Biomedical subjects
Publications and source records attributed to D T Mason.
Explore the source record for details and available documents.
In congestive heart failure, patients appear to have alimited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur...
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Canine cardiac myosin, which was synthesized in a 14-day tissue culture, based on L-[3H] leucine incorporation, was precipitated with goat gamma G antimyosin (cardiac-specific) and analyzed on dodecylsulfate gels. Incorporation of 32PO4 into myosin chains occurring in culture was the same as that obtained in vivo and appeared to be coupled with translation. Removal of 32PO4 from myosin heavy chains with base treatment indicated the presence of phosphoserine and phosphothreonine in canine cardiac myosin heavy chains. Further acid hydrolysis confirmed the data. The system described here, i.e., analyses of 32PO4 and L[3H] leucine incorporation into myosin heavy chains, could be used as a system for assaying hypertrophying factors.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The moles of calcium bound by the left ventricle were 1.5 +/- 0.1, while those of the right ventricle were 2.9 +/- 0.2. The calcium binding constants were the same between myosins of the two cardiac ventricles. The Ca2+ binding constants were approximately 1.1 X 10(5) M-1 for both left and right ventricular myosins. Left ventricular myosin bound 1.3 +/- 0.1 mol of Mn2+, whereas right ventricular myosin bound 2.8 +/- 0.1 mol of Mn2+. The divalent cation Mn2+ only partially competed out Ca2+ (50%). Because of the partial competition, it seemed that Ca2+ and Mn2+ had some sights in common. These studies demonstrate a twofold difference in divalent cation binding (Ca2+, Mn2+) between left and right ventricular myosins. This variation in cation binding between the two ventricles is reflected in similar differences in myosin ATPase activity between the two ventricles.
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.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.