Energetics of isometric contraction in porcine carotid artery.
Energetics of isometric contraction in porcine carotid artery.
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猪颈动脉等长收缩的能量学。
DOI：
10.1152/ajpcell.1984.246.5.c510
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Paul,RJ
中科院分区：
文献类型：
--
作者：
Krisanda,JM;Paul,RJ
通过对猪颈动脉在张力形成和维持过程中ATP利用率（JATP）和无负荷缩短速度（Vus）的测定，探讨了其维持张力的高经济性机制。我们实验室以前的工作确定，O2消耗率（JO 2）可用于测量收缩开始后30 s的组织磷酸酶原利用率。在37 ℃下对组织JO 2的研究表明了以下内容。1)基础JO 2为0.069 +/- 0.017 mumol O2 X min-1 X g-1）（n = 10）。在稳态张力维持期间，KCl刺激的组织（n = 11）的基底上JO 2为0.079 +/- 0.012 mumol O2 X min-1 X g-1，KCl +组胺刺激的组织为0.213 +/- 0.022（n = 3）。2)对于这两种刺激条件下，观察到初始升高（峰值）的基底上JO 2与张力发展的速率相关。刺激后10分钟测得的峰值基底上JO 2约为稳态基底上JO 2的两倍。3)在刺激后15-20 min，在快速长度步进后的张力重建期间，JO 2无显著变化（n = 4）。Vus的研究表明了以下几点。1)在稳态张力维持期间，对于KCl刺激的组织（n = 13），Vus为0.008 +/- 0.001组织长度/s，对于KCl +组胺刺激的组织（n = 6），Vus为0.008 +/- 0.001组织长度/s。2)在KCl刺激后0.25-0.5 min观察到Vus的初始双重峰，在KCl刺激后4 min降至稳态水平，而在KCl +组胺刺激后10-20 min仍发生Vus的轻微降低。3)Vus中测得的瞬态（尽管是双相的）与JO 2中的瞬态在时间上不相关，即使在针对O2扩散和电极响应时间导致的延迟校正了JO 2时程之后。在JATP和Vus中观察到的最大变化为2 - 4倍的机制不足以解释张力维持的高经济性。
The rate of ATP utilization ( JATP ) and unloaded shortening velocity ( Vus ) of porcine carotid artery were studied during tension development and maintenance to assess the importance of mechanisms proposed to account for its high economy of tension maintenance. Previous work from our laboratory established that the rate of O2 consumption ( JO2 ) can be used to measure rates of tissue phosphagen utilization as early as 30 s after initiation of contraction. Studies at 37 degrees C of tissue JO2 indicated the following. 1) The basal JO2 was 0.069 +/- 0.017 mumol O2 X min-1 X g-1) (n = 10). During steady-state tension maintenance suprabasal JO2 was 0.079 +/- 0.012 mumol O2 X min-1 X g-1 for tissues stimulated with KCl (n = 11) and 0.213 +/- 0.022 (n = 3) for tissues stimulated with KCl + histamine. 2) For both stimulation conditions an initial elevated (peak) suprabasal JO2 was observed that correlated with the rate of tension development. The peak suprabasal JO2 was approximately twice the steady-state suprabasal JO2 measured 10 min after stimulation. 3) There was no significant change in JO2 during tension redevelopment after a rapid length step at 15–20 min after stimulation (n = 4). Studies of Vus indicated the following. 1) During steady-state tension maintenance Vus was 0.008 +/- 0.001 tissue lengths/s for tissues stimulated with KCl (n = 13) tissue lengths/s for tissues stimulated with KCl + histamine (n = 6). 2) An initial twofold peak in Vus was observed at 0.25–0.5 min in that decreased to steady-state levels by 4 min after KCl stimulation, whereas minor decreases in Vus still occurred until 10–20 min after KCl + histamine stimulation. 3) The measured transient in Vus , although biphasic, does not temporally correlate with the transient in JO2 even after the JO2 time course was corrected for delays resulting from O2 diffusion and the electrode response time. The mechanism underlying the observed maximum change of two- to fourfold in both JATP and Vus is not sufficient to account for the high economy of tension maintenance.