Chloride

Brief ischemic episodes that induce myocardial and coronary endothelial dysfunction may alter the responses to inotropic drugs. To determine the effects of inotropic drugs in stunned myocardium, the coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and regional mechanical function in response to intracoronary dobutamine, epinephrine, amrinone, and calcium chloride (CaCl2) were measured before (normal) and 30 min after a 15-min-period occlusion of the left anterior descending artery (stunned) in an open-chest canine model. Percent segment shortening (%SS) and post-systolic shortening (%PSS) were determined. Myocardial extraction of oxygen (EO2) and lactate (E(lac)) was calculated. The inotropic drugs increased %SS, CBF, and MVO2 in normal myocardium. Epinephrine and amrinone decreased, while dobutamine and CaCl2 did not affect EO2. The ischemia and reperfusion itself significantly reduced %SS and E(lac), and increased %PSS. In stunned myocardium, the responses to inotropic drugs were not significantly altered, except that they progressively reduced %PSS and epinephrine did not affect EO2. These findings indicate that a brief episode of ischemia does not affect the mechanical and metabolic coronary flow responses to inotropic drugs, although it abolishes direct vasodilator responses to epinephrine.

Interaction between Intrathecal Gabapentin and Adenosine in the Formalin Test of Rats

Spinal gabapentin and adenosine have been known to display an antinociceptive effect. We evaluated the nature of the interaction between gabapentin and adenosine in formalin-induced nociception at the spinal level. Male Sprague-Dawley rats were prepared for intrathecal catheterization. Pain was evoked by injection of formalin solution (5%, 50 microliter) into the hindpaw. After examination of the effects of gabapentin and adenosine, the resulting interaction was investigated with isobolographic and fractional analyses. Neither gabapentin nor adenosine affected motor function. Gabapentin or adenosine decreased the sum of the number of flinches during phase 2, but not during phase 1 in the formalin test. Isobolographic analysis, in phase 2, revealed an additive interaction between gabapentin and adenosine. Taken together, intrathecal gabapentin and adenosine attenuated the facilitated state and interacted additively with each other.

The Effect of Doxapram Hydrochloride on the Ventilation Responses during General Anesthesia with Volatile Agent by Laryngeal Mask Airway / 대한마취과학회지

BACKGROUND: Inhalation anesthetics are known to depress ventilatory response to hypercapnea. Doxapram hydrochloride is an analeptic drug, which acts as a respiratory stimulant via peripheral and central chemoreceptors. Although the postoperarive infusion of doxapram hydrochloride is known to attenuate the impairment of respiratory function, no report is available on respiratory response to this drug when applied during anesthesia. Therefore, the present study aimed to evaluate the effect of doxapram hydrochloride on respiratory function during anesthesia. METHODS: Sixty adult patients undergoing operation under spontaneous ventilation via laryngeal mask airway (LMA) were randomly categorized into 3 groups: A control group, which received 5% dextrous infusion, and two groups in which patients were infused with doxapram hydrochloride (0.5 or 2 mg/kg/hr) starting 15 min after commencement operation. Anesthesia was maintained with 1 MAC sevoflurane - 4 L N2O - 2 L O2 under spontaneous ventilation via LMA. Tidal volume (VT), respiratory rate (RR), and arterial carbon dioxide tension (PaCO2) were measured just before and 15 min after the induction of anesthesia, 15 min after the start of operation and 15, 30, 45, and 60 min after the start of doxapram hydrochloride infusion. RESULTS: Measured values of RR and PaCO2 were significantly elevated during anesthesia venous those measured just before the induction of anesthesia in all groups. VT was significantly reduced during anesthesia venous just before the induction of anesthesia in all groups. All percent changes of VT, RR and PaCO2 were similar all any measurement times, and showed no significant changes after the infusion of doxapram hydrochloride in all groups. CONCLUSIONS: Intraoperative doxapram hydrochloride treatment did not produce any significant respiratory response improvement during 1 MAC sevoflurane anesthesia.

Effects of Nitrous Oxide on Cardiovascular Response to Laryngoscopy and Endotracheal intubation / 대한마취과학회지

BACKGORUND: Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia. Nitrous oxide (N2O), which is frequently used during the induction of anesthesia, is known to augment sympathetic nervous activity in humans. The aim of the present study was to investigate whether N2O affects cardiovascular response to intubation. METHODS: After iRB approval, 100 ASA i patients (aged 35 60 yr) were assigned randomly to receive one of four concentrations (0, 25, 50 or 75%; n = 25 for each) of N2O in oxygen throughout the study period, beginning 3 min before intubation. Anesthesia was induced with iV thiopental (5-7mg/kg) and tracheal intubation was faciliated with iV vecuronium (0.12 mg/kg), while patients were ventilated with the designated concentrations of N2O in oxygen. After intubation, all patients received 2% sevoflurane and N2O in oxygen via a semiclosed anesthesia circuit. Systolic arterial pressure (SAP), heart rate (HR) and rhythm were recorded before and after intubation at intervals for up to 5 min. Plasma concentrations of catecholamines were measured before and 3 min after induction, and 1 and 5 min after intubation. RESULTS: The intubation caused significant increases in SAP and HR in all groups (P<0.05). increasing concentrations of N2O gradually attenuated the pressor response to intubation, without affecting the tachycardiac response. No significant differences were observed between the groups in plasma concentrations of either norepinephrine or epinephrine:norepinephrine concentration increased significantly 1 min after intubation in all N2O-treated groups, while it remained unchanged in the control group. in contrast, the epinephrine concentration remained unaltered in all N2O-treated groups, but increased significantly in the control group. incidence of tachycardia, bradycardia, and arrhythmia was not different among the groups. CONCLUSiONS: These results indicate that N2O suppresses the pressor but not the tachycardiac response associated with endotracheal intubation, while it enhances the increases in plasma norepinephrine concentrations.