scholarly journals Perfusion-induced changes in cardiac contractility depend on capillary perfusion

1998 ◽  
Vol 274 (2) ◽  
pp. H405-H410 ◽  
Author(s):  
Marieke A. Dijkman ◽  
Johannes W. Heslinga ◽  
Pieter Sipkema ◽  
Nico Westerhof
Keyword(s):  
Perfusion Pressure ◽  
Cardiac Contractility ◽  
Segment Length ◽  
Active Tension ◽  
Internal Perfusion ◽  
Loss Of Function ◽  
Capillary Perfusion ◽  
Muscle Contractility ◽  
Induced Changes ◽  
Control State

The perfusion-induced increase in cardiac contractility (Gregg phenomenon) is especially found in heart preparations that lack adequate coronary autoregulation and thus protection of changes in capillary pressure. We determined in the isolated perfused papillary muscle of the rat whether cardiac muscle contractility is related to capillary perfusion. Oxygen availability of this muscle is independent of internal perfusion, and perfusion may be varied or even stopped without loss of function. Muscles contracted isometrically at 27°C ( n = 7). During the control state stepwise increases in perfusion pressure resulted in all muscles in a significant increase in active tension. Muscle diameter always increased with increased perfusion pressure, but muscle segment length was unaffected. Capillary perfusion was then obstructed by plastic microspheres (15 μm). Flow, at a perfusion pressure of 66.6 ± 26.2 cmH2O, reduced from 17.6 ± 5.4 μl/min in the control state to 3.2 ± 1.3 μl/min after microspheres. Active tension developed by the muscle in the unperfused condition before microspheres and after microspheres did not differ significantly (−12.8 ± 29.4% change). After microspheres similar perfusion pressure steps as in control never resulted in an increase in active tension. Even at the two highest perfusion pressures (89.1 ± 28.4 and 106.5 ± 31.7 cmH2O) that were applied a significant decrease in active tension was found. We conclude that the Gregg phenomenon is related to capillary perfusion.

Coronary pressure-flow autoregulation protects myocardium from pressure-induced changes in oxygen consumption

1994 ◽  
Vol 266 (6) ◽  
pp. H2359-H2368 ◽  
Author(s):  
X. J. Bai ◽  
T. Iwamoto ◽  
A. G. Williams ◽  
W. L. Fan ◽  
H. F. Downey
Keyword(s):  
Oxygen Consumption ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Coronary Perfusion ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Anesthetized Dogs ◽  
Induced Changes

Pressure-flow autoregulation minimizes changes in coronary blood flow (CBF) when coronary perfusion pressure (CPP) is altered. This investigation determined if autoregulation also minimizes CPP-induced changes in coronary vascular volume (CVV) and CVV-dependent changes in myocardial oxygen consumption (MVO2). In 11 anesthetized dogs, the left anterior descending coronary artery was cannulated, and responses to 20-mmHg changes in CPP were examined over a range of CPP from 60 to 180 mmHg. Changes in CPP had no significant effect on systemic hemodynamics or on left ventricular end-diastolic segment length, end-systolic segment length, or percent segment shortening. In hearts with effective pressure-flow autoregulation [closed-loop gain (GC) > 0.4], CVV increased 0.06%/mmHg change in CPP. For the same hearts, MVO2 increased 0.04%/mmHg change in CPP. In hearts with ineffective autoregulation (GC < 0.4), CVV increased 0.97%/mmHg (P < 0.001 vs. autoregulating hearts), and MVO2 increased 0.41%/mmHg (P < 0.001 vs. autoregulating hearts). MVO2 and CVV were correlated (r = 0.69, P < 0.0001) independently of autoregulatory capability, but only when autoregulation was poor and capacitance was elevated did CPP significantly affect MVO2. We conclude that pressure-flow autoregulation protects myocardium from CPP-induced changes in CVV, which in turn produces changes in oxygen consumption.

scholarly journals Complementary vasoactivity and matrix remodelling in arterial adaptations to altered flow and pressure

2008 ◽  
Vol 6 (32) ◽  
pp. 293-306 ◽  
Author(s):  
A Valentín ◽  
L Cardamone ◽  
S Baek ◽  
J.D Humphrey
Keyword(s):  
Smooth Muscle ◽  
Continuum Theory ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Rates Of Change ◽  
Biomechanical Loading ◽  
Smooth Muscle Proliferation ◽  
And Function ◽  
Diverse Data ◽  
Induced Changes

Arteries exhibit a remarkable ability to adapt to sustained alterations in biomechanical loading, probably via mechanisms that are similarly involved in many arterial pathologies and responses to treatment. Of particular note, diverse data suggest that cell and matrix turnover within vasoaltered states enables arteries to adapt to sustained changes in blood flow and pressure. The goal herein is to show explicitly how altered smooth muscle contractility and matrix growth and remodelling work together to adapt the geometry, structure, stiffness and function of a representative basilar artery. Towards this end, we employ a continuum theory of constrained mixtures to model evolving changes in the wall, which depend on both wall shear stress-induced changes in vasoactive molecules (which alter smooth muscle proliferation and synthesis of matrix) and intramural stress-induced changes in growth factors (which alter cell and matrix turnover). Simulations show, for example, that such considerations help explain the different rates of experimentally observed adaptations to increased versus decreased flows as well as differences in rates of change in response to increased flows or pressures.

scholarly journals Mechanisms Underlying Muscle Protein Imbalance Induced by Alcohol

2018 ◽  
Vol 38 (1) ◽  
pp. 197-217 ◽  
Author(s):  
Scot R. Kimball ◽  
Charles H. Lang
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Protein ◽  
Cardiac Contractility ◽  
Metabolic Phenotype ◽  
Alcoholic Myopathy ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
Induced Changes ◽  
Skeletal Muscle Strength

Both acute intoxication and longer-term cumulative ingestion of alcohol negatively impact the metabolic phenotype of both skeletal and cardiac muscle, independent of overt protein calorie malnutrition, resulting in loss of skeletal muscle strength and cardiac contractility. In large part, these alcohol-induced changes are mediated by a decrease in protein synthesis that in turn is governed by impaired activity of a protein kinase, the mechanistic target of rapamycin (mTOR). Herein, we summarize recent advances in understanding mTOR signal transduction, similarities and differences between the effects of alcohol on this central metabolic controller in skeletal muscle and in the heart, and the effects of acute versus chronic alcohol intake. While alcohol-induced alterations in global proteolysis via activation of the ubiquitin-proteasome pathway are equivocal, emerging data suggest alcohol increases autophagy in muscle. Further studies are necessary to define the relative contributions of these bidirectional changes in protein synthesis and autophagy in the etiology of alcoholic myopathy in skeletal muscle and the heart.

Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels

2002 ◽  
Vol 282 (4) ◽  
pp. H1334-H1340 ◽  
Author(s):  
R. R. Lamberts ◽  
M. H. P. van Rijen ◽  
P. Sipkema ◽  
P. Fransen ◽  
S. U. Sys ◽  
...  
Keyword(s):  
Ion Channels ◽  
Perfusion Pressure ◽  
Cardiac Contractility ◽  
No Synthase ◽  
Coronary Perfusion ◽  
Channel Blockade ◽  
No Release ◽  
Sustained Increase ◽  
Stretch Activated Ion Channels

The role of stretch-activated ion channels (SACs) in coronary perfusion-induced increase in cardiac contractility was investigated in isolated isometrically contracting perfused papillary muscles from Wistar rats. A brief increase in perfusion pressure (3–4 s, perfusion pulse, n = 7), 10 repetitive perfusion pulses ( n = 4), or a sustained increase in perfusion pressure (150–200 s, perfusion step, n = 7) increase developed force by 2.7 ± 1.1, 7.7 ± 2.2, and 8.3 ± 2.5 mN/mm2 (means ± SE, P < 0.05), respectively. The increase in developed force after a perfusion pulse is transient, whereas developed force during a perfusion step remains increased by 5.1 ± 2.5 mN/mm2 ( P < 0.05) in the steady state. Inhibition of SACs by addition of gadolinium (10 μmol/l) or streptomycin (40 and 100 μmol/l) blunts the perfusion-induced increase in developed force. Incubation with 100 μmol/l N ω-nitro-l-arginine [nitric oxide (NO) synthase inhibition], 10 μmol/l sodium nitroprusside (NO donation) and 0.1 μmol/l verapamil (L-type Ca2+ channel blockade) are without effect on the perfusion-induced increase of developed force. We conclude that brief, repetitive, or sustained increases in coronary perfusion augment cardiac contractility through activation of stretch-activated ion channels, whereas endothelial NO release and L-type Ca2+channels are not involved.

Chronic alcohol-induced changes in cardiac contractility are not due to changes in the cytosolic Ca2+ transient

1998 ◽  
Vol 275 (1) ◽  
pp. H122-H130 ◽  
Author(s):  
Vincent M. Figueredo ◽  
Kevin C. Chang ◽  
Anthony J. Baker ◽  
S. Albert Camacho
Keyword(s):  
Cardiac Contractility ◽  
Left Ventricular Pressure ◽  
Alcohol Exposure ◽  
Left Ventricular ◽  
Polyacrylamide Gel ◽  
Chronic Alcohol ◽  
Protein Levels ◽  
Chronic Alcohol Exposure ◽  
Induced Changes ◽  
And Control

Long-standing heavy alcohol consumption acts as a chronic stress on the heart. It is thought that alcohol-induced changes of contractility are due to altered Ca2+ handling, but no measurements of cytosolic Ca2+([Ca2+]c) after chronic alcohol exposure have been made. Therefore experiments were performed to determine whether alcohol-induced changes in contractility are due to altered Ca2+ handling by measuring [Ca2+]c(indo 1) in hearts from rats drinking 36% ethanol for 7 mo and age-matched controls. Peak left ventricular pressure was depressed (−16%), whereas rates of contraction (12%) and relaxation (14–20%) were faster in alcohol-exposed hearts. Systolic [Ca2+]c(808 ± 45 vs. 813 ± 45 nM), diastolic [Ca2+]c(195 ± 11 vs. 193 ± 10 nM), and rates of [Ca2+]crise and decline were the same in alcohol-exposed and control hearts. Protein levels of Ca2+-handling proteins, sarcoplasmic reticulum Ca2+-ATPase and phospholamban, were the same in myocytes isolated from alcohol-exposed and control hearts (SDS-polyacrylamide gel). These data suggest that chronic alcohol-induced contractile changes are not due to altered Ca2+ handling but may be due to changes at the level of the myofilament. As a first step in elucidating the mechanism(s) of alcohol-induced changes at the myofilament, we assessed myosin heavy chain (MHC) isoform content (SDS-polyacrylamide gel). α-MHC was decreased relative to β-MHC ( a/ a+ b = 0.55 ± 0.03 vs. 0.66 ± 0.02; P < 0.02) in alcohol-exposed hearts, which cannot account for the observed alcohol-induced contractile changes. In conclusion, changes of myocardial contractility due to chronic alcohol exposure do not result from altered Ca2+ handling but from changes at the level of the myofilament that do not involve MHC isoform shifts.

Mapping of capillary flow, cellular redox state, and resting membrane potential in hypoperfused rat myocardium

1999 ◽  
Vol 277 (5) ◽  
pp. H2050-H2064 ◽  
Author(s):  
Frank Brasch ◽  
Marion Neckel ◽  
Rolf Volkmann ◽  
Gerhard Schmidt ◽  
Gerhard Hellige ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Trypan Blue ◽  
Redox State ◽  
Capillary Flow ◽  
Resting Membrane Potential ◽  
Capillary Perfusion ◽  
Cellular Redox ◽  
Nadh Fluorescence ◽  
Induced Changes ◽  
Tetramethylrhodamine Methyl Ester

The influence on myocyte viability of ischemia-induced changes in capillary perfusion was studied in the hearts of anesthetized rats subjected to partial occlusion of the left coronary artery for 45 min. Timed plasma labeling was applied to determine perfusion patterns. Changes in the fluorescence of preloaded potential-sensitive dyes [tetramethylrhodamine methyl ester (TMRM) and bis-oxonol], of trypan blue, and of endogeneous NADH were utilized in characterizing myocyte viability in histological sections of the heart. Within the hypoperfused zone, localized areas appeared vascularly nonlabeled for periods of at least 10 min. Within these areas a reduction in TMRM fluorescence occurred in 82.5% of the tissue, signaling a reduced resting membrane potential. In the same areas 37.7% of the myocytes revealed an NADH fluorescence lower than that regularly found in anoxic tissues. This correlated with an especially low level of TMRM, with increased fluorescence bis-oxonol and with an accumulation of trypan blue. In conclusion, in localized hypoperfusion-induced zones lacking capillary flow, an inhomogeneous pattern of reductions in myocyte viability develops, which appears to be relevant in ischemia-induced arrhythmias.

Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs

1992 ◽  
Vol 73 (3) ◽  
pp. 995-1003 ◽  
Author(s):  
S. M. Scharf ◽  
L. M. Graver ◽  
S. Khilnani ◽  
K. Balaban
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Perfusion Pressure ◽  
Intrathoracic Pressure ◽  
Left Ventricular ◽  
Pleural Pressure ◽  
Segment Length ◽  
Coronary Resistance ◽  
Direct Measurements ◽  
Pericardial Pressure

Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.

Cardiac lymph flow in conscious dogs

1979 ◽  
Vol 237 (3) ◽  
pp. H311-H317 ◽  
Author(s):  
L. H. Michael ◽  
R. M. Lewis ◽  
T. A. Brandon ◽  
M. L. Entman
Keyword(s):  
Surgical Stress ◽  
Cardiac Metabolism ◽  
Left Ventricular ◽  
Lymph Flow ◽  
Conscious Dogs ◽  
Lymph Vessel ◽  
Segment Length ◽  
Flow Probe ◽  
Lymphatic Duct ◽  
Control State

The cardiac lymphatic duct was cannulated in dogs and the exteriorized cannula allowed chronic collection of lymph during the awake state for as long as 3 wk. The surgical methodology and inherent difficulties in the technique are describ:d. Cardiac lymph flow ranged from 0.45--5.6 ml/h in the control state in 14 dogs. An occluding device and flow probe were placed on the circumflex coronary artery (CFX); ultrasonic segment length crystals were placed in the left ventricular free wall in 4 dogs. Occlusion of the CFX in these conscious dogs caused lymph flow to fall as great as 46% below control during the 1st half-hour. Reperfusion of the occluded vessel caused an increase in lymph flow as great as 67% above control. The effect on cardiac lymph flow was demonstrated for a few select drugs that have known effects on the cardiovascular system. Cardiac lymph flow was altered from control as follows: isoproterenol, 42 +/- 11% increase; RO 2-2985, 118 +/- 8% increase; verapamil, 101 +/- 10% increase; propranolol caused no significant change. The conscious dog with cardiac lymph vessel cannulated should provide a model to further study the complexities of cardiac metabolism and physiology without interference of anesthesia and surgical stress.

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