The Myocardial Protective Effect and Change of the Monophasic Action Potential Duration by Adenosine Receptor, Protein Kinase C and KATP Channel in Ischemic Preconditioning in Cats

BACKGROUND AND OBJECTIVES: The myocardial protective effect of ischemic preconditioning is well known. However, the mechanism is remains unclear. The purpose of this study is to determine the role of adenosine, protein kinase C, KATP channel and the change of monophasic action potential duration on cardioprotective effect of ischemic preconditioning in cat. Materials AND METHODS: In this experiment, 66 cats were allocated into 7 groups:control (n=10), ischemic preconditioning (n=10), adenosine pre-treated (n=10), SPT (8-p-sulfophenyl theophylline) pre-treated (n=9), polymyxin B pre-treated (n=9), glibenclamide pre-treated (n=9) and nicorandil pre-treated (n=9) groups. Ischemic preconditioning was performed in ischemic preconditioning, SPT pre-treated, polymyxin B pre-treated and glibenclamide pre-treated groups by 3 episodes of 5 minutes ischemia and 10 minutes reperfusion. All animals were subjected to 40 minutes of ischemia and 40 minutes reperfusion. Monophasic action potential duration at 50% repolarization (MAP50) was measured in the ischemic and non-ischemic area respectively by epicardial probe throughout the experiment. The effect of ischemic preconditioning was determined by infarct size (% area at risk). RESULTS: Ischemic preconditioning, adenosine pre-treatment and nicorandil pre-treatment groups demonstrated a significant reduction in infarct size (26+/-4%, 25+/-4% and 34+/-8% infarction of the risk zone, respectively, p<0.01, p<0.01 and p<0.05 vs. control) with respect to control (41+/-8% infarction of the risk zone). However, pretreatment with SPT, polymyxin B or glibenclamide abolished the effect of ischemic preconditioning. Ischemic preconditioning group exhibited a significant reduction of MAP50 duration in the ischemic area during preconditioning;at the first preconditioning 128+/-11 msec vs. 144+/-10 msec control, at the second preconditioning 110+/-10 msec vs.147+/-10 msec control (p<0.01), at the third preconditioning 114+/-10 msec vs. 145+/-11 msec control (p<0.05). But, pretreatment with SPT, polymyxin B and glibenclamide prevented the reduction of MAP50 in the ischemic area during ischemic preconditioning. During 40 minutes ischemia, the shortening of MAP50 was more pronounced in the preconditioned group than in control group;at 5 minutes 112+/-13 msec vs. 124+/-10 msec control, at 10 minutes 89+/-12 msec vs. 133+/-11 msec control (p<0.05 ), at 20 minutes 93+/-12 msec vs. 136+/-11 msec control (p<0.05), and at 30 minutes 107+/-19 msec vs. 144+/-14 msec control (p<0.05). In adenosine pre-treated group, the MAP50 was significantly shortened than control group throughout 40 minutes occlusion period;at 5 minutes 90+/-8 msec (p<0.05), at 10 minutes 77+/-9 msec (p<0.05), at 20 minutes 92+/-8 msec (p<0.05), and at 30 minutes 103+/-8 msec (p<0.05). Nicorandil pretreatment pronounced the ischemic shortening of MAP50 in ischemic area and the effect was significant during early ischemic period;at 10 minutes 98+/-22 msec (p<0.05 vs. control). In pretreatment groups with SPT, polymyxin B or glibenclamide, the ischemic preconditioning of MAP50 measured in non-ischemic area was not significantly different compared with control group. MAP50 measured in ischemic area during reperfusion was not significantly different between groups. CONCLUSION: Based on this study, adenosine receptor-protein kinase C-KATP channel activation and monophasic action potential duration shortening during ischemia play an important role in myocardial protection during ischemic injury.

Prevention of Hypokalemia before Induction of Anesthesia by Clonidine or Midazolam / 대한마취과학회지

BACKGROUND: Selective 2-agonists cause decrease in serum K+ concentration. Midazolam is an anxiolytic, sedative, and amnestic drug. Premedication of midazolam prevents increase of catecholamine with anxiety. Clonidine, alpha 2-adrenergic receptor agonist, supresses sympathetic outflow from central nervous system. So we can expect that premedication of clonidine or midazolam will prevent hypokalemia before induction of anesthesia. METHODS: Twenty two patients received 300 mcg clonidine per oral, 22 patients 0.05 mg/kg midazolan IM and 22 patients had no premedication. We measured serum K+ level at out-patient Department (T1), at 11:00 P.M. of the day before surgery (T2) and immediately before induction of anesthesia (T3). RESULTS: Serum K+ levels at T2 decreased compared to serum K+ level at T1 in all groups. Serum K+ levels T3 decreased compared to serum K+ level at T2 in control and midazolam groups but clonidine group did not decrease in serum K+ level. CONCLUSIONS: We can not prevent decrease of serum K+ level with premedication of midazolam but we can prevent decrease of serum K+ level with premedication of clonidine. So premedication of clonidine is more effective than midazolam in prevention of hypokalemia before induction of anesthesia.

Effects of Drug Dose, Volume, and Concentration on the Spinal Anesthesia with Isobaric Tetracaine / 대한마취과학회지

BACKGROUND: The patient's position cannot be changed in the hyperbaric spinal anesthesia until the anesthesia level is fixed because gravity has an effect on the spread of hyperbaric solutions. The isobaric spinal anesthesia has the advantage that the patient's position can be changed soon after drug is injected into the subarachnoid space because gravity has no effect on the spread of isobaric solutions. Most studies of isobaric spinal anesthesia had been made using plain bupivacaine. In this study, effects of drug dose, volume, and concentration on the spinal anesthesia with isobaric tetracaine were investigated. METHODS: Eighty patients were randomly allocated to four groups: 1), group 1 received 1% tetracaine 14mg, 1.4ml (N=20), 2), group 2 received 0.74% tetracaine 14mg, 1.9ml (n=20), 3), group 3 received 0.5% tetracaine 14mg, 2.8ml (n=20), 4), group 4 received 1% tetracaine 19mg, 1.9ml (n=20). Drugs were administered in lateral position at L3~4 level. Neural block was assessed by pinprick. Changes of analgesic level were evaluated with time. RESULTS: Peak analgesic level of group 4 was higher than that of group 2 after 12 minutes and no difference in analgesic level between group 1, 2, and 3 after 18 minutes. Group 4 resulted in longer duration and a higher peak level of sensory block than group 2. CONCLUSIONS: In spinal anesthesia with isobaric tetracaine, the volume is the major factor affecting initial spread of isobaric tetracaine and the dosage was the major factor affecting peak level. High concentration results in longer duration, and higher peak level.

Comparision of Effects and Complications of Diprivan (ICI Pharm Co.) and Pofol (Dong - guk Pharm Co.) / 대한마취과학회지

BACKGROUND: Propofol is a rapidly acting alkylphenol compound. Pofol is another alkylphenol compound that was made by Dong-guk Pharm Co. in Korea. This study was performed to evaluate the efficacy and complications of pofol in comparison with diprivan. METHOD: Fourty three unpremedicated patients were randomly allocated to receive one of two i.v. anesthetic agents(pofol and diprivan). We assessed the induction dose, the time to loss of consciousness, time to opening eyes on command, changes of vital sign and various complications of the two drugs. RESULT: There were no differences in induction dose and maintenance dose between pofol group (P) and diprivan group (D). The induction times of P were shoter than those of D and the recovery times of P longer than those of D. Both groups produced a significant fall in mean arterial pressure(MAP) and heart rate(HR) but there were no differences in changes of vital sign between two groups. There was no difference in incidence of pain between D and P (83% Vs 80%). Even though the characters of adverse events to P and D, the incidence rate was not different between two groups. CONCLUSION: There is no differences in efficacy and complication of pofol in comparison with diprivan except differences in induction times and recovery times between two groups. So we can use the pofol as the i.v. anesthetics as diprivan and further evaluations in induction times and recovery times are needed.

The Relationship between ST-T Electrical Alternans on EKG and Ventricular Arrhythmia

In order to observe the development of ventricular arrhythmia during regional myocardial ischemia and reperfusion, especially under the presence or absence of ST-T electrical alternans on epicardial EKG. The proximal left descending coronary artery(LAD) was ligated for 20 minutes and then reperfused suddenly in twenty-three cats. Standard lead EKG(Lead??, chest lead EKG and epicardial lead EKG were recorded simultaneously during the occlusion and reperfusion respectively. During the ligation of LAD, STEA was observed in thirteen cats(56.5%). In occlusion period, the incidence of ventricular tachycardia in STEA positive group was significantly higher than in the negative group(p<0.01) and arrhythmic score was significantly higher(p<0.005) also In the reperfusion period the incidence of vefntricular fibrillation in STEA positive group was significantly higher than in the negative group(p<0.025). But there was the tendency to be higher in arrhythmic score of STEA positive group. There were no differences in heart rate, systolic left ventricular pressure, ST elevation and ST width in both groups. Most forms of ST-T of sinus rhythm before and after development of ventricular premature beat was low form(L). It was concluded that at the presence of STEA on EKG, the incidence of ventricular arrhythmia was more prevalent. So, STEA can be available as a marker of ventricular arrhythmia and prognostic factor.