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Saturday, April 18, 2020 | History

3 edition of Developmental changes in myocardial intropic responsiveness found in the catalog.

Developmental changes in myocardial intropic responsiveness

Michael Artman

Developmental changes in myocardial intropic responsiveness

  • 155 Want to read
  • 7 Currently reading

Published by R.G. Landes in Austin .
Written in English

    Subjects:
  • Myocardium -- Growth.,
  • Myocardium -- Effect of drugs on.,
  • Pediatric cardiology.,
  • Myocardial Contraction -- physiology.,
  • Myocardial Contraction -- drug effects.,
  • Cyclic AMP -- metabolism.,
  • Cardiotonic Agents -- pharmacology.,
  • Heart -- growth & development.

  • Edition Notes

    Includes bibliographical references and index.

    StatementMichael Artman.
    SeriesMedical intelligence unit, Medical intelligence unit (Unnumbered)
    Classifications
    LC ClassificationsQP113.2 .A78 1994
    The Physical Object
    Pagination121 p. :
    Number of Pages121
    ID Numbers
    Open LibraryOL1114309M
    ISBN 10157059127X
    LC Control Number94040260

    Hypertension is a significant health concern. Hypertension leads to compensatory pathologic hypertrophy and impaired cardiac function. Lifestyle modifications such as exercise are encouraged for hypertensive patients. Some studies have shown that exercise training can reverse pathological hypertrophy. Conversely, studies on animal models of hypertension have Cited by: 5. These molecular changes in the myocardial β-AR system led to improved β-AR responsiveness and corresponding inotropic reserve in the aged rat heart. β-ARs are members of the family of G-protein-coupled receptors that are critical in the regulation of myocardial inotropy, lusitropy, and chronotropy (6, 36).Cited by: The rat myocardium may exhibit a greater α-AR-induced inotropic responsiveness than does the human myocardium. Thus α-AR-mediated inotropic upregulation may not contribute to maintaining intrinsic myocardial function in human heart failure. Last, the present study was conducted in male rats by:


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Developmental changes in myocardial intropic responsiveness by Michael Artman Download PDF EPUB FB2

Covering the developmental changes in myocardial contractile function and inotropic responsiveness, this text discusses the morphological, physiological and biochemical basis for changes in inotropic responsiveness during perinatal maturation.

Author(s): Artman,Michael, Title(s): Developmental changes in myocardial inotropic responsiveness/ Michael Artman. Country of Publication: United States. Thus, knowledge of the alterations in the intrinsic cardiac responsiveness to positive inotropic agents that occur at the extremes of age is deficient in animals and even more so in man (Boréus, ; Pappano, ; Goldberg & Roberts, ).Cited by: 2.

Inotropic Support. Inotropic support may be required for patients with septic shock. In the context of severe sepsis-induced myocardial depression or if the patient has severe preexisting myocardial dysfunction, an inotrope may be necessary to augment cardiac output.

We recommend that dobutamine be the inotrope selected; however, dopamine could have an inotropic effect. To investigate the mechanisms by which angiotensin-converting enzyme inhibitor therapy may modulate inotropic responsiveness with long-term pressure overload, we studied the effects of captopril treatment on cardiac gene expression.

The intrinsic contractile properties of papillary muscles isolated from female Wistar rats during post-natal development were examined. In addition, t Cited by: 2. Nakanishi T, Jarmakani JM: Developmental changes in myocardial mechanical function and subcellular organelles.

Am J Physiol H–H, PubMed Google Scholar Author: P. Achterberg. Altered Responsiveness of Hypertrophied Rat Hearts to Alpha- and Beta-adrenergic Stimulation. journal of Molecular and Cellular Cardiology () 23, Inotropic responsiveness to a- and fl-adrenergic agents was examined in pressure-overload hypertrophied rat hearts.

Pressure overload was induced in rats by abdominal aortic by: Developmental changes in the myocardial alpha-receptor density were studied using rabbit, rat and dog hearts.

In all species studied, alpha-receptor density in the newborn was greater than in the adult. The inotropic effect of phenylephrine was measured using the isolated arterially perfused heart preparation of rabbit and by: Important changes occur in myocardial cells during embryonic development, including ultrastructural, metabolical, pharmacological, and electrophysiological changes.

For example, striking changes occur in the electrical properties of ventricular myocardial cells during embryonic development of chick by: Changes in action potential parameters by and inotropic responses to nicardipine, verapamil, ryanodine and cyclopiazonic acid were examined in isolated ventricular myocardial preparations from neonatal and adult by: The development of the mammalian heart is characterized by substantial changes in myocardial performance.

We studied the ontogeny of myocardial function with and without various inotropic. Michael Artman has written: 'Developmental Changes in Myocardial Inotropic Responsiveness' Asked in Biology, Human Behavior, Psychological Disciplines, Wolfgang Amadeus Mozart What. Altered inotropic responsiveness to isoproterenol of hearts from spontaneously hypertensive rats during development.

that functional beta adrenergic inotropic receptors are present in the embryonic hearts of both strains and undergo changes during development that are strain dependent. PMID: Myocardial Contraction/drug effects Cited by: 1. Post-natal developmental changes in myocardial contractility of the female Wistar rat.

Capasso JM, Sonnenblick EH. The intrinsic contractile properties of papillary muscles isolated from female Wistar rats during post-natal development were examined. In addition, the myocardial responsiveness to certain inotropic interventions was by: 2.

performance and reduce myocardial responsiveness to catecholamines. The normal arterial blood pH is to and any significant deviation from the norm can cause serious life-threatening dis-turbances throughout the body.

The development of acidosis results from either a. Heart failure is a multisystem disorder which is characterised by abnormalities of cardiac, skeletal muscle, and renal function; stimulation of the sympathetic nervous system; and a complex pattern of neurohormonal changes.

Developments in our understanding of the pathophysiology of heart failure have been essential for recent therapeutic advances in this. To investigate the mechanisms by which angiotensin-converting enzyme inhibitor therapy may modulate inotropic responsiveness with long-term pressure overload, we studied the effects of captopril treatment on cardiac gene expression, LV muscle mechanical contraction, and intracellular calcium (Ca 2+) transients from spontaneously hypertensive Cited by:   Preload and Right Ventricular Infarct.

Those of us that have worked in cardiac care have seen changes in the management of myocardial infarctions. As we have changed our protocols and treatment regimens, we have drastically decreased mortality.

PDE5 inhibition restores the inotropic and chronotropic response to catecholamine stimulation. Since HF is associated with a reduced responsiveness to β Author: Michael Lawless. The Role of SR Ca2+-Content in Blunted Inotropic Responsiveness of Failing Human Myocardium Article in Journal of Molecular and Cellular Cardiology 34(4).

When inotropic stimulation is prolonged, short-term hibernation is impaired and myocardial infarction develops. The mechanisms responsible for the development of short-term myocardial hibernation remain unclear at present. Significant involvement of adenosine and activation of ATP-dependent potassium channels have been by: 8.

Inotropes have been fundamental to resuscitation of acute cardiogenic shock for decades. Heart failure and cardiogenic shock, in severe cases, are syndromes characterized in many patients by a reduction in myocardial contractile force. While inotropes successfully increase cardiac output, their use has been plagued by excessive mortality due to increased tachycardia and myocardial.

Shock-induced myocardial dysfunction was characterized by altered contractile responsiveness to low-Ca2+ medium ( mM), gentamicin (4 mM), and hypoxia; altered inotropic reactivity to these interventions followed similar temporal development as the postendotoxin changes in basal contractile by: Nevertheless, it must be considered that myocardial responsiveness to β-adrenergic stimulation is decreased in septic patients [57, 58].

Alteration of intracellular calcium influx is a. Modification of myofibrillar responsiveness to Ca++ as an inotropic mechanism. Blinks JR, Endoh M. Intracellular Ca++ transients were monitored in preparations of mammalian heart muscle in which multiple superficial cells had been microinjected with the Ca++-sensitive bioluminescent protein by: altered, suggesting that receptor gene expression did not induce pathologic changes.

Given the substantial reduction in /]-adrenergic receptor density and resultant reduction in inotropic responsiveness observed in chronic heart failure, these findings represent a novel approach for increasing myocardial function with important clinical.

Therefore, PLB is a crucial determinant of both myocardial contractility and β-adrenergic signaling. 11 Given that PLB is robustly expressed in adult CMs but virtually absent in hESC-CMs, 10,12 here, we investigated the functional consequences of expressing this differentially expressed gene product in single hESC/iPSC-vCMs, as well as their 3 Cited by: and myocardial oxygen requirements increase as afterload and MAP rise.

α-adrenergic stimulation does result in mild inotropic stimulation but this is masked by the increase in afterload. A pure vasopressor will typically cause a relative bradycardia. However, if there is a major element of β1 stimulation, tachycardia may be Size: 99KB.

Altered myocardial sensitivity and responsiveness to alpha₁-adrenoceptor agonists have been reported in experimental diabetes mellitus. Stimulation of alpha₁-adrenoceptors is known to produce a positive inotropic effect and has been recently shown to stimulate the hydrolysis of phosphoinositides.

In addition, the relationship of thyroid state to endogenous norepinephrine stores and myocardial responsiveness to certain inotropic interventions were studied. In muscles from hyperthyroid cats, the velocity of shortening and the rate of tension development were markedly augmented, while duration of active state was decreased, compared to Cited by: been concentrated on as a mechanism explaining myocardial ischaemia.

However, not only is it plausible that changes in oxygen delivery influence the process of myocardial ischaemia, but to explain the day to day symptoms of patients with angina, changes in both MV˙ O 2 and oxygen delivery together or separately must by: As in the case with short-term iNOS inhibition, the disruption of iNOS gene improved β-adrenergic inotropic responsiveness in TG but not in WT mice, suggesting that myocardial induction of iNOS may play a pivotal role in the development of β-adrenergic inotropic hyporesponsiveness in cytokine-induced by:   MYOCARDIAL OXYGEN CONSUMPTION.

MV̇ o 2 is determined in large part by the parameters shown in table 1. 1 Some of these, on a daily basis, remain relatively fixed (for example, myocardial mass), but it is the change in myocardial workload that is the most obvious when talking to patients who give a clear story of a relation (though not precise Cited by:   The primary goal of intra-aortic balloon pump (IABP) treatment is to increase myocardial oxygen supply and decrease myocardial oxygen demand.

Decreased urine output after the insertion of IABP can occur because of juxta-renal balloon positioning. Haemolysis from mechanical damage to red blood cells can reduce the haematocrit by up to 5%.Cited by: Background—Contrary to β 1 - and β 2-adrenoceptors, β 3-adrenoceptors mediate a negative inotropic effect in human ventricular assess their functional role in heart failure, our purpose was to compare the expression and contractile effect of β 3-adrenoceptors in nonfailing and failing human hearts.

Methods and Results—We analyzed left ventricular samples from Cited by: No, they are drugs that counteract the effect of catecholamines between synapses and suppress inotropic effect of the heart muscle.

Decreased myofilament responsiveness in myocardial stunning follows transient calcium overload during ischemia and reperfusion. Predictors of long-term outcome after percutaneous balloon mitral valvuloplasty.

Expression of dihydropyridine receptor (Ca2+ channel) and calsequestrin genes in the myocardium of patients with end-stage heart failure.

Pressure overload–induced concentric hypertrophy is associated with a reduction in β-adrenergic receptor responsiveness and subsequent altered myocardial contractile function. 1,2 Concentric hypertrophy is regarded as an adaptational process to normalize wall stress with hypertension.

3 Increased systolic performance with diastolic dysfunction has been documented during this Cited by: This causes irritation to the myocardial nerve fibers and the afferent sensory nerve fibers in the area transmit these pain impulses to the spinal tract for detection.

mental status change, deterioration of responsiveness hypotension, prolonged cap refill times (positive inotropic drugs, possibly slow down the heart rate to reduce heart. Inotropic Drugs Inotropic drugs work by increasing the force of ventricular contraction, for indication impaired myocardial systolic function.

Although each drug in this group work through a different mechanism they generally all work through to improve cardiac contraction by increasing intracellular calcium concentration/5(12).Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest.

Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac by: Heart failure syndrome is defined as the inability of the heart to deliver adequate blood to the body to meet end-organ metabolic needs and oxygenation at rest or during mild exercise.

Myocardial dysfunction can be defined as systolic and/or diastolic, acute or chronic, compensated or uncompensated, or uni- or biventricular.

Several counterregulatory mechanisms are activated Cited by: 3.