| Japanese |
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| Title | 末梢化学受容器による循環調節と麻酔 |
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| Subtitle | 特集 |
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| Authors | 白幡眞知子* |
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| Organization | *Departments of Environmental Health Sciences and Anesthesiology/Critical Care Medicine The Johns Hopkins University |
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| Journal | 循環制御 |
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| Volume | 12 |
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| Number | 3 |
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| Page | 395-406 |
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| Year/Month | 1991/ |
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| Article | 報告 |
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| Publisher | 日本循環制御医学会 |
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| Abstract | 「1. はじめに」生体が全身的ストレスにさらされた時, 循環系の機能は, ストレスの中枢への影響及びその局所作用によって大きく変化する. 循環中枢の活動状態は種々の末梢性受容器からの情報に大きく依存しており, 末梢化学受容器はその中でも重要な役割を担っている. 主な末梢化学受容器としては, 頚動脈小体と大動脈小体がある. 頚動脈小体は, その位置から大動脈小体より研究しやすいため, その機能や呼吸循環反射作用についてよりよく知られている. 本論文では的を頚動脈小体に絞り, 化学受容のメカニズム, 末梢化学受容器刺激の循環系への影響, 頚動脈小体の機能に対する麻酔薬の影響, 頚動脈小体刺激による循環系の反応に対する麻酔薬の影響について, 最近の知見を加えながら概説する. 「2. 頚動脈小体の機能と化学受容のメカニズム」頚動脈小体は, 総頚動脈が内頚動脈と外頚動脈に分岐する部分に存在するほぼ球形の感覚器官で(Fig.1)動脈血中のPo2, Pco2, pHの変化に敏感に反応する. PaO2の低下, PaCO2の上昇, PHの低下は, 求心神経であるcarotid sinus nerve(舌咽神経の枝)中chemoreceptor成分の神経活動の増加に変換され, 延髄孤束核へ送られる. この他, chemorecepterからの神経活動はニコチン, シアン, アセチルコリン等により増加し, また低血圧によっても増加することが知られている12,13). |
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| Practice | 基礎医学・関連科学 |
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| Keywords | Carotid body, hypoxia, hypercapnia, ion chnnels, reflex |
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| English |
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| Title | Control of Circulation by Arterial Chemoreceptors and Anesthesia |
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| Subtitle | |
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| Authors | Machiko Shirahata |
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| Organization | Departments of Environmental Health Sciences and Anesthesiology/Critical Care Medicine The Johns Hopkins University |
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| Journal | Circulation Control |
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| Volume | 12 |
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| Number | 3 |
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| Page | 395-406 |
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| Year/Month | 1991/ |
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| Article | Report |
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| Publisher | Japan Society of Circulation Control |
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| Abstract | The peripheral arterial chemoreceptors have long been known to have a significant influence on cardiovascular responses to hypoxia, hypercapnia and acidosis. The peripheral arterial chemoreceptors are the carotid body and the aonic body. A decrease in O2 tension, an increase in CO2 tension, and a decrease in pH in the arterial blood increase neural activities from these receptors. The signal is transferred to and integrated in the central nervous system via nucleus tractus solitarius. When a spontaneously breathing animal is exposed to hypoxia, increases in heart rate, cardiac output, arterial blood pressure, and total peripheral resistance are generally observed. There are some disagreements among the investigators about the direct effects of peripheral arterial chemoreceptors on these changes in cardiovascular parameters. In general, a decrease in heart rate and an increase in total peripheral resistance are accepted as the direct effects of arterial chemoreceptor stimulation. Most studies exploring the chemotransducing mechanisms have been carried out on the carotid body, because anatomically it is relatively easy to approach. Although the mechanisms of chemotransduction are poorly understood, most carotid body researchers agree that the Type I cells in the carotid body play a fundamental role in the chemotransducing process. In our hypothesis hypoxia, hypercapnia, and acidosis depolarize the Type I cells, allowing an activation of voltage-gated calcium channels (VGCC) with subsequent release of neurotransmitters from these cells. This hypothesis was tested using selective perfusion technique of the carotid body. Selective perfusion of the carotid body with hypoxic or hypercapnic Krebs solution increased chemoreceptor neural activity as much as systemic hypoxia or hypercapnia, when the Po2, Pco2 and pH of the solution were matched to the arterial blood. On the other hand, chemoreceptor neural activity was significantly attenuated during a selective perfusion of the carotid body with a hypoxic calcium-free Krebs solution, hypoxic Krebs solutions containing VGCC blockers (nifedipine, verapamil, diltiazem), or hypercapnic Krebs solutions containing VGCC blockers. These results support our hypothesis. Our recent work suggests the involvement of chloride channels for hypercapnic chemotransduction. In addition, the possibility that potassium channels play a role for hypoxic chemotransduction has been suggested by several laboratories. Anesthetics could influence the function of the carotid body by affecting channel activities in the Type I cells or in the afferent nerves. Recent neurophysiological studies have started revealing that anesthetics modify the channel kinetiks of the Na, K, Ca or Cl channels in nerve cells. However, up to now, there have been no studies concerning the effects of anesthetic effects on the ion channels in the Type I cells or the afferent sinus nerve. Chemoreceptor neural activity seems certainly to be affected by the anesthetics. The effects of halothane, enflurane, isoflurane, ether, etomidate, propofol, and thiopental have been reported. Halothane is the only anesthetic which was studied by more than one investigator, and the results have been inconsistent. More studies are needed. The effects of anesthetics on cardiovascular reflexes by the carotid body would be very complex, because the anesthetics would work on the carotid body, central nervous system, the heart and the vessels. Although not many studies have been conducted, most clinically used anesthetics seem to depress the cardiovascular chemoreflex. During anesthesia or even during the recovery phase from anesthesia the anesthesiologist should not use the stability of cardiovascular parameters as an index of the adequacy of respiration in the patient. |
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| Practice | Basic medicine |
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| Keywords | Carotid body, hypoxia, hypercapnia, ion chnnels, reflex |
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