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|標題:||合併使用Dexmedetomidine及Atropine對犬Cardiac troponin I濃度的影響|
The Effect of Dexmedetomidine Combine with Atropine on Cardiac troponin I Concentration in dogs
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|摘要:||Dexmedetomidine 為α-2 adrenergic 致效劑，具有鎮靜、止痛及肌肉鬆弛效果，麻醉使用可減少其他氣體麻醉或液體麻醉藥物的用量，其藥理機制會使周邊血管平滑肌收縮，造成暫時性高血壓、心搏徐緩、心輸出量可下降約50%。若使用抗膽鹼類藥物，例如atropine，來提升心跳速率，在先前的文獻中認為會增加心肌耗氧、高血壓等現象，可能造成心臟的負擔，因此不建議此兩種藥物合併使用，但未有實際對心臟受損的程度做檢測。本實驗的目的是利用檢測心肌受損標誌cTnI的濃度變化，監控合併此兩種藥物是否的確會造成心肌的傷害。在國立中興大學獸醫教學醫院進行絕育或骨科手術的18隻狗，隨機且平均分成SD10組(saline-Dexmedetomidine 10)、AD10組(atropine- Dexmedetomidine 10)及AD5組(atropine- Dexmedetomidine 5)。以生理食鹽水或atropine搭配兩種劑量Dexmedetomidine作為麻醉前給藥，術中以MLK連續靜脈輸注方式止痛。於麻醉給藥前、給藥後6、12、48、72小時測量cTnI，紀錄術中各項生理數值，予以分析。結果顯示cTnI濃度於給藥後6及12小時在AD10上升最多且與SD10和AD5有統計學上顯著差異，心跳速率以SD10組下降最多，於導入時(T0)及導入10分鐘(T10) SD10和AD10有顯著差異，收縮壓以AD5為三組中最低，且在T20及T30與AD10組有顯著差異，舒張壓以AD10為最高，且於T20、T30及T60與AD5有顯著差異，平均壓以AD10最高，於T20和T30與AD5有顯著差異。根據實驗結果，atropine 於dexmedetomidine 前給予，在dexmedetomidine 10 µg/kg組別，造成血壓升高且cTnI上升，可能增加心肌耗氧及損傷。在dexmedetomidine 5 µg/kg組別，心跳速率維持100次/分鐘左右，cTnI在正常範圍，因此以atropine來減少dexmedetomidine造成的心搏徐緩，增加心輸出量，在5 µg/kg dexmedetomidine，不會造成心臟的損傷。|
Dexmedetomidine is an α-2 adrenergic agonist with effects of sedation, analgesia and muscle relaxation. When used in combination with other drugs, it is able to reduce the dosage such as the inhalant anesthetic and intravenous anesthetics. The mechanism of dexmedetomidine is to induce peripheral vasoconstriction, which results in temporary hypertension, bradycardia and 50% reduction of cardiac output. Anticholinergics such as atropine were used for increasing heart rate, but it was considered to increase myocardial oxygen consumption and hypertension in previous studies. As a result, combination of atropine with dexmedetomidine was not recommended. But the extent of myocardial damage has not been confirmed. The purpose of this study is to find out whether the combination of these two drugs will cause myocardial damage by the change in cTnI concentration. Eighteen dogs were distributed randomly into group SD10, group AD10 and group AD5. Orthopedics or OHE were performed at Veterinary Medicine Teaching Hospital of National Chung Hsing University. 5 µg/kg and 10 µg/kg of dexmedetomidine were accompanied by saline or atropine as premedication, MLK was given by constant rate infusion during surgery. Concentration of cTnI was recorded before premedication, and 6, 12, 24, 48, 72 hours after premedication. Physiological parameters during anesthesia were recorded for analysis. Results showed that cTnI level increased the most in group AD10 at 6 and 12 hours after premedication and was significantly different from SD10 and AD5. Heart rate decreased most in group SD10, and showed significant differences with AD10 at induction (T0) and T10. Systolic blood pressure was lowest in group AD5, showed significant differences with group AD10 at T20 and T30. Diastolic blood pressure was highest in group AD10, showed significant differences with group AD5 at T20, T30 and T60. Mean arterial pressure was highest in group AD10, showed significant differences with group AD5 at T20 and T30. According to our study, atropine followed by dexmedetomidine 10 µg/kg would result in increasing blood pressure and cTnI level, which lead to increasing myocardial oxygen consumption and injury. Somehow when atropine was followed by dexmedetomidine 5 µg/kg, heart rate was able to maintain around 100 beats/minute and cTnI level remained normal. Therefore, when atropine was used as compensation for bradycardia caused by dexmedetomidine, cardiac output would increase and no myocardial injury was found.
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