Wikman-Coffelt J, Kamiyama T, Salel A F, Mason D T
Recent Adv Stud Cardiac Struct Metab. 1976;12:367-72.
Mild pulmonic stenosis, induced in dogs by banding the pulmonary artery, elevated right ventricular peak systolic pressure to 60% above the control and elevated right ventricular K+- and Ca2+- activated myosin ATPase activities. In contrast, severe pulmonic stenosis, which elevated right ventricular peak systolic pressure to 300% above the control, did not produce an increase in myosin enzymatic ATPase Vmax values but caused a decrease in myosin activity. Mild aortic stenosis, induced by banding the ascending aorta, forcing a transaortic pressure gradient of 25 mm Hg, caused an elevation in left ventricular muosin ATPase, whereas severe aortic banding, brought about by creating a transaortic pressure gradient of 55 mm Hg, never caused an elevation in left ventricular myosin enzymatic Vmax values, but, like severe pulmonic banding, caused a decrease in K+- and Ca2+- activated myosin activities. Normal left ventricular myosin Vmax values in mumol of PO4/mg-min at 37 degrees C were: K+ = 2.84 +/- 0.22, and Ca2+ = 0.97 +/- 0.14. For right ventricular myosin they were: K+ = 2.15 +/- 0.16, and Ca2+ =0.74 +/- 0.10. Analyses of tissue gases, based on mass spectrometry data, showed that the hypertrophied ventricles had an elevated tissue pCO2 and an elevation in the cGMP/cAMP ratio.
通过结扎肺动脉在犬身上诱发的轻度肺动脉狭窄，使右心室收缩压峰值比对照组升高60%，并提高了右心室K⁺和Ca²⁺激活的肌球蛋白ATP酶活性。相比之下，严重肺动脉狭窄使右心室收缩压峰值比对照组升高300%，并未使肌球蛋白酶促ATP酶Vmax值增加，反而导致肌球蛋白活性降低。通过结扎升主动脉产生25 mmHg的跨主动脉压力梯度诱发的轻度主动脉狭窄，导致左心室肌球蛋白ATP酶升高，而通过产生55 mmHg的跨主动脉压力梯度造成的严重主动脉结扎，从未使左心室肌球蛋白酶促Vmax值升高，但与严重肺动脉结扎一样，导致K⁺和Ca²⁺激活的肌球蛋白活性降低。在37℃时，正常左心室肌球蛋白Vmax值以μmol PO₄/mg·min计为：K⁺ = 2.84 ± 0.22，Ca²⁺ = 0.97 ± 0.14。右心室肌球蛋白的相应值为：K⁺ = 2.15 ± 0.16，Ca²⁺ = 0.74 ± 0.10。基于质谱数据的组织气体分析表明，肥厚的心室组织pCO₂升高，cGMP/cAMP比值升高。
