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PubMed1988

Prostacyclin biosynthesis and phospholipase activity in hypoxic rat myocardium.

Phospholipid metabolism was studied in rat myocardial slices that were incubated under normoxia or hypoxia for up to 24 hours. Phospholipid degradation was prominent in hypoxic myocardium, particularly phosphatidylcholine, which markedly decreased after 24 hours of hypoxia. In contrast, lysophosphatidylcholine increased. The mechanism of phospholipid degradation in hypoxic myocardium was studied. The highest activity for phospholipase A2 among subcellular fractions was found in microsomal fraction. In hypoxic myocardium, this phospholipase A2 activity markedly increased and had substrate specificity toward phosphatidylcholine and phosphatidylethanolamine. Phosphatidylcholine was slightly hydrolyzed in control myocardium, but it was markedly hydrolyzed in hypoxic myocardium. Phospholipase C activity was found in cytosol and had a high substrate specificity toward phosphatidylinositol. In hypoxic myocardium, its activity gradually decreased during hypoxic incubation. Prostacyclin biosynthesis was also determined. The synthesis of prostacyclin in hypoxic myocardial microsomes did not increase. These results suggest that hypoxia causes phospholipid degradation and activates phospholipase A2 activity.

Animals↗
PubMed1991

Effects of acidic fibroblast growth factor on normal and ischemic myocardium.

We sought to determine the effects of acidic fibroblast growth factor (FGF) on ischemic and normal myocardium and to determine whether direct application of acidic FGF to the heart could promote angiogenesis. Eighteen dogs underwent placement of an ameroid constrictor on the left anterior descending coronary artery (LAD). Three weeks later, a left internal mammary artery (IMA) pedicle was positioned over the LAD territory, with a sponge saturated with acidic FGF (n = 12) or saline (n = 4) interposed between the pedicle and the heart. Polytetrafluoroethylene fiber or collagen I sponges were used to deliver the acidic FGF. Weekly angiography of the IMA was performed in all dogs, but significant IMA to coronary collaterals were not demonstrable in any dog. Eight dogs had histological evidence of subendocardial infarction in the LAD territory (five acidic FGF, three control, p = NS). Striking smooth muscle cell hyperplasia was present in arterioles and small arteries exclusively in areas of subendocardial infarction in all of the acidic FGF-treated dogs but in none of the control dogs (p less than 0.05). Noninfarcted myocardium appeared normal in all dogs. In two additional dogs, ameroid constrictors were not placed on the LAD, such that acidic FGF-treated sponges were placed on normally perfused myocardium of the LAD territory. Histological evaluation of those hearts revealed normal myocardium, without evidence of myocardial infarction or smooth muscle cell hyperplasia. Thus, when acidic FGF is delivered to the myocardium via an epicardial sponge in dogs whose coronary flow is compromised, acidic FGF does not cause an angiogenic response in viable myocardium but causes vascular smooth muscle cell hyperplasia in areas subjected to ischemic injury.

Animals↗
PubMed1985

Metabolic fate of extracted glucose in normal human myocardium.

Glucose is an important substrate for myocardial metabolism. This study was designed to determine the effect of circulating metabolic substrates on myocardial glucose extraction and to determine the metabolic fate of glucose in normal human myocardium. Coronary sinus and arterial catheters were placed in 23 healthy male volunteers. [6-14C]Glucose was infused as a tracer in 10 subjects. [6-14C]Glucose and [U-13C]lactate were simultaneously infused in the other 13 subjects. Simultaneous blood samples were obtained for chemical analyses of glucose, lactate, and free fatty acids and for the the isotopic analyses of glucose and lactate. Glucose oxidation was assessed by measuring myocardial 14CO2 production. The amount of glucose extracted and oxidized by the myocardium was inversely correlated with the arterial level of free fatty acids (r = -0.71; P less than 0.0001). 20% (range, 0-63%) of the glucose extraction underwent immediate oxidation. Chemical lactate analysis showed a net extraction of 26.0 +/- 16.4%. However, isotopic analysis demonstrated that lactate was being released by the myocardium. In the 13 subjects receiving the dual-carbon-labeled isotopes, the lactate released was 0.09 +/- 0.04 mumol/ml and 49.5 +/- 29.5% of this lactate was from exogenous glucose. This study demonstrates that the circulating level of free fatty acids plays a major role in determining the amount of glucose extracted and oxidized by the normal human myocardium. Only 20.1 +/- 19.4% of the glucose extracted underwent oxidation, and 13.0 +/- 9.0% of the glucose extracted was metabolized to lactate and released by the myocardium. Thus, 60-70% of the glucose extracted by the normal myocardium is probably stored as glycogen in the fasting, resting state.

Adult↗
PubMed1998

Basic fibroblast growth factor increased regional myocardial blood flow and limited infarct size of acutely infarcted myocardium in dogs.

Basic fibroblast growth factor (bFGF), a growth factor potent in promoting angiogenesis, has been shown to reduce infarct size in experimentally induced acute myocardial infarction. However, the effect of bFGF on regional myocardial blood flow (Qm) in the acutely infarcted myocardium has not been well clarified. In 20 open-chest dogs, the left anterior descending (LAD) coronary artery was occluded and animals were maintained in this condition for 4 weeks. In eight of these dogs, bFGF (300 microg) was injected into the myocardium supplied by the LAD and the artery was ligated (bFGF group), and in the other 12 dogs, saline was injected (control group). Nonradioactive colored microspheres were used to measure Qm. The amount of viable myocardium as percent of visual field in the microscope and the extent of fibrosis scored histologically from 0 to 5 in the infarcted area 4 weeks after occlusion were measured. In the outer layer, the Qm values immediately after and 4 weeks after occlusion were 26 +/- 2% and 70 +/- 6%, respectively, in the control group, and 46 +/- 5% and 121 +/- 13%, respectively, in the bFGF group. The Qm at both times in the bFGF group was significantly higher than the corresponding control group values (p < 0.01). The Qm at 4 weeks in the inner and the middle layers also significantly increased in the bFGF group. There was more viable myocardium (control vs bFGF group; 41 +/- 5 vs 61 +/- 7%, p < 0.05) and less fibrosis (3.1 +/- 0.2 vs 2.0 +/- 0.4, p < 0.01) at the outer layer in the bFGF group. It was found that bFGF caused a marked increase in Qm, an increase of viable myocardium, and a decrease of fibrosis in the infarcted myocardium in dogs.

Animals↗
PubMed2002

Mibefradil improves beta-adrenergic responsiveness and intracellular Ca(2+) handling in hypertrophied rat myocardium.

The present study investigated the effects of mibefradil, a novel T-type channel blocker, on ventricular function and intracellular Ca(2+) handling in normal and hypertrophied rat myocardium. Ca(2+) transient was measured with the bioluminescent protein, aequorin. Mibefradil (2 microM) produced nonsignificant changes in isometric contraction and peak systolic intracellular Ca(2+) concentration ([Ca(2+)](i)) in normal rat myocardium. Hypertrophied papillary muscles isolated from aortic-banded rats 10 weeks after operation demonstrated a prolonged duration of isometric contraction, as well as decreased amplitudes of developed tension and peak Ca(2+) transient compared with the sham-operated group. Additionally, diastolic [Ca(2+)](i) increased in hypertrophied rat myocardium. The positive inotropic effect of isoproterenol stimulation was blunted in hypertrophied muscles despite a large increase in Ca(2+) transient amplitude. Afterglimmers and corresponding aftercontractions were provoked with isoproterenol (10(-5) and 10(-4) M) stimulation in 4 out of 16 hypertrophied muscles, but were eliminated in the presence of mibefradil (2 microM). In addition, hypertrophied muscles in the presence of mibefradil had a significant improvement of contractile response to isoproterenol stimulation and a reduced diastolic [Ca(2+)](I), although a mild decrease of peak Ca(2+)-transient was also shown. However, verapamil (2 microM) did not restore the inotropic and Ca(2+) modulating effects of isoproterenol in hypertrophied myocardium. Mibefradil partly restores the positive inotropic response to beta-adrenergic stimulation in hypertrophied myocardium from aortic-banded rats, an effect that might be useful in hypertrophied myocardium with impaired [Ca(2+)](i) homeostasis.

Adrenergic beta-Agonists↗
PubMed1982

beta-Adrenergic receptors and catecholamine sensitive adenylate cyclase in developing rat ventricular myocardium: effect of thyroid status.

The present study was designed to describe the relationships among thyroid status, myocardial growth and myocardial beta-adrenergic receptors in the developing rat ventricle. In normal rat myocardium the beta-adrenergic binding capacity (Bmax) for (-)-[3H] DHA decreased with increasing age and heart size. In order to determine the effect of thyroid status on ventricular growth characteristics and beta-adrenergic receptors, animals were rendered: (1) hypothyroid with propylthiouracil (PTU), (2) euthyroid with PTU and daily thyroxine (T4) replacement, (3) hyperthyroid for several days with daily thyroxine injections or (4) normal controls with sham saline injections. Growth characteristics were similar in euthyroid and normal rat myocardium; ventricular weight, protein and DNA content were similar at postnatal days 5, 15 and 28. Growth in hypothyroid pups was normal until postnatal day 14 at which time the heart weight and protein content were significantly lower than in normal or euthyroid pups, whereas the number of beta-adrenergic receptors was decreased in hypothyroid myocardium at all ages studied. On postnatal day 5 the (-)-[3H]DHA binding (Bmax) was 37 +/- 9 in hypothyroid myocardium compared to 63 +/- 8 fmole per mg protein mean +/- S.D. in euthyroid myocardium. The function of the beta-adrenergic receptors was also decreased in hypothyroid as compared to euthyroid or normal myocardium as demonstrated by a decrease in maximal catecholamine sensitive adenylate cyclase activity in myocardial membranes at 28 days of age. Treatment of hypothyroid or normal pups with T4 resulted in an increase in heart size, protein content and beta-adrenergic receptors. Ventricular DNA content, which describes hyperplastic growth, was not decreased in hypothyroid rats demonstrating that postnatal hypertrophic but not hyperplastic ventricular growth is dependent on thyroid hormone.

Adenylyl Cyclases↗
PubMed1994

Sodium-calcium exchange in neonatal myocardium: reversible inhibition by halothane.

Neonatal myocardium is distinctly more sensitive to extracellular calcium levels than is mature myocardium. This has been ascribed to the poorly developed sarcoplasmic reticulum of neonatal myocardium. Recent evidence has suggested that there is an increased dependence of neonatal myocardium on the sodium-calcium exchange current, and that sodium-calcium exchange may be a major source of calcium influx in neonatal myocardial cells. We determined the effect of halothane on the sodium-calcium exchange current on single neonatal (2- to 5-day-old) rabbit ventricular myocytes by means of the whole cell voltage clamp. Lower (1.5%) halothane decreased sodium-calcium exchange current by 49%, from 29 +/- 3 to 15 +/- 6 pA. Higher (3%) halothane decreased this current by 66%, from 50 +/- 9 to 17 +/- 9 pA. Thus halothane has a reversible inhibition of sodium-calcium exchange current in neonatal myocardium. Inhibition of sodium-calcium exchange current would be expected to have a magnified effect on contractility in neonatal as opposed to adult myocardium, and could theoretically ameliorate reperfusion injury due to influx of calcium via the sodium-calcium exchanger.

Animals↗
PubMed1989

The protection of the acute ischemic myocardium: merits and demerits of the coronary reperfusion.

At first, in order to know the causes of reperfusion injury, we studied myocardial injury by reperfusion in comparison with by Ca overloading, and the salvage of the myocardium from reperfusion and from Ca overloading by Ca antagonist, diltiazem (DIL), in 52 anesthetized open-chest dogs. In myocardial mitochondria (Mit), Ca content was increased and Mg content and oxidative phosphorylation (State III) were decreased both by 120 min reperfusion after 60 min occlusion and by Ca overloading. Ca and Mg contents and oxidative phosphorylation of Mit were similarly changed by reperfusion as by Ca overloading. Electron-microscopically, myocardial injury by Ca overloading resembled reperfusion injury. Therefore, Ca inflow to myocardial cells may be one of the determinant factors which induce reperfusion injury. Although myofibrils were disorganized and contraction band necrosis appeared in these two types of myocardial injury, amorphous densities and glanular densities which indicated the irreversible injury of Mit appeared only in reperfusion injury. Then, the myocardial injury by Ca overloading is suspected of being mainly composed of the injury of myofibrils. The myocardial injury by reperfusion and by Ca overloading was prevented by DIL. These facts suggest that DIL may suppress Ca inflow and Mg outflow to myocardial cells. Second, to know the effect of positive inotropic agents on pump failure in acute myocardial infarction, we studied the effect of dobutamine (DOB) on the ischemic myocardium and the salvage of the ischemic myocardium from DOB-induced injury by DIL in 39 anesthetized open-chest dogs. After occlusion, the regional mechanical function of the acute ischemic myocardium was rapidly lost and % systolic shortening was negative level. In this situation, myocardial Pco2 quickly increased and myocardial pH rapidly decreased. These parameters reached peak level after 20 min occlusion. Then, paradoxical improvement phenomenon appeared so that Pco2 decreased and pH increased after that. Myocardial blood flow measured by thermocouples was stable at almost 10% of the preoccluded level for a 90 min occlusion. These data suggest that anaerobic metabolism and residual aerobic metabolism can not supply the ischemic myocardium with enough energy and that irreversible injury may appear in the ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Pathophysiology and pathogenesis of contractile failure in stunned myocardium.

To investigate excitation-contraction coupling in stunned myocardium, intracellular free calcium concentration [( Ca2+]i) was measured before and after ischemia in perfused hearts using gated 19F NMR and the Ca2+ indicator 5F-BAPTA. Maximal Ca(2+)-activated force was also measured in parallel experiments. Stunned myocardium was created by reperfusion after 15 min global ischemia at 37 degrees C in isolated ferret hearts. In stunned myocardium, peak [Ca2+]i was paradoxically higher than that in control, but maximal Ca(2+)-activated pressure was lower in stunned hearts. These results indicate that contractile failure in stunned myocardium is due to a decrease in the myofilament sensitivity to Ca2+ as well as to a decrease in maximal Ca(2+)-activated force; failure of activator Ca2+ delivery cannot be implicated. The role of intracellular calcium overload in the pathogenesis of stunned myocardium was also investigated. Time-averaged 19F NMR measurements directly revealed the increase in [Ca2+]i during ischemia and in the early phase of reperfusion. The strategies to prevent Ca overload during reperfusion with modified reperfusate succeeded in preserving contractile function. Transient Ca overload without ischemia induced by different causes, i.e., high [Ca]0 perfusion, ventricular fibrillation or treatment with adriamycin, also produced contractile dysfunction that outlasted the interventions themselves. Thus, we propose that transient Ca overload during ischemia and early reperfusion initiates long-lasting contractile dysfunction in stunned myocardium.

Animals↗
PubMed2006

Focalized contractile impairment at hypertrophied myocardium proven in consideration of wall stress in patients with hypertrophic cardiomyopathy.

In hypertrophic cardiomyopathy (HCM) a hyperkinetic state is sometimes observed in spite of impaired systolic function in the hypertrophied myocardium. The aim of the present study was to determine the mechanism of this paradox. Seventeen patients with HCM and 10 normal subjects underwent cine magnetic resonance (MR) imaging to measure percent systolic wall thickening and percent fractional shortening. The ratio of systolic radial wall stress of the LV at the hypertrophied myocardium over that at the nonhypertrophied myocardium was evaluated to describe the focal advantageous condition for wall thickening. The ratio was 0.66 +/- 0.36 at the start of contraction and 0.78 +/- 0.31 at early-systole, indicating consistently smaller radial wall stress at the hypertrophied myocardium. Although the condition for contraction was favorable (a ratio less than 1.00), percent systolic wall thickening at the hypertrophied myocardium (23.0 +/- 11.8%) was smaller than that at the nonhypertrophied myocardium (70.5 +/- 32.3%). Smaller end-diastolic dimension (HCM group; 45.2 +/- 4.2 mm, reference group; 48.9 +/- 4.1 mm, P = 0.04) with a statistically identical value of systolic decrease in intraventricular dimension (HCM group; 19.7 +/- 3.9 mm, reference group; 18.9 +/- 3.2 mm, P = 0.60) yielded high percent fractional shortening in patients with HCM (43.5 +/- 7.6%). Although contractile impairment was proven at the hypertrophied region with low radial wall stress in the HCM group, the smaller end-diastolic dimension in this group resulted in high percent fractional shortening.

Cardiomyopathy, Hypertrophic↗
PubMed2002

Decreased expression of Na+/H+ exchanger isoform 1 (NHE1) in non-infarcted myocardium after acute myocardial infarction.

Although cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in non-infarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury.

Animals↗
PubMed2005

Hibernating myocardium in heart failure.

Ischemic left ventricular systolic dysfunction may result from myocardial necrosis or from hypocontractile areas of viable myocardium. In some cases, recovery of contractility may occur on revascularization--this reversibly dysfunctional tissue is commonly referred to as hibernating myocardium. Observational data suggest that revascularization of patients with ischemic left ventricular systolic dysfunction and known viable myocardium provides a survival benefit over medical therapy. Identification of viable, dysfunctional myocardium may be especially worthwhile in deciding which patients with ischemic left ventricular systolic dysfunction will benefit from revascularization procedures. Randomized, prospective trials evaluating this are currently ongoing. This review will provide an overview of the complex pathophysiology of viable, dysfunctional myocardium, and will discuss outcomes after revascularization. Of the techniques used to determine the presence of hibernating myocardium, functional methods such as stress echocardiography and cardiac magnetic resonance appear more specific, but less sensitive, than the nuclear modalities, which assess perfusion and metabolic activity. Currently, the availability of all methods is variable.

Heart Failure↗
PubMed1999

[The basis of chronic ischemic reversible left ventricular dysfunction (hibernating myocardium)].

The term "Hibernating myocardium" refers to the presence of a chronic left ventricular dysfunction that could be partially or completely improved after revascularization. Formerly, the myocardial hibernation was considered to be an adaptive response to a sustained reduction of the resting myocardial blood flow. Recently, several studies with positron emission tomography have revealed a normal or almost normal resting myocardial blood flow. The reduced coronary flow reserve of the hibernating myocardium brings about multiple episodes of demand-induced ischemia and may evoce recurrent stunning of the myocardium. It is the basis of structural changes in the myocardium and the contractile dysfunction. Cellular degeneration rather than adaptation prevails in the hibernating myocardium. The longer the process continues, the smaller is the chance for a complete structural and functional recovery after the reperfusion. Thus the early revascularization becomes important for the patients with hibernating myocardium.

Chronic Disease↗
PubMed1996

[Effects of simulated weightlessness on ultrastructures and oxygen supply and consumption of myocardium in rats].

Weightlessness causes atrophy of myocardium in rats, however, properties of ultra-structural changes and oxygen supply and consumption in myocardium are still unclear. Changes in ultrastructures of left ventricular myocardium in rats tail-suspended for 8W were observed. Qualitative analysis showed that the lysosomes, lipofuscins and degenerate mitochondria increased in myocytes of left ventricle in tail-suspended rats (SUS). The sarcoplasmic reticula were reduced in quantity and shrunken in appearance. The number of extended endothelial projections into the lumen of capillaries increased. Quantitative analysis showed that volume densities of mitochondria and sarcoplasmic reticulum in SUS were reduced by 14.5% and 22.2%, respectively. The number density of mitochondria also had a 12.5% decrease in SUS. The morphometric data-estimated oxygen demand of the myocardium in SUS showed a 16.7% decrease. These results suggested that the feature of the changes be chronic degeneration without the evidence of acute hypoxia in myocardium. The decrease of oxygen consumption of myocardium in SUS didn't cause a reflex reduction in the oxygen supply.

Animals↗
PubMed2002

[Cell transplantation of 5-aza cytidine induced bone marrow stromal cells transfected by angiogenin gene ex vivo into infarcted myocardium, an experimental study].

OBJECTIVE: To investigate the effect of transfection of 5-aza cytidine (5-aza) induced BMSCs that were transfected with Ad. ANG ex vivo into infarcted myocardium. METHODS: Lewis rat BMSCs were cultured in vitro and incubated together with 5-aza (3 micro mol/l) for 24 hours, and the induced BMSCs were transfected with Ad. ANG with a infection multiple of 50. ELISA method was applied to assay the expression and secretion of ANG in the medium. Then such BMSCs expressing ANG were transplanted into the ischemic myocardium of 14 Lewis rats whose left descending branch of coronary artery had been ligated 4 weeks ago (Group I). Eight rats with infarcted myocardium were transplanted with such BMSCs too (group II). Another eight rats received only Ad. ANG injection (group III). Twelve rats receiving serum-free medium injection were used as controls (Group IV). Four weeks after the ligation of LDA (for group I) and 4 weeks after the beginning of experiment (for all groups), the parameters of heart function, such as ejection fraction (EF) and end-diastole volume of left heart (EDLV), were examined by echocardiography. Four weeks after the beginning of experiment, the rats were killed, and the survival and differentiation of transplanted BMSCs and angiogenesis were observed by immunohistochemistry and transmission electron micrography. RESULTS: One day after the beginning of experiment, the concentration of ANG in the supernatant of medium was 162 +/- 10 pg/ml, significantly higher than that in the supernatant of medium in control group (86 +/- 5 pg/ml, P < 0.01). The concentration of ANG gradually increased and reached its peak at the 4th to 7th day; ANG could still be assayed 15 days later. 4 weeks after the transplantation, most of the 5-aza-induced BMSCs in group I and group II had differentiated into cardiomyogenic cells in the transplanted area. The EF value was 0.42 +/- 0.114 weeks after ligation of LAD, and was 0.69 +/- 0.034 weeks after the transplantation in group I. The EF value was 0.46 +/- 0.06 at the beginning of experiment and was 0.64 +/- 0.144 weeks after the transplantation in group II. The improvement of EF in Group I was significantly than that in other 3 groups (P < 0.05 or P < 0.01). The number of new vessels in group I was 36.3/high-power field (HPF), significantly higher than those in the other three groups (10.5/HPF in Group II, 23.1/HPF in Group III, and 0.9/HPF in Group IV). CONCLUSION: Induced by 5-aza, BMSCs differentiate into cardiomyogenic cells in infracted myocardium. ANG-expressing BMSCs transplantation is one of the safe and beneficial new strategies for repairing damaged myocardium and enhancing angiogenesis in ischemic myocardium.

Animals↗
PubMed1976

[Morphological analysis of the adaptive changes in the myocardium under individually measured physical load].

Studying morphological changes of the myocardium in the organic, cellular and subcellular levels of experimental animals (dogs) has shown that standard physical load on tradmill band graded only by external parameters of work (time of running, its speed etc.) causes different changes in different animals. In contrast to it, the method of individually graded physical load proposed by the author (1970, 1972) considers the depth of myocardium responses, the degree of its morphofunctional changes corresponding to certain stages of changes in the parameters of cardio-vascular activity and respiratory system. Using the relationship of pulse rate and frequency of respiration as a diagnostic test made it possible to establish 6 stages of myocardium responses to physical load. Each of these stages has a complex of morpho-functional changes in the myocardium and corresponds to certain adaptive shifts on the organism level. On these foundations one can prognoze the depth of morphological changes in the myocardium basing upon diagnostic tests. So, the proposed experimental model of individual selection of the value of physical load according to responses of the organism rather than to external parameters of work as well as the established principle of the stage character of adaptive responses may be used in the practice of investigators for directed influence on the myocardium to form its certain qualities.

Adaptation, Physiological↗
PubMed2003

[Remodeling myocardium and skeletal muscle in chronic heart failure].

The spread and progression of chronic heart failure (CHF) is viewed presently from the standpoint of remodeling the myocardium and skeletal peripheral vessels. However, it is not clear yet, if such remodeling is a common adaptive mechanism in CHF for the myocardium and skeletal muscle. The study aim was to investigate the morphological changes in the myocardium and their interrelations with the skeletal muscle condition in CHF patients. For this purpose the biopsy materials of the left ventricle and pectoral muscles obtained from 36 patients with CHF (functional classes I-IV according to NYHA) of various etiologies as well as biopsy materials of the rectus abdominal muscle obtained from 8 patients without CHF were examined by light and electron microscopy. It was established that the development and progression of CHF is accompanied by similar changes in the morphology of the myocardium and skeletal muscle at the tissue, cellular and subcellular levels. As CHF aggravates, the manifestations of hypertrophy and heteromorphism of tissue fibers equally progress in the myocardium and skeletal muscle. A reliable correlation was detected between changes of cellular-stromal ratio in the myocardium and in the skeletal muscle (r = 0.57; p < 0.05).

Adult↗
PubMed1976

[Maximum velocity of load-free shortening Vmax, myocardial capacity and "contractility indices" in the hypertrophic myocardium].

Based upon literature and our own experimentation on Goldblatt rats, the significance of a decrease of the maximal shortening velocity of the myocardium at zero load (Vmax) in the hypertrophied, chronically pressure-loaded heart is discussed. In the hypertrophied myocardium with varying concentrations of the contractile structures, the developed tension under isometric conditions (sigma) and the maximum rate of tension development (d sigma/dtmax) can indicate significant deviations from the values of controls of the same age, without, however, making it possible to draw from these changes absolute conclusions about the elementary contractile process. With the enhanced concentration of contractile proteins, the mentioned isometric values, as well as the maximum instantaneous power (cross-sectionally related) of the myocardium can be increased during a stage of hypertrophy in which Vmax is already reduced. The decrease of Vmax shows a rough correlation with the reduction of the specific ATPase activity of actomyosin and is already observed at moderate degrees of hypertrophy (30 to 50%). The time course of the change of both parameters in experimental hypertrophy suggests a causal relation between the changes of those two parameters and the failure of the myocardium in later stages of a chronic overload. Under the condition of reliable estimation, Vmax allows for, also with changed actomyosin concentration, an assessment of the elementary contractile process. On the other hand, Vmax does not present a sufficient measure for the cross-sectionally related power capacity of the hypertrophied myocardium. The possible dissociation between the unloaded shortening velocity and the cross-sectionally related power capacity could, in certain cases, explain an unsatisfactory correlation between Vmax and the clinical state of the heart. The so-called empirical indices of contractility, which are not always clearly related to basic physiological characteristics of the myocardium, should be interpreted with particular reserve in relation to the hypertrophied cardiac muscle.

Actomyosin↗