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Biomedical subjects

R L Coulson

Publications and source records attributed to R L Coulson.

28 records · Page 2Linked to original sources
PubMed1978

Normal cardiac myosin ATPase and mechanics in pressure overload with digitalis treatment.

Cardiac muscle myosin ATPase activity is depressed and contractile function impaired when the heart is subjected to a chronic pressure overload. Administering digitalis in the presence of chronic pressure overload significantly attenuates the decline in mechanical function. The current study sought to determine if the cardiac muscle myosin ATPase activity of cats treated with digitalis in the presence of pressure overload remains normal in parallel with the mechanical function. Four groups of cats were studied: normal controls (C), animals with pressure-overload hypertrophy with or without failure (HF), normal cats that received treatment with digitalis (D), and animals that received digitalis prior to and together with pressure overload (DHF). Compared to C, the maximum myosin ATPase activity of HF was significantly (P less than 0.05) depressed, but the maximum ATPase activity of D and DHF was not altered significantly (P greater than 0.05) from C. In parallel with the enzyme maximum activity, the papillary muscle isometric rate of force development was significantly (P less than 0.005) depressed in HF compared to C; D and DHF were not significantly (P greater than 0.05) different from C. It is concluded that the depression of myosin ATPase observed in HF is not present when digitalis is administered concomitant with the pressure overload.

Adenosine Triphosphatases↗
PubMed1977

Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat.

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.

Animals↗
PubMed1976

Energetics of isovolumic contractions of the isolated rabbit heart.

1. In the isolated beating rabbit heart the heat production (measured by Dewar-flask calorimetry) and oxygen consumption (measured polarographically) increased in a similar way to force development (assessed as the time integral of left ventricular developed pressure) when the diastolic size of the heart was increased. 2. The energy expenditure of the heart consists of an element which is independent of the force developed and another which varies with the force developed. 3. The calorific equivalent of oxygen in the beating heart when it was provided with pyruvate as a substrate was found to be 20-48 mJ/mul: O2 at 25 degrees C. 4. The anaerobic metabolism was well below 5% of the total energy liberation and was constant at all levels of mechanical activity.

Anaerobiosis↗
PubMed1970

Observations on coronary collateral communications and the control of flow in the coronary circulation of the dog.

1. Pressure was measured in the small arterial anastomosing branches of the coronary vascular network. The mean value was 30 mm Hg not significantly different from the mean value of 33 mm Hg for peripheral coronary pressure measured distal to a ligature on the anterior descending branch of the left coronary artery. Evidence was adduced to show that either the anterior descending or the circumflex artery had the capacity to maintain network pressure at levels adequate for tissue perfusion.2. The network has both capacity and compliance. Filling of the network compliance during systole probably accounts for the systolic phase of coronary flow. Flow through the microcirculation is probably entirely diastolic, the combined compliance of the aorta and large vessels together with the network provides the necessary reservoir, the potential energy indicated by diastolic pressure provides the perfusion pressure head.3. Resistance of vessels between the aorta and network cannula (pre-net) was approximately double that of the microcirculation (post-net). The smaller pre-network vessels are of the order 70 mum in diameter. Both pre- and post-network vessels are vaso-active and respond similarly to adrenaline and haemorrhage.

Animals↗
PubMedDate not supplied

Cytochalasin D inhibits penetration of hamster eggs by guinea pig and human spermatozoa.

Fertilization experiments using zona-free hamster eggs and spermatozoa from both guinea pig and human were conducted in the presence of cytochalasin D to evaluate the possible role of actin filaments in fertilization processes. When the actin filament inhibitor, cytochalasin D, was added to fertilization media at concentrations of 10 to 30 microM, penetration of eggs was significantly inhibited. Preincubation of the eggs with cytochalasin D and washing prior to addition of spermatozoa had no effect on penetration as quantitated by the number of swollen heads in the egg cytoplasm. However, spermatozoa preincubated with cytochalasin D and subsequently washed prior to egg addition showed reduced penetration of the same magnitude as when spermatozoa and eggs were coincubated with cytochalasin D. Both the percentage of zona-free eggs showing decondensed sperm heads and the penetration indices (total decondensed spermatozoa/total eggs) were significantly affected when spermatozoa were exposed to cytochalasin D. The DMSO vehicle used to dissolve cytochalasin D had little effect on the number of decondensed heads. When the concentration of cytochalasin D was increased (DMSO remaining constant) in human sperm experiments, percent penetration decreased and progressively fewer decondensed spermatozoa were recorded, indicating dose-responsiveness to cytochalasin D. Motility parameters of human spermatozoa were not altered at any of the concentrations of cytochalasin D tested. Neither guinea pig sperm motility nor acrosome reaction was altered significantly by cytochalasin D or the DMSO vehicle. These experiments suggest that cytochalasin D may be an inhibitor of some fertilization processes such as sperm penetration or sperm head decondensation.

Actins↗