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P B Hultgren

Publications and source records attributed to P B Hultgren.

9 recordsLinked to original sources
PubMed1992

Reduced isotonic sarcomere shortening in rabbit right ventricular pressure overload hypertrophy.

We found previously that sarcomere shortening was reduced in hypertrophied rabbit right ventricular (RV) trabeculae, even when total isometric force and damaged end compliance were the same as normal. Here we studied isotonic shortening of similar preparations force-clamped with a servomotor. A force clamp holds the length of damaged end compliance constant. Sarcomere length (SL) was measured with laser diffraction in twitches with single and optimally paired stimuli. delta SL was sarcomere shortening divided by SL at the onset of shortening. Muscle shortening divided by unloaded muscle length (ML) at the onset of shortening was delta ML. RV hypertrophy was produced with pulmonary artery constriction in 11 rabbits and there were eight normal rabbits. delta SL was smaller than normal in hypertrophy, but delta ML was unchanged from normal. delta SL/delta ML in hypertrophy, 0.90 +/- 0.02, was significantly less than normal, 2.40 +/- 0.07 (mean +/- S.E.M.) (P less than 0.01). delta SL/delta ML did not depend on sarcomere shortening, load, time during shortening or stimulus pattern. Therefore, the reduced delta SL in hypertrophy was independent of contractile state parameters. The ratio was also independent of resting SL (normal = 2.29 +/- 0.07 microns; hypertrophy = 2.23 +/- 0.03 microns; P greater than 0.05) or where diffraction was sampled along central muscle length. One explanation for the findings includes reduced compliance of series viscoelastic elements within the central undamaged region of a hypertrophied muscle. This explanation is consistent with changes from normal in myocardial mechanics and connective tissue in cardiac hypertrophy. Ventricular function remains adequate in hypertrophy without heart failure perhaps because reduced delta SL/delta ML in hypertrophy results in less sarcomere work at any level of muscle work.

Animals↗
PubMed1986

Sarcomere shortening in pressure overload hypertrophy.

Sarcomere shortening during contraction was measured by using laser diffraction, in thin, rabbit right ventricular (RV) trabeculae from normal hearts (N) (n = 5) and from hearts subjected to RV pressure overload by pulmonary banding (H) (n = 5). Banding resulted in substantial RV hypertrophy after 2 wk. Hypertrophied preparations had the same resting muscle length (H = 3.15 +/- 0.29 mm) and resting sarcomere lengths (H = 2.16 +/- 0.005 micron) as the normal preparations (3.10 +/- 0.37 mm, 2.16 +/- 0.008 micron, respectively). Total tension at the peak of isometric twitches was the same as normal in the hypertrophied muscles (N = 8.06 +/- 1.20, H = 8.51 +/- 1.95 g/mm2). However, the amount of auxotonic sarcomere shortening was much less than normal in the hypertrophied preparations (N = 0.39 +/- 0.028, H = 0.19 +/- 0.034 micron; P less than 0.001). In isotonic contractions in which the ratio of muscle shortening to resting muscle length was the same in both the normal and hypertrophied muscles (ratio of 0.05 in both groups), the extent of sarcomere shortening relative to resting sarcomere length was less in the hypertrophied muscles than in the normal preparations (N = 0.14 +/- 0.01), H = 0.07 +/- 0.01; P less than 0.01). Series elasticity was the same as normal in the hypertrophied muscle P less than 0.05). Less auxotonic sarcomere shortening for a given level of isometric tension development and less isotonic sarcomere shortening per unit muscle shortening indicate that there is less than normal work per sarcomere during contraction in hypertrophied myocardium. These findings may have important implications for intracellular compensatory adaptation in pressure overload cardiac hypertrophy.

Animals↗
PubMed1985

Decreased auxotonic sarcomere shortening in hypertrophied rabbit myocardium.

Auxotonic sarcomere length change occurs during isometric twitches of isolated cardiac muscle preparations. To assess the amount of internal work in hypertrophied myocardium, we measured auxotonic sarcomere length change during isometric tension development over a range of initial muscle and sarcomere lengths. Hypertrophy was produced by banding the pulmonary artery, which resulted in an increase in the ratio of right ventricular free wall weight to total ventricular weight (normal 0.19 +/- 0.004; hypertrophy 0.35 +/- 0.008; P less than 0.001). Right ventricular free wall trabeculae and papillary muscles were studied with optical and mechanical instrumentation, including a helium-neon laser, to measure sarcomere length and isometric twitch parameters. The resting sarcomere length-resting tension relationship was shifted to the left of normal in the hypertrophied preparations (P less than 0.001). The relationship of sarcomere length at the peak of the twitch with total tension at the same instant was shifted downward and to the right of normal in hypertrophy (P less than 0.01). For the same amount of total tension development there was less than normal sarcomere shortening in the hypertrophied preparations (P less than 0.001). Consequently, there is less than normal work per sarcomere during auxotonic sarcomere shortening in hypertrophied heart muscle. Less sarcomere work for a particular functional state is important to consider in the assessment of the basis of myocardial function in compensated pressure overload hypertrophy.

Adaptation, Physiological↗
PubMed1981

Myocardial blood flow and mechanics in volume overload-induced left ventricular hypertrophy in dogs.

Chronic volume overload and subsequent left ventricular hypertrophy (LVH) were produced by a surgical shunt between the left subclavian artery and the left atrial appendage in eight dogs. A sham operation was performed on six control dogs. Analysis of biplane ventriculograms showed no significant differences in ejection fraction, mean wall stress, tension-time index, or stress-time index. A significant increase was found in stroke work per gram of left ventricle (P less than 0.005). Myocardial blood flow (MBF) was measured using 9 micrometers, radioactive microspheres at rest, at a constant treadmill workload (CWL) of 2 mph, 2% grade, and at a constant heart rate (CHR) of 175 beats.min-1. Total LVMBF (cm3.min-1) in the shunt dogs was increased at rest (P less than 0.05) with CWL (P less than 0.05) and a CHR (P less than 0.05). However, no differences were found between the groups in the LVMBF.g-1 of myocardium (cm3.g-1.min-1) at rest or during exercise, or in the endocardial to epicardial blood flow ration. Volume overload hypertrophy, without the presence of heart failure, is associated with normal haemodynamic and mechanical function at rest, normal LVMBF.g-1 of myocardium and normal flow distribution at rest and during exercise.

Animals↗
PubMedDate not supplied

Increased active elastic stiffness in tetanized papillary muscles from hypertrophied rabbit hearts.

Studies of skeletal muscle suggest that the ratio of stiffness to tension will increase in the presence of a slower rate of crossbridge head rotation from the attached perpendicular state (non-force generating) to the attached 45 degree angle state (force generating). Maximum shortening velocity is depressed proportionate with adenosinetriphosphatase activity in pressure overload cardiac hypertrophy. The maximum rate of isometric force generation also is less than normal but active isometric force levels are normal. The myosin isoenzymes of hypertrophied heart muscle are shifted to predominantly slower than normal types. Among a number of possibilities, the overall rate of crossbridge cycling may be less than normal and crossbridge head rotation may be slower. We reasoned that a greater than normal ratio of active elastic stiffness to total tension development in hypertrophy would be suggestive of an alteration from normal in crossbridge dynamics. We studied right ventricular septal papillary muscles from normal rabbits and from rabbits with hypertrophy induced by pulmonary artery constriction. A high level of mechanical activation was obtained by tetanizing the muscles in solutions containing caffeine. Small (less than or equal to 2% muscle length) and rapid (0.8 ms) length perturbations were applied to the preparations with a servo-controlled motor. Active elastic stiffness was estimated from the linear relationship of minimum (for releases) or maximum (for stretches) tension reached during a length change with muscle length change (strain). Although total tetanic tension development was normal in the hypertrophied muscles (p greater than 0.1), active elastic stiffness was greater than normal in hypertrophy (p less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Isotonic muscle and sarcomere shortening in rabbit right ventricular preparations.

Cardiac muscle fibers are suspended within and attached to an elaborate connective tissue matrix that includes numerous compliant interconnections. Myocardial muscle fibers are not branched, but connect at small angles to each other to form a branched array. Therefore, fiber shortening occurs as a vector within a connective tissue framework and individual fiber work may exceed external muscle work. To evaluate the latter we measured isotonic muscle shortening simultaneous with sarcomere shortening. The hearts were obtained from rabbits (n = 4) anesthetized with intravenous pentobarbital sodium. We isolated right ventricular trabeculae or free wall papillary muscles in Krebs-Ringer's solution (2.5 mM Ca2+, 28 degrees C). Cross-sectional area was 0.038 +/- 0.003 mm2 (+/- SE throughout) and resting sarcomere length was 2.33 +/- 0.12 microns. Sarcomere length was measured with laser diffraction (He-Ne, lambda = 632.8 nm) during force clamps in single- and paired-stimulation twitches. Relative sarcomere shortening (delta SL) was isotonic sarcomere shortening divided by sarcomere length at the onset of isotonic shortening. Relative muscle shortening (delta ML) was isotonic muscle shortening divided by muscle length at zero load; the latter was estimated from the stress-strain relation of elastic recoil at the onset of load clamps. Average delta SL/delta ML at peak shortening was 3.38 +/- 0.16 and was independent of stimulus pattern, isotonic load, amount of shortening, time during a twitch or laser beam position along a muscle. Therefore, the ratio greater than 1 was neither a function of activation nor heterogeneous sarcomere length change.(ABSTRACT TRUNCATED AT 250 WORDS)

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