Van Eyk, Dunn - Proteomic and Genomic Analysis of Cardiovascular Disease - 2003 (522919), страница 87
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Van EykThe function of an organ, including muscle, is impaired when its supply of energy (oxygen) is diminished. The best-known and best-studied examples includecerebrovascular accidents (stroke), myocardial infarction (heart attack), hemorrhage, sepsis, acute respiratory distress syndrome, and multi-organ system failure.While there is an understandable tendency to study these and other conditions inisolation in order to minimize confounding variables, diseases and/or injury inone organ system can and do affect others.
Aliverti and Macklem [1], for example,have convincingly argued that limited oxygen delivery to limb (skeletal) muscles isthe common element underlying their impaired contraction in health, chronic obstructive pulmonary disease (COPD), and heart failure (HF).The finely tuned interplay of the cardiovascular and respiratory systems is critical for ensuring adequate oxygen delivery to individual organs. Inadequate oxygendelivery can result from low perfusion (ischemia), low arterial oxygen levels (hypoxemia), or some combination. The former is typical of reduced cardiac output,the latter of reduced oxygen uptake by the lungs. A reduction in cardiac outputcan be caused by impaired contraction due to myocardial stunning infarction or agenetic disorder.
A reduced oxygen uptake is, in turn, the result of either inadequate alveolar ventilation due to reduced convection (impaired contractile performance of the respiratory muscles or high resistance and/or low compliance of thelung) or impaired diffusion. Whatever the cause, low perfusion or hypoxemia willresult in further reductions in oxygen delivery, leading to a vicious circle in whichthe contractile performance of muscles, whether cardiac or skeletal (including respiratory), worsens, accelerating the patient’s deterioration.HF, the inability of the heart to maintain an adequate cardiac output, is achronic progressive disease.
It is often characterized by the remodeling of the leftventricle (hypertrophy) during the initial compensatory stage which can becomedetrimental and eventually end in failure and death. Breathlessness is a commonsymptom experienced by patients with HF due, in part, to changes in the positionand function of the diaphragm as well as changes in the respiratory muscles [2–4]. In fact, the extent of reduction in inspiratory muscle strength with heart failure (HF) is an independent predictor of prognosis [5].
Skeletal muscle is affectedin HF, leading to exercise intolerance, although the proximate cause remains controversial. Alterations to skeletal muscle (i.e., its proteome or the protein compliProteomic and Genomic Analysis of Cardiovascular Disease.Edited by Jennifer E. van Eyk, Michael J. DunnCopyright © 2003 WILEY-VCH Verlag GmbH & Co. KGaA, WeinheimISBN: 3-527-30596-331819 Myofilament Proteomicsment of a biological sample at a given time) may be a cause of this exercise intolerance (for review, see [6]), but extensive analysis is required to determine the underlying mechanism for skeletal muscle dysfunction.COPD, a term commonly applied to patients with chronic bronchitis, emphysema or some mixture of the two, is an insidiously progressive airway disease characterized by a gradual loss of pulmonary function that is not fully reversible [7].In COPD, there can be a large strain on the right ventricle as a result of the increase in pulmonary vascular resistance.
As the disease progresses, problems begin to develop because of right ventricular hypertrophy; the heart’s rhythm is disrupted by abnormal beats and the interventricular septum is “pushed” leftward,thereby decreasing left ventricular volume and compliance. As a result, patientstend to tire more easily and additional strain (on either the lungs or heart) can result in an inadequate left ventricular output, leading to liver and kidney problemsand edema [7]. Many COPD patients succumb to right ventricular failure as a result of pulmonary hypertension. All these problems are compounded by a decrease in skeletal, including respiratory, muscle function, especially in advancedCOPD (for reviews, see [1, 8]).The analysis of skeletal muscle injury is confounded, compared to that of cardiac muscle, by the presence of multiple fiber types.
Rather than the injury beingdistributed among all fibers, it can be specific to a particular fiber type (slow oxidative, type I fibers or fast glycolytic, type II fibers). For example, one would notexpect equal damage to fast and slow fibers of the quadriceps during a marathon.In addition, injury could occur within a specific group of muscles (limb musclesfor movement, postural muscles for balance, and respiratory muscles for breathing). Moreover, injury can be distributed unequally within a synergistic group ofmuscles (e.g., diaphragm versus other respiratory muscles; [9]). Thus, unlike thecardiac proteome, the skeletal proteome involves different fiber types and/orgroups of muscles that can be differentially affected.Identification and characterization of both the skeletal and cardiac proteomesare important steps in understanding contractile function in health and disease.In disease, skeletal (including respiratory) and/or cardiac muscle function (contraction or contractility) is impaired.
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