The effect of progesterone on biosynthetic pathways in mammary tissue.
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Animals↗
Biomedical subjects
J Wikman-Coffelt
Publications and source records attributed to J Wikman-Coffelt.
Changes in cAMP concentrations during chronic cardiac hypertrophy.
Mild pulmonic stenosis in the dog, where right ventricular peak systolic pressure was increased approximately 150% at the time of sacrifice, induced 100% or more increase in right ventricular free wall weight by 3 weeks postoperative. Accompanying cardiac hypertrophy at these postoperative times, there was a decrease in both tissue PO2 levels and cAMP concentrations in the hemodynamically stressed ventricle, the right ventricle. Myosin ATPase activity was elevated as well as the velocity of contractile element shortening. The hemodynamically nonstressed left ventricle did not hypertrophy at these early postoperative times.
Adenosine Triphosphatases↗
Chemomechanics of altered perfusion pressure in rat hearts.
In an apex-ejecting isolated perfused working rat heart, as well as isovolumic preparations of rat hearts, perfusion pressure was studied independent of afterload. A decrease in perfusion pressure caused an immediate decrease in developed pressure (10s). There was a significant increase in free Pi and the phosphorylation potential after 20-30 min of perfusion at a reduced coronary flow induced by a reduction in perfusion pressure. Developed pressure decreased prior to the phosphorylation potential and inorganic phosphate; however, the phosphorylation set a limit to maximum work performance. At a perfusion pressure of 140 cm H2O and an afterload of 140 cm H2O, work imposed on the heart was maximum; there was no further increase in work.
Adenosine Diphosphate↗
Glycolysis in heart failure: a 31P-NMR and surface fluorometry study.
Glycolysis is slow in the heart, especially in the cardiomyopathic heart. Glycolysis is partially rate-limited by phosphofructokinase (PFK), an enzyme which is inhibited by calcium (Ca2+)i and hydrogen ions (H+)i and activated by cAMP. (H+)i and (Ca2+)i are augmented in cardiomyopathy. With glucose as the only substrate (NADH)/(NAD) the phosphorylation potential and developed pressure were significantly lower, and concentrations of phosphomonoester sugars and hydrogen ions (H+)i were significantly higher in isolated cardiomyopathic hearts as compared to healthy hamster hearts. Pyruvate lowered diastolic (Ca2+)i in cardiomyopathic hamster hearts. With pyruvate as the substrate (NADH)/(NAD), the phosphorylation potential and developed pressure increased significantly and concentrations of phosphomonoester sugars (PME), (H+)i and diastolic (Ca2+)i decreased significantly in myopathic hamster hearts. The results suggest that late heart failure in the myopathic hamster is associated with calcium and/or hydrogen ion-induced inhibition of glycolysis.
Animals↗
Mechanism of physiologic versus pathologic ventricular hypertrophy process: enhanced or depressed myosin ATPase activity and contractility governed by type, degree and duration of inciting stress.
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Adenosine Triphosphatases↗
Influence of ischemia on [Ca2+]i transients following drug therapy in hearts from aortic constricted rats.
Intracellular calcium transients were studied prior, during and after 30 min of global ischemia in control and aortic constricted rat hearts, with and without acute treatment with verapamil. Calcium transients [Ca2+]i continued to occur in verapamil treated animals for 18-20 min following the onset of global ischemia, whereas untreated hearts demonstrated calcium transients for only 3-8 min following global ischemia. Following the onset of global ischemia calcium transients continued to occur even though there was no measurable developed pressure. When calcium transients occurred for shorter periods of time during global ischemia the rise in diastolic calcium was greater and recovery was less. Addition of bradykinin to the perfusate showed that an increase in diastolic [Ca2+]i was related to a decrease in amplitude of developed [Ca2+]i transients and a decrease in developed pressure, but not to a change in coronary flow.
Animals↗
Binding of divalent cations by canine cardiac myosin: differences in normal right and left ventricles dependent upon number of light chains.
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.
Adenosine Triphosphatases↗
Differential responses of canine myosin ATPase activity and tissue gases in the pressure-overloaded ventricle dependent upon degree of obstruction: mild versus severe pulmonic and aortic stenosis.
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.
Adenosine Triphosphatases↗