1987 Fiscal Year Final Research Report Summary
An X-ray diffraction study on heart muscle during diastole
Project/Area Number |
60570035
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
General physiology
|
Research Institution | TOHOKU UNIVERSITY |
Principal Investigator |
MATSUBARA Ichiro Department of Pharmacology, Tohoku University School of Medicine, 医学部, 助教授 (90010040)
|
Co-Investigator(Kenkyū-buntansha) |
YAGI Naoto Department of Pharmacology, Tohoku University School of Medicine, 医学部, 助手 (80133940)
|
Project Period (FY) |
1985 – 1987
|
Keywords | Heart muscle / Myosin / Actin / Muscle contraction / X線回析 |
Research Abstract |
1. X-ray diffraction patterns were recorded from canine heart muscles perfused with an oxygenated artificial blood containing perfluorobutylamine. The integrated intensity of the myosin-related meridional reflection at 1/14.3 mn^<-1> did not change significantly between the systolic and the diastolic phases. These results indicated that the alignment of myosin heads along the filamentaxis did not change significantly during the cardiac cycle. 2. Rat heart muscles undergoing cyclic contractions were exposed to strong X-rays of 0.15-nm wavelength produced by the synchrotron at Tsukuba (Photon Factory). The diastolic tension increased gradually during exposure. At the end of 1-min exposure, the peak active tension decreased by 30 %. The X-ray diffraction patterns indicated that heart muscles went into partial rigor during exposure. On the other hand, chemically skinned heart muscles bathed in an ATP-rich solution were unaffected by an exposure of the same duration. These observations suggested that X-rays damaged the cellular membranes or mitochondria, leading to ATP depletion. 3. Rat heart muscles at 22 ゜C were contracted at frequencies ranging from 0.2 to 1 Hz. The 1,0 and 1,1 equatorial reflections from the hexagonal myofilament lattice were recorded with a fast X-ray diffraction technique. Based on the intensities of these reflections, the number of myosin heads associated with actin was calculated. During the systolic phase, the number increased approximately in parallel with tension development. A detailed examination, however, revealed that the number reached its maximum about 10 msec before the peak tension. During the diastolic phase, the number decreased with a time constant of 3-4 sec. The duration of this decrease was determined by the contraction frequency. Therefore, the number of actin-myosin links at the end-distolic state was dependent on the frequency of the cardiac cycle.
|