Skeletal muscle vasodilation during electrical stimulation of the preoptic recess.
Skeletal muscle vasodilation during electrical stimulation of the preoptic recess.
复制标题
电刺激视前隐窝期间骨骼肌血管舒张。
DOI：
10.1152/ajpheart.1986.250.2.h221
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Bealer,SL
中科院分区：
文献类型：
--
作者：
Proctor,KG;Bealer,SL
在电刺激下丘脑室周区视前隐窝（AV 3V区）的过程中，用视频显微镜观察大鼠脊髓背角肌中的横向（第三级）小动脉（直径12 ± 2 μ m，n = 6），以测试主动骨骼肌血管舒张是否由β-肾上腺素能机制介导。在实验前3-7天将双极丝电极植入AV 3V。持续灌注普萘洛尔（10（-5）M）导致小动脉直径的稳态减小（3 +/- 1微米），并减少由持续灌注异丙肾上腺素（10（-6）M）引起的稳态血管舒张（26 +/- 2 vs. 11 +/- 2微米）。在四种频率的AV 3V刺激（8-15 V，0.2-0.5 ms脉冲持续时间; 10、15、20和25 Hz; 1 min刺激持续时间）期间，观察了有和无普萘洛尔的六条小动脉。刺激引起频率相关的动脉血压降低（10-20 mmHg），普萘洛尔可持续且不改变。在30 +/- 7 s后观察到瞬时峰直径;时间与刺激频率无关或受普萘洛尔影响。溶剂组的峰直径平均为14-17微米，普萘洛尔组的峰直径平均为11-12微米（最大直径32 +/- 3）。峰值血管舒张显著，但与溶媒或普萘洛尔相同（平均值3 +/- 1微米），与刺激频率无关。仅在15和20 Hz期间（溶剂）和仅在20 Hz期间（普萘洛尔），直径稳定在高于基线的稳态值。我们的结论是，AV 3V刺激引起短暂的血管扩张，在spinoadrenozius肌肉，这可能不是由β-肾上腺素能受体介导的。（250字处删节）
Transverse (3rd-order) arterioles (diam 12 +/- 2 micron, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a beta-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10(-5) M) caused steady-state reduction (3 +/- 1 microns) in arteriolar diameter and reduced steady-state vasodilation (26 +/- 2 vs. 11 +/- 2 microns) caused by a continuous superfusion of isoproterenol (10(-6) M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 +/- 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 microns during vehicle and 11-12 micron during propranolol (maximum diam 32 +/- 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 +/- 1 microns) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)