Effects of Ischemic Preconditioning on the Left Ventricular Function, Myosin Isozyme, Myofibrillar ATPase Activity and Ultrastructure of the Rabbit Heart

Myocardial contractility and the enzymatic (ATPase) activity of cardiac contractile proteins were examined after exercise training using the chronically instrumented, unanesthetized dog as an experimental model. Before training, heart rate and the maximum rate of left ventricular pressure development (max dP/dt) were measured at rest and during submaximal exercise. Animals were then subjected to an 8- to 10-wk treadmill running program. Training was verified by the establishment of a 10- to 20-beat/min reduction in heart rate during submaximal exercise. After training max dP/dt was within normal limits at rest, but significantly elevated during submaximal exercise. When max dP/dt was plotted as a function of heart rate, either with the animal standing quietly on the treadmill or during submaximal exercise, a marked elevation in max dP/dt at any given heart rate was observed following training. Myofibrillar protein yield and ATPase activity values were nearly identical in left ventricles from exercise-trained and sedentary control dogs. Although exercise training by treadmill running improved contractile function in the unanesthetized dog myocardium, this response does not appear to involve alterations in myofibrillar ATPase activity.

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Nutritional modification of rat heart postnatal development

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1984.246.3.h332 ◽

1984 ◽

Vol 246 (3) ◽

pp. H332-H338 ◽

Cited By ~ 3

Author(s):

R. T. Dowell

Keyword(s):

Atpase Activity ◽

Postnatal Development ◽

Contractile Function ◽

Left Ventricular ◽

Activity Level ◽

Myofibrillar Atpase ◽

Fast Growing ◽

Growing Rats ◽

Myofibrillar Atpase Activity ◽

Slow Growing

Postnatal development of the mammalian myocardium encompasses increases in cellularity, energy producing and energy utilizing systems, and concurrent augmentation of heart contractile performance. The present study disrupted normal developmental sequences by adjusting the number of newborn rats per litter at 4 days postbirth. Fast-growing (4 rats/litter), normal (8 rats/litter), or slow-growing (16 rats/litter) animals were studied when 21 days old. Left ventricular cellularity (total DNA) increased as a function of the nutritionally modified growth of the heart, having values of 562 +/- 27, 625 +/- 33, and 791 +/- 20 (SE) micrograms in 16, 8, and 4 rats/litter groups, respectively. Low levels of systolic pressure (55 + 5 mmHg) and rate of pressure development (dP/dt, 2,670 +/- 130 mmHg/s) were noted in the slow-growing rats. Growth-related augmentation of pressure and dP/dt occurred such that adult levels (104 +/- 4 mmHg; 5,810 +/- 290 mmHg/s) were observed in 21-day-old, fast-growing rats. An enzymatic marker for aerobic metabolism (malate dehydrogenase) indicated mitochondrial accumulation in excess of ventricular tissue, thereby establishing progressive increases in aerobic capacity. Myofibrillar ATPase activity was not significantly different among all groups. Thus heart contractile function during nutritionally induced changes in postnatal development is augmented in proportion to increases in heart DNA content. A positive relationship also exists between dP/dt and number of mitochondria; however, enhanced contractile function is achieved independently of myofibrillar ATPase activity level.

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Endotoxin and myocardial failure: role of the myofibril and venous return

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.2.h150 ◽

1978 ◽

Vol 235 (2) ◽

pp. H150-H156 ◽

Cited By ~ 4

Author(s):

F. D. Bruni ◽

P. Komwatana ◽

M. E. Soulsby ◽

M. L. Hess

Keyword(s):

Atpase Activity ◽

Venous Return ◽

Normal Activity ◽

Left Ventricular ◽

Myofibrillar Atpase ◽

Myocardial Failure ◽

Myofibrillar Atpase Activity ◽

Myofibril Preparation

The effects of gramnegative endotoxin-induced myocardial failure in the pentobarbital-anesthetized dog were examined by monitoring its influence on cardiac myofibrillar ATPase activity. Myofibrils were isolated from endo- and epicardial portions of the left ventricular wall. ATPase activities were determined in animals treated with 4 mg/kg endotoxin and monitored 5 h, in animals monitored for 5 h without endotoxin (controls), and in animals implanted with a unilateral femoral shunt and given endotoxin. No differences were seen in the activities between the endo- and epicardial portions of any preparation. Activity was significantly depressed in endotoxemic animals. Increasing venous return by 313 +/- 71 ml/min significantly increased coronary flow by reducing coronary vascular resistance and prevented any observed depression of myofibrillar ATPase activity. In in vitro studies, adding endotoxin directly to a myofibril preparation did not modify normal activity. It appears that the mechanical and myofibrillar dysfunctions are due to the action of endotoxin at sites not associated with the actomyosin ATPase, but may be due to the production of an intermediary agent in concert with a decreased venous return.

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Altered Expression of Cardiac Myosin Isozymes Associated with the Malignant Hyperthermia Genotype in Swine

Anesthesiology ◽

10.1097/00000542-200011000-00026 ◽

2000 ◽

Vol 93 (5) ◽

pp. 1312-1319 ◽

Cited By ~ 3

Author(s):

Ying-Ming Liou ◽

Meei Jyh Jiang ◽

Ming-Che Wu

Keyword(s):

Atpase Activity ◽

Malignant Hyperthermia ◽

Myofibrillar Atpase ◽

Cardiac Myosin ◽

Long Term Effects ◽

Altered Expression ◽

Cardiac Symptoms ◽

Myofibrillar Atpase Activity ◽

Malignant Hyperthermia Susceptible ◽

Myosin Isozyme

Background Anesthetic-induced malignant hyperthermia (MH) in humans and pigs is associated with dramatic alterations in cardiac function. However, it remains controversial as to whether MH-associated cardiac symptoms represent a primary difference of myocardium or a secondary alteration consequent to increases in the hyperthermic stress. Here the authors describe changes in myosin isoform expression in the hearts of MH-susceptible pigs with and without prior exposure to halothane. Methods One group of pigs was diagnosed as MH susceptible by halothane challenge and Hal-1843 nucleotide examination. To determine if there is an effect of halothane exposure, another group of pigs was diagnosed by simple MH genotyping without exposure to halothane. After diagnosis and genotyping, animals with and without exposure to halothane were killed to study cardiac myosin isozyme distributions, cardiac myofibrillar adenosine triphosphatase (ATPase) activity, and the steepness of the Ca2+-ATPase activity relation in the hearts of normal and susceptible pigs. The altered myosin isozyme expression was analyzed by pyrophosphate gel electrophoresis. Results Malignant hyperthermia-susceptible animals with the prior halothane challenge showed an increased V1 myosin (-44%) expression, increased myofibrillar ATPase activity (-25%) and increased steepness of the Ca2+-ATPase activity relation. Without exposure to halothane, no change of myofibrillar ATPase activity was found in the hearts of different genotyped pigs, but there was a small increase in expression of V1 myosin (-5%) in the mutant (TT). Conclusions The potential modulation of V1 myosin expression occurs in the hearts of MH-susceptible pigs. The added stress by halothane challenge would further cause a V3 --> V1 shift, which may be attributed to the long-term effects of hyperthermic stress.

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