Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of decreasing pH from 7.40 to 6.20 on the tension developed by direct activation of the myofilaments and by Ca2+ release from the sarcoplasmic reticulum were studied comparatively in segments of single cells of skeletal muscle (frog semitendinosus) and cardiac muscle (rat ventricle) from which the sarcolemma had been removed by micro-dissection (skinned muscle cells). 2. The concentration of free Ca2+ in the solutions was buffered with ethylene glycol-bis (beta-aminoethylether N,N'-tetraacetic acid (EGTA). The change of the buffer capacity of a given [total EGTA] caused by varying pH and the uncertainty about the value of the equilibrium constant for Ca-EGTA have been taken into account in the interpretation of the results. 3. Decreasing pH from 7.40 to 6.20 produced an increase in the [free Ca2+] required for the myofilaments to develop 50% of the maximum tension by a factor of about 5 in skinned cardiac cells but of only 3 in skeletal muscle fibres. In addition, acidosis depressed the maximum tension developed in the presence of a saturating [free Ca2+] by approximately the same amount in the two tissues. 4. The pH optimum for loading the sarcoplasmic reticulum of skinned fibres from skeletal muscle decreased when the pCa (-log [free Ca2+]) in the loading solution decreased. The optimum was pH 7.40-7.00 for a loading at pCa 7.75, pH 7.00-6.60 at pCa 7.00 and pH 6.60-6.20 at pCa 6.00. 5. The pH optimum for loading the sarcoplasmic reticulum of skinned cardiac cells with a solution at pCa 7.75 was about pH 7.40 as in skeletal muscle fibres. But the cardiac sarcoplasmic reticulum could not be loaded with a [free Ca2+] much higher than pCa 7.75 because a higher [free Ca2+] triggered a Ca2+-induced release of Ca2+ from the sarcoplasmic reticulum. 6. The pH optimum of about 7.40 for the loading of the cardiac sarcoplasmic reticulum was also optimum for the Ca2+-induced release of Ca2+ from it. 7. It was concluded that the effects of acidosis on the cardiac sarcoplasmic reticulum accentuate the depressive action of decreasing pH on the myofilaments. This may explain the pronounced depression of contractility observed during acidosis in cardiac muscle. In contrast, a moderate acidosis causes an effect on skeletal muscle sarcoplasmic reticulum that could compensate for the depressive action on the myofilaments, which is, in addition, less pronounced than in cardiac muscle.
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PMID:Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiace and skeletal muscles. 2 57

Like all inhalation anesthetics, halothane (CF3CHBrCl) has a dose-dependent negative inotropic effect on cardiac muscle. The mechanism of the action has not been determined, although effects on glycolysis, mitochondrial respiration and calcium kinetics, and sarcoplasmic reticulum ATPase activity have been suggested. Previous studies of the effect of halothane on the ATPase of contractile protein suffered from design and dosing defects. We have measured ATP splitting by canine cardiac natural actomyosin using extraction and equilibration procedures described previously (Honig, C. R. and Reddy, Y. C. 1973, J. Pharmacol. 184: 330-338). Drug dosing calculations were facilitated by measurement of the partition coefficient of halothane in protein. Halothane shifted the Ca++ concentration effect curve for actomyosin ATPase activity to the right. The maximum depression occurred at pCa 7.0 or 6.5. The effect was dose dependent with less than 10 percent depression at threshold and 50-60 percent depression at peak. Enzyme inhibition was antagonized by high Ca++ concentration, and was reversed by removing halothane from the reaction mixture. We suggest that inhibition of ATP utilization by the contractile system may be a mechanism of the in vivo myocardial depression produced by halothane.
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PMID:Halothane decreases actomyosin ATPase activity: a possible mechanism of the negative inotropic effect. 12 60

The contractile properties and contractile protein enzymatic activity of skeletal muscle can be altered by neural influences. To determine whether similar influences apply to cardiac muscle, adult rats were chemically sympathectomized by intravenous injection of 6-hydroxydopamine (6-OHDA). After 2 weeks of treatment, rats were anesthetized and an index of myocardial contractility (max dP/dt) was measured in situ. Max dP/dt was depressed in 6-OHDA-treated rats [4560 +/- 420 (mean +/- SE) mm Hg/sec] when compared to controls (6710 +/- 580 mm Hg/sec). Sympathectomy was verified by reduced hemodynamic responsiveness to tyramine injections. After functional measurements had been completed, the heart was excised. Myofibrils were prepared from left ventricular tissue and analyzed for ATPase activity. Myofibrillar protein yield averaged 38 +/- 2 mg/g in controls and was not significantly different in 6-OHDA rats. Myofibrillar ATPase activity was 0.314 +/- 0.014 mumol P1/mg per min in controls. Enzyme activity was significantly reduced to 0.230 +/- 0.020 mumol P1/mg per min in 6-OHDA rats. The results demonstrate that a chronic reduction in sympathetic stimulation to the heart results in a depression of an index of myocardial contractile function which is accompanied by reduced myofibrillar ATPase activity. Acute (16-18 hours) chemical sympathectomy depressed the contractile function index without altering ATPase activity. Bilateral adrenalectomy produced no further decrement in myofibrillar ATPase activity in chronically (2 weeks) sympathectomized rats. Therefore, it appears that the changes in contractile protein enzymatic properties are mediated by sympathetic neural influences and may involve the synthesis of new contractile protein(s) with altered enzymatic properties.
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PMID:Myocardial contractile function and myofibrillar adenosine triphosphatase activity in chemically sympathectomized rats. 13 56

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.
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PMID:Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. 13 86

In Goldblatt rats (GV) 4-24 weeks after coarctation of one renal artery the following characteristics were registered as compared to controls (CV) of the same age: Arterial blood pressure increased to 190-200 mmHg in comparison to 105-110 mmHg in controls. This pressure overload induced an increase in ventricular weights (34%-54%). Noteworthy differences in myocardial water, total protein, and nonprotein substance contents were found. Hydroxyproline concentration in GV did not increase significantly until 24 weeks after onset of pressure overload. No significant alterations were detected in the relationship of myocardial, sarcoplasmic, and stromal protein fractions. However, greater changes could be registered in the concentration of the myofibrillar protein fraction and its single components. Furthermore, a correlative depression in specific actomyosin ATPase activity and in maximum shortening velocity of the unloaded cardiac muscle (2,3) was observed.
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PMID:Characteristics of the hypertrophied left ventricular myocardium in Goldblatt rats. 14 Jun 72

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.
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PMID:Normal cardiac myosin ATPase and mechanics in pressure overload with digitalis treatment. 14 32

Myocardial failure is uniformly fatal when associated with post-traumatic sepsis and multisystem failure. Controversy exists as to whether endotoxin has a direct effect on the myocardium. A nonanoxic isolated arterially perfused rabbit interventricular septum was used in this study to evaluate the effects of endotoxin, live E. coli, and endotoxin/septic shock plasma on myocardial function and ultrastructure. Purified E. coli endotoxin and live E. coli bacteria did not have a significant direct effect on rabbit cardiac muscle function or ultrastructure. Perfusion of the rabbit septum with plasma from rabbits exsanguinated following a 2-hour septic or endotoxin shock insult, however, caused significant (p less than 0.02) myocardial depression when compared with control septa perfused with normal rabbit plasma. Septa perfused with shock plasma demonstrated ultrastructural alterations of mitochondria that were not noted in control preparations.
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PMID:Myocardial depression in sepsis. 36 63

The nature of the myocardial depression observed in patients with septic shock, and in animals late in shock induced by endotoxin, is still under examination. These studies, in cats and kittens administered an LD80 dose of E coli endotoxin, were designed to examine the relationship between changes in myocardial contractility, in cellular electrophysiology and in ultrastructural morphology. There was no difference between tension developed in vitro by cardiac muscle removed from cats five hours after endotoxin administration and from cats not administered endotoxin. There was also no difference in their responses to calcium chloride or to anoxia. The action potential characteristics of ventricular muscle isolated from endotoxin treated cats were also not different from control, and ultrastructural damage was minimal and not extensive. Endotoxin (100 microgram/ml) had no effect on cardiac muscle in vitro, even after a one-hour contact time. It is concluded that the integrity of the myocardium is maintained even late in shock and that endotoxin has no direct effects on the heart.
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PMID:Myocardial function in feline endotoxin shock: a correlation between myocardial contractility, electrophysiology, and ultrastructure. 49 26

An hemodynamic study has been performed in eight patients (age 68 +/- 7) suffering from complete atrioventricular block. They had to undergo the definitive implantation of a cardiac pace maker under general anesthesia. The fixed cardiac frequency may help to understand the effect of the anesthetic agent used on the cardiac muscle function. Ketamine is the only agent used directly at an initial intravenous dose of 3 mg.kg-1 followed by a perfusion in a constant rate of 0.20 mg.kg-1. min-1. Hemodynamic data (arterial pressure, pulmonary pressures, thermodilution cardiac output) are performed before induction, then every 5 minutes after induction for a 20 minute period. The absence of respiratory depression (PaCO2: 38 +/- 3 mm Hg) shows that hemodynamic changes are entirely due to ketamine. The peak of these changes takes place after 5 minutes (significant rise (p < 0.05) in systemic and pulmonary resistances, in systemic arterial pressure and in pulmonary arterial pressure). Stroke index decreases moderately. After 20 minutes all the parameters have returned to control values. Use of ketamine is not desirable for two reasons: 1 degree The rise of the afterload may alter the hemodynamic state which can be previously deteriorated in patients suffering from atrio-ventricular block. 2 degree Post-anesthetic agitation can displace the right ventricular electrode.
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PMID:[Ketamine anesthesia for definitive implantation of a cardiac pace maker (author's transl)]. 55 78

Clarification of the mechanisms of the myocardial depression produced by thiamylal was sought by studying the effect of thiamylal upon the sensitivity of contractile proteins to calcium (Ca2+), by using glycerinated muscle fibres from the canine right ventricle. The dose--response relationship between the concentration of Ca2+ and the force of contraction of the glycerinated cardiac muscle fibres was not shifted from the control curve by the administration of thiamylal 67 microgram ml-1. This result suggests that the changes in the sensitivity of contractile proteins to Ca2+ are not responsible for the depression of myocardial performance produced by thiamylal.
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PMID:Effect of thiamylal on the sensitivity of glycerinated cardiac fibres to calcium. 70 54


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