• Journal of Veterinary Science
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• v.21 no.1
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• pp.8.1-8.11
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• 2020

This study reports the clinical use of two sevoflurane-based anesthetic techniques in dogs undergoing craniectomy. Twenty-one animals undergoing elective rostrotentorial or transfrontal craniectomy for brain tumor excision, anesthetized with sevoflurane, were enrolled in this retrospective, observational study. Anesthetic records were allocated to two groups: Sevo-Op (sevoflurane and short acting opioid infusion): 8 dogs and Sevo-Dex (sevoflurane and dexmedetomidine infusion): 13 dogs. Average mean arterial pressure (MAP), heart rate, end-tidal carbon dioxide, end-tidal sevoflurane and intraoperative infusion rates during surgery were calculated. Presence of intra-operative and post-operative bradycardia, tachycardia, hypotension, hypertension, hypothermia, hyperthermia was recorded. Time to endotracheal extubation, intraoperative occurrence of atrioventricular block, postoperative presence of agitation, seizures, use of labetalol and dexmedetomidine infusion were also recorded. Data from the two groups were compared with Fisher's exact test and unpaired t tests with Welch's correction. Odds ratio (OR) and 95% confidence interval (CI) were calculated for categorical variables. Intra-operatively, MAP was lower in Sevo-Op [85 (± 6.54) vs. 97.69 (± 7.8) mmHg, p = 0.0009]. Time to extubation was longer in Sevo-Dex [37.69 (10-70) vs. 19.63 (10-25), p = 0.0033]. No differences were found for the other intra-operative and post-operative variables investigated. Post-operative hypertension and agitation were the most common complications (11 and 12 out of 21 animals, respectively). These results suggest that the infusion of dexmedetomidine provides similar intra-operative conditions and post-operative course to a short acting opioid infusion during sevoflurane anesthesia in dogs undergoing elective rostrotentorial or transfrontal intracranial surgery.

• Journal of Chest Surgery
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• v.30 no.3
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• pp.253.1-262
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• 1997

Hypothermia during lung preservation decreases metabolic processes. After the rabbit lung was flushed with modified Euro-Collins solution, heart-lung block was harvested and the left lung was assessed after ligation of the right pulmonary artery and right main-stem bronchus. Heart-lung block was immersed in the same solution for 6 hours. The modified Euro-Collins solution and storage temperature of group 1(10 cases) was 4t, roup 2(10 cases) was l$0^{\circ}C$. On completion of the storage period, the left lung was ventilated and reperfused with blood u:high used a cross-circulating paracorporeal rabbit as a "biologic deoxygenator" for 60 minutes. Pulmonary artery pressure, airway pressure, difference in oxygen tension between mow and outflow perfusate and degree of pulmonary edema were assessed at 10-minute intervals while the left lung was ventilated at 0.8 of the inspired oxygen fraction. The mean pulmonary venous oxygen tensions at 10 and 60 minutes after reperfusion were 209.52$\pm$42.46 and 103.48$\pm$ 15.96 mmHg in group I versus 247.78$\pm$36.19 and 147.91 $\pm$ 11.07 mmHg in group II(p=0.049, (0.0001). The mean alveolar-arterial oxygen differences at 20 and 60 minutes after reperfusion were 357. 95$\pm$ 12.84 and 437.31 14.26 mmHg in group I versus 310.88$\pm$3).47 and )90.93$\pm$ 15.86 mmHg in group II (p=0.0092, (0.0001). The mean pulmonary arterial pressures at 10 and 60 minutes after reperfusion were 40.56$\pm$ 18.66 and 87. 2$\pm$ 17.22 mmHg in group I versus 31.22$\pm$6.84 and 65.78$\pm$ 11.02 mmHg in group rl (p : 0.048, 0.0062). The mean pulmonary vascular resistances at 10 and 60 minutes after reperfusion were 2.69$\pm$0.85 and 4.36$\pm$0.86 mmHg/ml/min in group I versus 1.99$\pm$0.39 and 3.29$\pm$0.55 mmHg/ml/min in group II(p : 0.0323, 0.0062). There were no difference between groups in peak airway pressure, lung compliance and degree of pulmonary edema. In conclusion that preservation of lung at l$0^{\circ}C$ was superior to preservation at 4$^{\circ}C$.}C$.

• Journal of Chest Surgery
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• v.39 no.4 s.261
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• pp.281-288
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• 2006

Background: Extracardiac pericardial-flap lateral tunnel Fontan operation has theoretical advantage of growth potentiality of the extracardiac tunnels. The mid-term results of this technique and morphologic change of the lateral tunnel were studied. Material and Method: Clinical data was reviewed in 42 patients who underwent extracardiac pericardial-flap lateral tunnel Fontan operation between November 1993 and December 2004. The age was $2.8{\pm}1.5$ years and the body weight was $12.3{\pm}3.2$ kg. Extracardiac tunnel was constructed using the pedicled pericardium with the base undetached. By reviewing the follow-up cardiac angiograms, the diameter and the cross-sectional area of the lateral tunnel was compared to those of inferior vena cava. Result: There were four operative mortality cases (9.8%) and the causes of death were low cardiac output for all four cases. Postoperatively, five patients had prolonged pleural effusion longer than two weeks and one patient required a permanent pacemaker due to complete heart block. Follow-up was possible in 37 patients and the follow up duration was $3.8{\pm}2.2$ years. During that period, one patient died, of upper gastrointestional bleeding combined with heart failure and one patient died a sudden death of unknown cause. Two patients required reoperation due to subaortic stenosis and anastomosis site stenosis between inferior vena cava and lateral tunnel. In one patient, bradyarrhythmia was anew but there was no thromboembolic complication. The lateral tunnel showed growth in proportion to the size of the inferior vena cava. Conclusion: Extracardiac pericardial-flap lateral tunnel Fontan operation is relatively simple and safe. The mid-term result was favorable and the extracardiac tunnel showed potential for growth.

• The Korean Journal of Nuclear Medicine
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• v.26 no.1
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• pp.72-81
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• 1992

Pharmacologic coronary vasodilation in conjunction with myocardial scintigraphy has become an accepted alternative to dynamic exercise testing for the diagnosis of coronary artery disease. Although dipyridamole has traditionally been used for this purpose, it causes frequent side effect, which at times can be life-threatening. Moreover, dipyridamole dose not elicit maximal coronary vasodilation in a substantial number of patients receiving the usual i.v. dose. Adenosine is an endogenously produced compound that has significant effects as a coronary vasodilator and rapid onset action and extremely short half-life (< 10 seconds). The diagnostic accuracy and safety profile of adenosine $^{99m}Tc-MIBI$ myocardial scintigraphy were evaluated and comparison with exercise $^{99m}Tc-MIBI$ was performed. Twenty-eight subjects underwent $^{99m}Tc-MIBI$ imaging after adenosine infusion and exercise $^{99m}Tc-MIBI$ imaging. Adenosine was infused intravenously at a dose of 0.14mg/kg/body weight per minute for 6 min and MIBI was injected at 3 minute. Adenosine caused an incerease in heart rate ($64{\pm}12$ at baseline versus $74{\pm}16$ beats/min at peak effect, p<0.001), a mild decrease in systolic and diastolic blood pressure and a slightly increase in PR interval(p; NS). Side effects were reported in 92% of patients and were mostly mild in nature and promptly resolved within 1 or 2 minutes of termination of adenosine infusion. Facial flushing (53%), chest pain (36%), mild dyspnea (39%), headache (21%), throat discomfort (21%) were frequent symptoms. ST segment depression (> 1 mm) and second degree AV block in electrocardiography occured in 11% of the patients, respectively. The overall sensitivity and specificity for individual coronary stenoses in 16 patients underwent coronary angiography were 88% and 95%, respectively. The agreement ratio of segmental perfusion between adenosine and exercise images was 92% (Kappa index=0.82). In conclusion, $^{99m}Tc-MIBI$ myocardial perfusion scintigraphy with intravenous adenosine is a feasible, safe and highly accurate noninvasive technique for the detection of coronary artery disease and results are at least comparable with those of exercise $^{99m}Tc-MIBI$ scintigraphy.

• Journal of Chest Surgery
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• v.16 no.2
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• pp.199-212
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• 1983

The inhibition/influences of adenine compounds on the heart have been described repeatedly by many investigators, since the first report by Druny and Szent-Gyorgyi [1929]. These studies have shown that adenosine and adenine nucleotides have an over-all effect similar to that of acetylcholine [ACh] by slowing and weakening the heartbeat. The basic cellular and membrane events underlying the inhibitory action of adenosine on sinus rate, however, are not well understood. Furthermore, the physiological role of adenosine in regulation of the heartbeat remains still to be elucidated. Therefore, this study was undertaken in order to examine the response of rabbit SA node to adenosine and to compare the response to that of ACh. Isolated SA node preparation, whole atrial pair, or left atrlal strip was used in each experiment. Action potentials of SA node were recorded through the intracellular glass microelectrodes, which were filled with 3M KCI and had resistance of 30-50 M. All experiments were performed in a bicarbonate-buffered Tyrode solution which was aerated with 3% $CO_2-97%$ $O_2$ gas mixture and kept at $35^{\circ}C$. Spontaneous firing rate of SA node at 35C [Mean + SEM, n=16] was 154 + 3.3 beats/min. The parameters of action potentials were: maximum astolic potential [MDP], -731.7mV: overshoot [OS], 9 + 1.4mV; slope of pacemaker potential [SPP], 94 3.0mV/sec.Adenosine suppressed the firing rate of SA node in a dose dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was potentiated in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine [2mg/l] and propranolol [$5{\times}10^{-6}M$]. ACh [$10^{-6}M$] responses on action potential were similar to those of adenosine by increasing MDP and decreasing SPP. These effects of ACh disappeared by pretreatment of atropine [2mg/1]. Inhibition/effects of adenosine and ACh on sinus rate were enhanced synergistically with the simultaneous administration of adenosine and ACh. Marked decrease of overshoot potential was the most prominent feature on action potential. Dipyridamole [DPM], which is known to block the adenosine transport across cell membrane, definitely potentiated the action of adenosine . Adenosine suppressed the sinus rate and atrial contractility in the same dosage range, even in the reserpinized preparation. Above` results suggest that adenosine suppresses pacemaker activity, like ACh, by acting directly on the membrane of SA node, increasing MDP and decreasing SPP.

• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.189-199
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• 1996

Myocardial ${\alpha}_1-adrenoceptors$ have been shown to mediate a biphaslc inotropic response that was characterized by a transient decline followed by a sustained increasing phase in guinea pig ventricular muscle. Recently one group reported that an ${\alpha}_1-adrenoceptors-induced$ intracellular $Na^+$ decrease is linked to fast $Na^+$ channel inhibition and another group reported that it is linked to $Na^+$-$K^+$ pump activation by ${\alpha}_{1b}-adrenoceptors$. But until now, its mechanism is not clear. Therefore, to see whether the $Na^+$channel or $Na^+-K^+$ pump is related to a decrease in intracellular $Na^+$ activity and/or the negative inotropic response, and which ${\alpha}_1-adrenoceptor$ subtype was involved in the decrease in intracellular $Na^+$activity by phenylephrine, we used conventional and sodium selective microelectrodes, and tension transducer to determine the effects of ${\alpha}_1-adrenergic$ stimulation on membrane potential, intracellular $Na^+$ activity, and twitch force in guinea pig ventricular muscles. $10^{-5}$ M Phenylephrine produced a slight hyperpolarization of the diastolic membrane potential, a decrease or increase in $a_N^i_a$, and a biphasic inotropic response. The negative inotropic response accompanied by a decrease in intracellular $Na^+$activity, whereas in muscles showing a remarkable positive inotropic response without initial negative inotropic effect was accompanied by an increase in intracellular $Na^+$ activity. The decrease in intracellular $Na^+$ activity was apparently inhibited by WB4101, an antagonist of the ${\alpha}_{1a}-adrenoceptors$. The decrease in intracellular $Na^+$ activity caused by phenylephrine was not abolished or reduced by a block of the fast $Na^+$ channels. $V_{max}$ also was not affected by phenylephrine. Phenylephrine produced an increase in intracellular $Na^+$ activity in the presence of a high concentration of extracellular $Ca^{2+}$ (in quiescent muscle) or phorbol dibutyrate, a protein kinase C activator(in beating muscle). These suggest that the ${\alpha}_{1a}-adrenoceptors-mediated$ decrease in intracellular $Na^+$ activity may be related to the protein kinase C.

• Molecules and Cells
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• v.25 no.3
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• pp.390-396
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• 2008

Calreticulin (CRT) is one of the major $Ca^{2+}$ binding chaperone proteins of the endoplasmic reticulum (ER) and an unusual luminal ER protein. Postnatally elevated expression of CRT leads to impaired development of the cardiac conductive system and may be responsible for the pathology of complete heart block. In this study, the molecular mechanisms that affect $Ca^{2+}$-dependent signal cascades were investigated using CRT-overexpressing cardiomyocytes. In particular, we asked whether calreticulin plays a critical role in the activation of $Ca^{2+}$-dependent apoptosis. In the cells overexpressing CRT, the intracellular calcium concentration was significantly increased and the activity of PKC and level of SECAR2a mRNA were reduced. Phosphorylation of Akt and ERKs decreased compared to control. In addition the activity of the anti-apoptotic factor, Bcl-2, was decreased and the activities of pro-apoptotic factor, Bax, p53 and caspase 8 were increased, leading to a dramatic augmentation of caspase 3 activity. Our results suggest that enhanced CRT expression in mature cardiomyocytes disrupts intracellular calcium regulation, leading to calcium-dependent apoptosis.

• Journal of Dental Anesthesia and Pain Medicine
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• v.20 no.6
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• pp.367-375
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• 2020

Background: Intraosseous anesthesia (IO) allows the anesthetic solution to be injected directly into the cancellous bone. The anesthetic solution immediately reaches the periapical region, and thus the axonal area of the nerve, where it can temporarily disable the sodium pump. The effect is felt almost without any time delay, and only a small amount of anesthetic solution is required. Methods: This study aims to investigate the efficacy of IO using the AnestoⓇ device after infiltration anesthesia (IA) and/or inferior alveolar nerve block anesthesia (IANB) failed to work in symptomatic irreversible pulpitis (hot tooth). The 33 patients included in the study were treated additionally with 1.7 ml articaine hydrochloride with 1:100,000 epinephrine hydrochloride (UltracainⓇ D-S, Sanofi-Aventis, Frankfurt, Germany) IO. Results: The electrical pulp test showed that 95.76% of the volunteers reacted positively to the combination of IANB or IA with the IO. In women, the additive IO was effective at 97.22%. In men, the IO led to pain elimination in 94.00% of cases. The duration of the IO was less than a quarter of an hour (13.03 min). The IO worked longer in women than in men (13.61 min vs. 12.33 min). Overall, more than every third tooth that needed trepanation was located in the posterior area of the mandible (36.4%). Treatment of hot teeth in this area was associated with an increased pulse rate and increased residual pain. There was a moderate correlation (Spearman-Rho [IRI] = 0.280) between the Visual Analog Scale (VAS) score and bone density, and a significant correlation (IRI = 0.612) between subjective residual pain and bone width. The IO resulted in a moderate, transient increase in the pulse rate by approximately 20 bpm. This is similar to the temporary increase in heart rate after conventional anesthesia techniques in non-preloaded patients and can be considered clinically irrelevant. Conclusion: IO with the AnestoⓇ device as an extension and deepening of local pain elimination is recommended for the treatment of hot teeth.

• The Korean Journal of Physiology
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• v.18 no.1
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.

• Journal of Chest Surgery
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• v.39 no.7 s.264
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• pp.527-533
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• 2006

Background: A retrospective study was conducted to analyze the results of St. Jude Medical mitral valve replacement at the Chonbuk National University Hospital since the initial implant in May 1984. Material and Method: Between May of 1984 and December of 1996, 95 patients underwent MVR with the St. Jude Medical mechanical valve prosthesis at Department of Medical Science of Chonbuk National University Hospital and follow-up ended in May of 2004. Result: Age ranged from 19 to 69 years. Follow-up (mean${\pm}$standard deviation) averaged $10.6{\pm}4.2\;year$. Thirty-day operative mortality was 4.2% (4/95). Nine late deaths have occurred and actuarial survival was $90.5{\pm}3.0%,\;87.9{\pm}3.4%\;and\;83.2{\pm}4.6%$ at 5, 10 and 20 years, respectively. Probability of freedom from valve-rotated death was $95.5{\pm}2.1%,\;94.3{\pm}2.4%\;and\;91.0{\pm}3.9%$ at 5, 10 and 20 years, respectively. Seven patients have sustained thromboembolic events (1,05%/patient-year). Fifteen patients had anticoagulation related hemorrhage (3.56%/patient-year). There was no structural valve deterioration. Probability of freedom from all complications was $82.0{\pm}3.9%,\;71.3{\pm}4.8%\;and\;42.4{\pm}10.5%$ at 5, 10 and 20 years, respectively. Conclusion: We confirm the effective and excellent durability of the St. Jude Medical prosthesis in the mitral position with a low event rate at long-term follow-up. It also demonstrates the commonly encountered practical difficulty of adjusting the anti-coagulation protocol in patients with prosthetic mitral valves.