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G H Templeton

Publications and source records attributed to G H Templeton.

At least 19 recordsLinked to original sources
PubMed1989

Left ventricular coordinate systems.

Three-dimensional kinematics of radiopaque markers in anterior, posterior, septal, and lateral regions of a major equatorial plane were evaluated in anesthetized dogs by biplane fluoroscopy. Stationary coordinate systems measured marker locations recorded during diastole and systole from a contractile origin at the center of contraction at end systole and from a geometric origin at the intersection with the equatorial plane of the ventricular long axis at end diastole. A time-indexed system measured marker locations at end diastole and at end systole, respectively, from the locations of the geometric origin at end diastole and end systole. Compared to the stationary system with the geometric origin, both the stationary system with the contractile origin and the time-indexed system reduced the variability of the radial components of the contractile displacements between ventricular regions. In contrast to the other two systems, the system with the contractile origin reduced circumferential components to values not significantly different from zero. These results indicate that 1) abnormally contracting regions of the ventricle may be located and their size measured by determining the region where the radial component differs from that in the rest of the equatorial plane and 2) rotation in a major equatorial plane of the ventricle is significant, but the influence of rotation can be minimized by referencing ventricular dimensions to a coordinate system with an origin at the center of contraction.

Animals↗
PubMed1989

Quantification of three-dimensional left ventricular segmental wall motion and volumes from gated tomographic radionuclide ventriculograms.

Tomographic radionuclide ventriculograms may be used for three-dimensional wall motion analysis. We propose that automatic quantification of these images is possible, and here we describe the implementation and validation of a method to perform this task. Automatic computer methods were developed to locate the left ventricular (LV) endocardial surfaces in all time frames of the cardiac cycle. Global, regional, and local motion and volume were computed. Results were displayed using three-dimensional graphics. The methods were validated using phantom, canine, and human studies. Actual phantom values correlated well with experimentally determined volumes, y = 1.01x + 1.29ml, r = 0.99. In the canine model, the LV endocardial surfaces were located to within an average of 1.9 mm and 3.7 mm at end-diastole and end-systole, respectively. Areas of obvious wall motion abnormalities in automatically processed patient studies corresponded well with angiographically documented coronary artery disease. End-diastolic and end-systolic volumes computed automatically from single photon emission computed tomography averaged errors of 9% and 38%, respectively, when compared with contrast ventriculographic volumes. These results indicate that it is possible to automatically identify the left ventricular endocardial surface in gated tomographic radionuclide ventriculograms. The location of these surfaces corresponds well with the location of implanted endocardial markers, and global volume computed from these surfaces corresponds well with known volumes.

Adult↗
PubMed1988

Ventricular ejection fractions of linear transformation and ellipsoid models.

Eigenvolumes calculated from a linear transformation model were found previously to be linearly related to balloon volumes in excised hearts. The present study analyzed endocardial marker kinematics in intact, contracting left ventricles by biplane cinefluorography. Ejection fractions of the linear transformation model were compared by linear regression analysis with those of an ellipsoidal model, whose ejection fractions had been documented previously in closed and open-chest dog preparations. Data from 10 dogs indicated a correlation coefficient of 0.98 and a regression equation with close similarity to the line of identity. Ejection fractions calculated from the linear transformation model are concluded to be proportional to actual ejection fractions in intact, beating left ventricles.

Algorithms↗
PubMed1988

Changes in fiber composition of soleus muscle during rat hindlimb suspension.

Chronic reduction of gravitational load in the rear limbs of rats to simulate the influence of near-zero gravity in skeletal muscles has been shown previously to elicit atrophy in the soleus muscle. Use of this model by the present investigation indicates that soleus atrophy was characterized by a decline in the number of fibers in groups that contained the slow isoenzyme of myosin and which were classified as type I from intensity of staining to myofibrillar actomyosin adenosinetriphosphatase (ATPase) and to NADH tetrazolium reductase. Furthermore total fiber number was not changed, whereas fibers containing the intermediate isoenzyme and those classified as type IIa increased. There results could be explained by either a change in the composition within existing fibers or a simultaneous loss of slow fibers and de novo synthesis of intermediate and fast fibers. Evidence for transformation included an absence of embryonic or neonatal myosin in muscles from suspended rats and the constant fiber number that was unchanged by 4 wk of suspension. Furthermore although fiber areas of both groups of type I and IIa fibers declined during suspension, variability of the fiber areas within each group did not increase.

Animals↗
PubMed1986

Influences of inactivity and indomethacin on soleus phosphatidylethanolamine and size.

Results of previous investigations indicate that muscular prostaglandins (PG) E2 and F2 alpha are biosynthesized during changes in muscular activity and stimulate protein degradation and synthesis, respectively. The results of the present investigation demonstrates a reduction by indomethacin of soleus hypertrophy, which occurred during a one week recovery period following rat hindlimb suspension. While this hypertrophic model evoked significant, rapid increases in soleus myosin and weight in control groups, continuous systemic release of indomethacin (3.5 mg/Kg/day) reduced the gain in soleus weight, Type I and II hypertrophy. Body weights of all groups were not significantly different. Additional analysis found a selective reduction in phosphatidylethanolamine (PE) during soleus atrophy and hypertrophy which were elicited by hindlimb suspension and recovery from suspension, respectively. Indomethacin enhanced PE recovery. Data from previous and present studies support a hypothesis that a change in soleus activity elicits PE catabolism, changes in cytosolic and muscular calcium, in calcium-dependent phospholipase activity, in PG biosynthesis, and in soleus size.

Animals↗
PubMed1984

Influence of suspension hypokinesia on rat soleus muscle.

Hindlimb hypokinesia was induced in rats by the Morey method to characterize the response of the soleus muscle. Rats suspended for 1-4 wk exhibited continuous and significant declines in soleus mass, function, and contractile duration. Soleus speeding was in part explained by an alteration in fiber type. The normal incidence of 70-90% type I fibers in the soleus muscle was reduced after 4 wk of suspension to 50% or less in 9 of 11 rats. A significant decline in type I myosin isozyme content occurred without a change in that of type II. Other observed histochemical changes were characteristic of denervation. Consistent with soleus atrophy, there was a significant increase in lysosomal (acid) protease activity. One week of recovery after a 2-wk suspension was characterized by a return to values not significantly different from control for muscle wet weights, peak contraction force, one-half relaxation time, and type I myosin. Persistent differences from control were observed in maximal rate of tension development, contraction time, and denervation-like changes.

Animals↗
PubMed1984

The influence of rat suspension-hypokinesia on the gastrocnemius muscle.

Hind-limb hypokinesia was induced in rats by the Morey method to characterize the response of the gastrocnemius muscle. A comparison of rats suspended for 2 weeks with weight, sex, and litter-matched control rats indicate no difference in gastrocnemius wet weight, contraction, or one-half relaxation times, but less contractile function as indicated by lowered dP/dt. Myosin ATPase staining identified uniform Type I (slow-twitch) and II (fast-twitch) atrophy in the muscles from 4 of 10 rats suspended for 2 weeks and 1 of 12 rats suspended for 4 weeks; muscles from three other rats of the 4-week group displayed greater Type I atrophy. Other histochemical changes were characteristic of a neuropathy. These data together with recently acquired soleus data (29) indicate the Morey model, like space flight, evokes greater changes in the Type I or slow twitch fibers of the gastrocnemius and soleus muscles.

Adenosine Triphosphatases↗
PubMed1982

Muscle diffraction theory. Relationship between diffraction subpeaks and discrete sarcomere length distributions.

A theoretical discussion is presented that describes the diffraction on monochromatic light by a three-dimensional sarcomere array having the following properties. The basic repetitive diffracting unit is the sarcomere. The contiguous arrangement of physically attached serial sarcomeres in the myofibril is contained within the model so that relative position of sarcomeres depend upon the lengths of intervening ones. Sarcomere length is described by a distribution function. This function may be discrete or continuous and contain one or more subpopulations. Two arrangements of sarcomeres are considered: (a) when sarcomeres of different lengths are arranged randomly in myofibrils the amplitude and width of mth order (m greater than or equal to 1) peaks and associated secondary diffraction maxima decrease and increase monotonically, respectively, as the standard deviation of the length distribution increases. No subpeaks are present regardless of the number of subpopulations within the distribution function. This behavior is shown to follow from the dependence of sarcomere position on the length of intervening sarcomeres. (b) When sarcomeres belonging to the same length subpopulation are arranged in serial contiguous fashion to form domains and more than one length subpopulation is present, then mth order diffraction peaks split to form subpeaks. The theoretical basis for this behavior is developed for the first time and may explain the subpeaks evident in diffraction patterns from cardiac and skeletal muscle.

Light↗
PubMed1979

Influence of aging on left ventricular hemodynamics and stiffness in beagles.

We studied the influence of aging on the contractile performance, stiffness, and contraction time of the canine left ventricle. Eight young (27 +/- 2.5 months, mean +/- SE) and seven old (128 +/- 20.5 months) beagles were placed on complete cardiopulmonary bypass, the arterial pressure was adjusted to 80 mm Hg, and the heart contracted isovolumically at a paced rate of 120 beats/min. Diastolic pressure-volume curves were established for each unpaced left ventricle at the beginning of each experiment, and the volume at the knee of the curve was used during the subsequent data collection when the heart was paced. Stiffness was measured with a sinusoidal forcing function, which imposed a sinusoidal displacement of 1 ml at 20 Hz into a balloon placed in the left ventricle. In each ventricle, stiffness was related linearly to pressure during the cardiac cycle, and was greater for any given pressure in the older beagles. Contraction duration was prolonged in the older dogs. In an additional seven old beagles during right heart bypass time, and duration of contraction were longer than in seven young beagles. Aging of the beagle heart is associated with an increase in left ventricular systolic and diastolic stiffness and prolonged duration of contraction.

Aging↗
PubMed1979

Ryanodine: its alterations of cat papillary muscle contractile state and responsiveness to inotropic interventions and a suggested mechanism of action.

Cat right ventricular papillary muscles responded biphasically to cumulative additions of ryanodine. A progressive and pronounced negative inotropic effect was observed with low to intermediate ryanodine concentrations (5 nM-1 muM) while a rebound or reversal of these initial changes back toward pre-drug values was obtained as the ryanodine concentration was further increased to 100 muM. Active force development (DF), the rate of force development (dF/dt), as well as the rate of relaxation all exhibited these bidirectional changes. In contrast, time to peak force underwent only a progressive prolongation over the entire concentration range tested. This response pattern was observed with both normal and K+-depolarized (isoproterenol- or dibutyryl cAMP-restored) preparations. The response to a single addition of 100 muM ryanodine, in the presence of 2.5 mM Ca++ mimicked both the qualitative and quantitative aspects of the cumulative concentration response curve. In the presence of 5.0 mM Ca++ the high concentration of ryanodine no longer caused depression but instead caused only a slowly developing, monophasic increase in DF. Ryanodine also changed the response of ventricular muscle to other inotropic interventions. Ryanodine (1 muM; 2.5 mM Ca++) abolished the normal increase in dF/dt following either paired electrical stimulation (PES) or 50 mOsM mannitol, but not that in response to a doubling of the stimulation rate (0.2--0.4 Hz). After ryanodine exposure, the potentiation of developed force by PES was shifted from the first (regular) to the second (premature) contraction, producing a summation-like waveform. Prior addition of the calcium channel antagonist D600 (1 muM) did not alter ryanodine-induced changes in PES. Caffeine (1 mM) produced alterations in the responses to PES and hyperosmolarity which were similar to those observed with ryanodine. In the presence of high concentrations of both ryanodine (100 muM) and calcium (5 mM) both the transient and steady-state responses to a doubling of the stimulation rate (0.2--0.4 Hz) were markedly depressed, whereas the decrease in DF or dF/dt normally accompanying a reduction in the rate of stimulation was attenuated. The data obtained in the present study are consistent with a functional inhibition of sarcoplasmic reticular calcium release by ryanodine.

Alkaloids↗
PubMed1978

Species differences in responses to hyperosmolality and D600 in cat and rat heart.

The direct inotropic effect of hypertonic mannitol was compared in isolated rat and cat papillary muscles. The inotropic effects of paired electrical stimulation and D600 were also evaluated in the same species. At extracellular calcium concentrations of 2.5 mM, hypertonic mannitol (25--100 mosmol/kg H2O above normal) depressed contractility in isolated rat myocardium; hyperosmolality exerted a positive effect only when extracellular Ca2+ was low (e.g., 0.3 mM). Paired pacing exerted a small but significant inotropic effect in rat heart when extracellular Ca2+ was 2.5 mM, and a larger effect at lower Ca2+. As previously noted, hypertonic mannitol and paired pacing both produced significant positive effects in isolated cat heart at an extracellular Ca2+ concentration of 2.5 mM. D600 exerted less of a depressant effect on contractility in rat than in cat heart at concentrations of 10(-6)--10(-7) M. The data suggest that 1) in contrast to results in cat heart, the positive inotropic effect of hyperosmolality in isolated rat cardiac muscle is apparent only when extracellular calcium concentration is reduced; 2) the inotropic effect of paired pacing in rat heart is greatest at low Ca2+ levels, but persists to a lesser degree at extracellular calcium concentrations of 2.5 mM; and 3) D600-inhibitable calcium channels appear to be relatively less important in the maintenance of cardiac contractility in rat than in cat cardiac muscle.

Animals↗
PubMed1978

Inhibitory effect of hypertonic mannitol on vasoconstrictor and vasodilator responses of isolated coronary arteries.

The effect of hypertonic mannitol on pressor responses to vasoactive agents was studied in isolated canine coronary arteries perfused with physiologic salt solution at a constant flow. When perfusion pressure was increased with 60 mM KCl, mannitol (50 mosM) consistently caused a decrease in perfusion pressure that lasted for at least 1 h. Withdrawal of mannitol from the perfusion media was associated with a vasoconstrictor response that was not prevented by alpha- or beta-adrenoceptor blockade or by the presence of either nitroglycerin or norepinephrine. Hypertonic mannitol also reduced the responsiveness of the isolated smooth muscle preparations to several different mechanistically unrelated vasodilator agents. The mechanism(s) responsible for the paradoxical ability of hypertonic mannitol to reduce vascular responsiveness to both vasoconstrictor and vasodilator interventions in isolated canine coronary arteries is not known, but future studies should be directed at elucidating it as well as determining whether similar phenomena occur in vivo.

Animals↗
PubMed1977

Influence of mannitol on contractile responses of isolated perfused arteries.

The influence of hyperosmotic mannitol on vascular smooth muscle contractile responses was examined in isolated arterial preparations. Vasoconstrictor effects of norepinephrine (NE) and potassium chloride (K+) in the perfused central artery of the rabbit's ear and in perfused mesenteric arteries of cats were significantly inhibited by infusion with Krebs bicarbonate solution made hyperosmotic with mannitol (50-200 mosM increase). Similarly, the magnitude and duration of vasoconstrictor responses to transmural stimulation of the central ear artery of the rabbit were decreased by hyperosmotic mannitol (50 mosM). Mannitol (50 mosM) produced a decrease in perfusion pressure when perfusion pressure was maintained at an increased level by K+ (60 mM). Mannitol-induced vasodilatation was not affected by ethacrynic acid (1.5 X 10(-5) M), beta adrenergic blockade or by the development of tachyphylaxis to the vasodilator effects of nitroglycerin. The concentration of cyclic adenosine-monophosphate was not changed by mannitol. Isotonic mannitol also inhibited NE-induced contractile responses. These data indicate that hyperosmotic mannitol produces vasodilatation in isolated arterial smooth muscle by a mechanism(s) that appears dissimilar from that of several other vasodilator substances and suggest that hypertonicity may not be the only factor involved in the vasodilator effect of mannitol.

Animals↗
PubMed1977

Contraction and resting stiffness of isolated cardiac muscle: effects of inotropic agents.

The purpose of this study was to test the hypothesis that either hypoxia and its combined effects with extracellular calcium (Ca), digoxin, and ouabain, or these positive inotropic agents acting alone or in combination, influence contraction and resting stiffness of isolated papillary muscle. Stiffness was measured utilizing the sinusoidal forcing function technique. Neither an increase in extracellular calcium concentration (from 2.5 to 4.0 mM) nor digoxin or ouabain in either Ca concentration altered contraction or resting stiffness in the well-oxygenated environment. Resting stiffness for any given resting tension was increased at the end of hypoxia only in the presence of digoxin, and this occurred in both 2.5 mM Ca (P less than 0.02) and in 4.0 mM Ca (P = 0.05). Contraction stiffness for any given tension was increased in 2.5 mM Ca by hypoxia alone (P less than 0.05) and by hypoxia in the presence of digoxin (P less than 0.005) and ouabain (P less than 0.02), but was not increased in any experiments conducted in 4.0 mM Ca. The conclusions from these data are that certain experimental conditions of the study evoked different directional changes in stiffness and contractility. Further, changes in contraction stiffness are not always paralleled by changes in resting stiffness.

Animals↗
PubMed1977

Lanthanum probe studies of cellular pathophysiology induced by hypoxia in isolated cardiac muscle.

This study was undertaken to evaluate directly the relationship between evolution of irreversible myocardial injury induced by hypoxia in an isolated papillary muscle preparation and the development of pathophysiological alterations related to severely impaired membrane function. An ionic lanthanum probe technique was employed as a cytochemical marker to monitor the progression of cellular injury, and data from this cytologic technique were correlated with ultrastructure and measurements of contractile parameters in a total of 67 muscles subjected to control conditions or to graded intervals of hypoxia with or without reoxygenation. Marked depression of developed tension and rate of tension development occurred after 30 min of hypoxia. Contractile function showed significant recovery with reoxygenation after 1 h and 15 min of hypoxia but remained depressed when reoxygenation was provided after 2 or 3 h of hypoxia. Examination by transmission and analytical electron microscopy (energy dispersive X-ray microanalysis) revealed lanthanum deposition only in extracellular regions of control muscles and muscles subjected to 30 min of hypoxia. After hypoxic intervals of over 1 h, abnormal intracytoplasmic and intramitochondrial localization of lanthanum were detected. After 1 h and 15 min of hypoxia, abnormal intracellular lanthanum accumulation was associated with only minimal ultrastructural evidence of injury; muscle provided reoxygenation after 1 h and 15 min of hypoxia showed improved ultrastructure and did not exhibit intracellular lanthanum deposits upon exposure to lanthanum during the reoxygenation period. After 2 to 3 h of hypoxia, abnormal intracellular lanthanum accumulation was associated with ultrastructural evidence of severe muscle injury which persisted after reoxygenation. Thus, the data support the conclusion that cellular and membrane alterations responsible for abnormal intracellular lanthanum deposition precede the development of irreversible injury but evolve at a transitional stage in the progression from reversible to irreversible injury induced by hypoxia in isolated feline papillary muscles.

Animals↗