Altered oscillatory work by ventricular myofilaments from a rabbit coronary artery ligation model of heart failure

Abstract

Reduced capacity for mechanical power, consistent with depressed haemodynamic performance in LVD hearts, is only partially attributable to crossbridge slowing; changes in the phase relationship will also contribute. These changes are not readily attributable to known alterations in contractile protein isoforms. Some deductions are drawn about which steps in the crossbridge cycle are modified in this model of LVD. Altered cardiac myocyte Ca-transients, reported to be associated with LVD, will be translated into pump work by a contractile machinery that is functionally altered, even though isometric force and myofilament Ca-sensitivity might remain near-normal at this stage.

Functional Consequences of Sarcomeric Protein Abnormalities in Failing Myocardium

“…This property of the myofilament suggests that both calcium cycling and myofilament function are modulated in a coordinated fashion to produce the observed FFR. Moreover, recent studies demonstrate a decrease in the optimal frequency of work and power production of the myofilament in experimental heart failure [49,56] as well as in patients with diabetic cardiomyopathy [63]. While comparable studies in patients with dilated cardiomyopathy have not yet been reported, the results in experimental heart failure suggest that altered myofilament function may contribute in a significant fashion to depression of the FFR in these patients.…”

“…Less severe depression of the FFR has been reported in patients with mitral regurgitation [59], pressure overload hypertrophy [60] and diabetic cardiomyopathy [61]. More recently, the possible contribution of the myofilament to the normal FFR has been recognized based on the results of sinusoidal analysis experiments performed in skinned myocardial strips [49,56]. This method probes the ability of activated strips to produce work and generate power as a function of sinusoidal length perturbations at varying frequencies [62].…”

“…This method probes the ability of activated strips to produce work and generate power as a function of sinusoidal length perturbations at varying frequencies [62]. The experiments demonstrate that the oscillatory work and power generation of the myofilament is highly frequency-dependent, with maximal values at stimulation frequencies similar to the optimal frequency of the FFR determined in excitable myocardial strips and the intact heart [49,56,62]. This property of the myofilament suggests that both calcium cycling and myofilament function are modulated in a coordinated fashion to produce the observed FFR.…”

“…New information is emerging in regard to frequency-dependent behavior of the myofilament and its modification in heart failure [49,56]. The markedly positive force-frequency relation (FFR) or Treppe effect in mammalian myocardium is a key mechanism whereby cardiac function is enhanced during stressful conditions such as exercise [57,58].…”

Συγκριτική Δράση Του Ισοφλουρανίου Και Του Σεβοφλουρανίου Σε Σήψη

“…Οι τιμές της ΔΑΚΤΔ ήταν κατά μέσο όρο 1,54 cm (χωρίς αναισθησία) και 1,48 cm (σε αναισθησία), ενώ της ΔΑΚΤΣ 1,01 και 1,07 cm, αντίστοιχα. Η ΔΑΚΤΔ και η ΔΑΚΤΣ των κονίκλων, σύμφωνα με άλλους ερευνητές, κυμαίνονται από 1,41 cm (Nagueh et al 2000) έως 1,75 cm (Miller et al 2004) και από 0,88 cm (Pennock et al 1997) έως 1,08 cm (Marian et al 1999), αντίστοιχα. Σε νεότερη μελέτη των Fontes-Sousa et al ( 2006), λήφθηκε υπερηχοκαρδιογράφημα σε 52 αρσενικούς κονίκλους, στους οποίους είχε χορηγηθεί κεταμίνη και μεδετομιδίνη, η ΔΑΚΤΔ ήταν 1,44 cm και η ΔΑΚΤΣ 1,025 cm.…”