| Japanese |
|---|
| Title | 急性低酸素および高炭酸血症下のイヌ頸部交感神経活動に及ぼす吸入麻酔薬の影響 |
|---|
| Subtitle | 原著 |
|---|
| Authors | 堂崎信一, 山村剛康, 大塚浩司, 村上富裕美, 劔物修 |
|---|
| Authors(kana) | |
|---|
| Organization | 北海道大学医学部麻酔学講座 |
|---|
| Journal | 循環制御 |
|---|
| Volume | 12 |
|---|
| Number | 4 |
|---|
| Page | 675-684 |
|---|
| Year/Month | 1991/ |
|---|
| Article | 原著 |
|---|
| Publisher | 日本循環制御医学会 |
|---|
| Abstract | 急性低酸素血症および高炭酸血症の頸部交感神経活動(CSA)に及ぼす影響, およびこれに対する4種類の吸入麻酔薬-ハロセン(H), エンフルレン(E), イソフルレン(1), セボフルレン(S)-の抑制効果について定量的に検討した. CSA, 脳波, 心電図, 心拍数, 動脈圧, 動脈血酸素飽和度(SaO2)および呼気終末炭酸ガス濃度(FETCO2)を連続的にモニタリングした. SaO2を6〜9%/分の速度で下降させて得られた急性低酸素血症に対してCSAは著明に増加した. CSAの反応はSaO2との関係から以下の2つの方法により評価した. (1)CSAが基礎値より3%以上増加し続ける時点のSaO2(閾値)および(2)SaO2の. 低下に対するCSAの増加の傾き(利得). 対照において, それぞれ92±1.8%と-1.88±0.14(平均±標準偏差)であった. H, E, IおよびSの1MAC投与下において, 各々89.2±3.4%と-1.16±0.16, 81±6.6%と-0.74±0.21, 84.2±3.6%と-1.16±0.08および86.2±4.4%と-0.94±0.11であった. 1MACのEとSは, HとIに比べ有意にCSAの反応を抑制した(p<0.05). 二酸化炭素を加えることによって得られた高炭酸血症に対してもCSAは著明に増加した. 反応の極値は, 吸入麻酔薬の濃度の上昇に伴い抑制された. 以上のことから, 急性低酸素および高炭酸血症に対するCSA反応に及ぼすEの抑制効果は, 等力価のHやIと比べて有意に強いことが示唆された. |
|---|
| Practice | 基礎医学・関連科学 |
|---|
| Keywords | Halothane, Enflurane, Isoflurane, Sevoflurane, Sympathetic Nervous System, Hypoxemia, Hypercarbia |
|---|
| English |
|---|
| Title | Effects of Volatile Anesthetics on Cervical Sympathetic Nerve Activity during Acute Hypoxemia or Hypercarbia in Dogs |
|---|
| Subtitle | Original |
|---|
| Authors | Shinichi Dozaki*, Takeyasu Yamamura*, Hiroshi Otsuka*, Fuyumi Murakami*, Osamu Kemmotsu* |
|---|
| Authors(kana) | |
|---|
| Organization | *Department of Anesthesiology Hokkaido University School of Medicine |
|---|
| Journal | Circulation Control |
|---|
| Volume | 12 |
|---|
| Number | 4 |
|---|
| Page | 675-684 |
|---|
| Year/Month | 1991/ |
|---|
| Article | Original article |
|---|
| Publisher | Japan Society of Circulation Control |
|---|
| Abstract | 「Abstract」The response of cervical symathetic nerve activity (CSA) to acutely induced hypoxemia and/or hypercarbia was studied in the absense and the presence of either halothane (H), enfulurane (E), isoflurane (I) or sevoflurane (S). Hypoxemia was produced by adding nitrogen to the inspired gas in amounts needed to decrease arterial oxygen saturation (SaO2) at a rate of 6-9% per minute. Hypercarbia was produced by adding carbon dioxide in amounts needed to maintain end tidal carbon dioxide concentration (FETCO2) at 10%. EEG, ECG, heart rate, arterial blood pressure, SaO2, FETCO2 and multifiber potentials of CSA were continuously monitored. CSA increased significantly in response to hypoxemia. The response of CSA was quantified as a function of SaO2 in two ways：First, a threshold value of SaO2 was determined at the SaO2 value at which CSA increased 3% over the baseline level. Second, a reflex gain was determined by dividing the net increase in CSA by the degree of change in SaO2 value. The threshold and gain were 92.0±1.8% and -1.88±0.14 (mean±SD), respectively, in the absence of volatile anesthetics. The threshold and gain significantly decreased in the presence of E, I and S at 1 MAC. They were 81.0±6.6%, -0.74±0.21 ; 84.2±3.6%, -1.16±0.08 and 86.2±4.4%, -0.94±0.11 for E, I and S, respectively, Suppression of the responses of CSA was significantly greater with both E and S than with H and I (p<0.05). H at 1 MAC attenuated the gain but changes of threshold was not signifcant. CSA also increased in response to acutely induced hypercarbia. The peak response was suppressed with increasing concentrations of volatile anesthetics. These results may indicate that the depressant effects of E on CSA responses to acutely induced hypoxemia and hypercarbia was significantly greater than that of equipotent H or I. |
|---|
| Practice | Basic medicine |
|---|
| Keywords | Halothane, Enflurane, Isoflurane, Sevoflurane, Sympathetic Nervous System, Hypoxemia, Hypercarbia |
|---|