1992 Fiscal Year Final Research Report Summary
The Experimental Study Regarded to the Mechanism of Centrally Induced Arrhythmia
| Project/Area Number |
02670694
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | KANSAI MEDICAL UNIVERSITY |
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Principal Investigator |
SAITO Keizo KANSAI MEDICAL UNIVERSITY MEDICINE Research Associate, 医学部, 助手 (50148524)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Sakahiro KANSAI MEDICAL UNIVERSITY MEDICINE Research Associate, 医学部, 助手 (70212769)
MATSUMOTO Sanae KANSAI MEDICAL UNIVERSITY MEDICINE Research Associate, 医学部, 助手 (20154156)
NIITSU Tateki KANSAI MEDICAL UNIVERSITY MEDICINE Assistant Professor, 医学部, 講師 (40098140)
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| Project Period (FY) |
1990 – 1992
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| Keywords | Subarachnoid hemorrhage / Electrocardiography / Basal cistern / ProstaglandinF_2alpha / Lidocaine / Rabbits / Plasma epinephrine / Pkasma norepinephrine |
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| Research Abstract |
We developed a new method for introducing drugs into the basal cistern of rabbits. In this model, injection of 0.5ml of 0.1% ProstaglandinF_2alpha ( PGF_2alpha )into the basal cistern produced ECG changes, which were normalized with intracisternal administration of 0.5ml of 0.1% lidocaine. In this study, to elucidate the cause of these electrocardiographic( ECG ) changes. Regional cerebral blood flow ( gammaCBF ) near the hypothalamus was measured continuously using crossed thermocouple type texture blood flow measuring system. Intracisternal injection of PGF_2alpha produced bradycardia and other ECG changes, bloodpressure rose, and the gammaCBF increased. Intracisternal injection of lidocaine immediately abolished the ECG changes however it did not show any tendency for the gammaCBF. Recently, some authors express that ischemia of the hypothalamus may produce arrhythmias. From this study we conclude that ischemic changes of the area near the basal cistern is not the only cause of the
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ECG changes. The ECG changes were considered to be normalized by lidocaine with effect on the brain cells. And the following study with reference to elucidating nerve pathways of PGF_2alpha produced stimulation, changes in ECG were examined in three groups of rabbits which underwent dissection of the spinal cord either at C_<2-3>, or at Th_<7-8>, or binding of bilateral suprarenal artery and vein, prior to the administration of PGF_2alpha into the basal cistern. The administration of PGF_2alpha decreased more significantly appearance rate of ECG alteration in the rabbits following spinal cord dissection at C_<2-3>, and binding of the suprarenal vessels than the rabbits with spinal cord dissection at Th_<7-8>. And we measured plasma epinephrine and norepinephrine concentration in a rabbit model simulating subarachnoid hemorrhage(SAH), following the injection of PGF_2alpha into the basal cistern. In this model, plasma epinephrine values increased significantly (to 4.2-fold those before injection), substantially more than norepinephrine (which increased 1.3-fold) at 5 minutes after PGF_2alpha injection. Dissection of autonomic outflow from the cervical spinal cord or ligation of the suprarenal veins reduced the changes in plasma catecholamine concentration associated with PGF_2alpha injection. These results suggest that the sympathetic discharge seen after PGF_2alpha injection into the basal cistern in rabbits occurred through the sympatho-adrenal pathways. Less
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