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Myocardial Oxygen Consumption (myocardial + oxygen_consumption)
Selected AbstractsCoronary Hemodynamics and Myocardial Oxygen Consumption During Support With Rotary Blood PumpsARTIFICIAL ORGANS, Issue 1 2009Peter Voitl Abstract Mechanical support offered by rotary pumps is increasingly used to assist the failing heart, although several questions concerning physiology remain. In this study, we sought to evaluate the effect of left-ventricular assist device (VAD) therapy on coronary hemodynamics, myocardial oxygen consumption, and pulmonary blood flow in sheep. We performed an acute experiment in 10 sheep to obtain invasively measured coronary perfusion data, as well as pressure and flow conditions under cardiovascular assistance. A DeBakey VAD (MicroMed Cardiovascular, Inc., Houston, TX, USA) was implanted, and systemic and coronary hemodynamic measurements were performed at defined baseline conditions and at five levels of assistance. Data were measured when the pump was clamped, as well as under minimum, maximum, and moderate levels of assistance, and in a pump-off condition where backflow occurs. Coronary flow at the different levels of support showed no significant impact of pump activity. The change from baseline ranged from ,10.8% to +4.6% (not significant [n.s.]). In the pulmonary artery, we observed a consistent increase in flow up to +4.5% (n.s.) and a decrease in the pulmonary artery pressure down to ,14.4% (P = 0.004). Myocardial oxygen consumption fell with increasing pump support down to ,34.6% (P = 0.008). Left-ventricular pressure fell about 52.2% (P = 0.016) as support was increased. These results show that blood flow in the coronary arteries is not affected by flow changes imposed by rotary blood pumps. An undiminished coronary perfusion at falling oxygen consumption might contribute to cardiac recovery. [source] Regional sympathetic denervation affects the relation between canine local myocardial blood flow and oxygen consumptionEXPERIMENTAL PHYSIOLOGY, Issue 3 2007David J. C. Alders Myocardial blood flow and oxygen consumption are heterogeneously distributed. Perfusion and myocardial oxygen consumption are closely correlated in the normal heart. It is unknown how this metabolism,perfusion relation is influenced by sympathetic denervation. We investigated this question in seven chloralose-anaesthetized dogs, 3,4 weeks after regional sympathetic denervation of the left circumflex coronary artery area of supply of the left ventricle. Measurements were made of local myocardial blood flow (MBF, in ml min,1 (g dry wt),1), measured with microspheres, and myocardial oxygen consumption (, in ,mol min,1 (g dry wt),1) in the same location, calculated from the 13C spectrum of tissue extracts after intracoronary infusion of 3,13C-lactate. Since both innervated and denervated regions are subject to the same arterial pressure, lower blood flow indicates higher resistance. Mean MBF was 5.56 ml min,1 (g dry wt),1 (heterogeneity of 3.47 ml min,1 (g dry wt),1) innervated, 7.48 ml min,1 (g dry wt),1 (heterogeneity of 3.62 ml min,1 (g dry wt),1) denervated (n.s.). Significant linear relations were found between MBF and of individual samples within the innervated and denervated regions. The slopes of these relations were not significantly different, but the adjusted mean was significantly higher in the denervated regions (+1.92 ml min,1 (g dry wt),1, an increase of 38% of the mean MBF at the pooled mean , P= 0.028, ANCOVA). The ratio (in ml ,mol,1) was significantly higher, being 0.296 ± 0.167 ml ,mol,1 in the denervated region compared with the innervated region, 0.216 ± 0.126 ml ,mol,1, P= 0.0182, Mann,Whitney U test. These results indicate that sympathetic tone under chloralose anaesthesia imposes a moderate vasoconstrictive effect in the myocardium that is not detected by comparison of the mean blood flow or resistance. [source] Cardiac 17O MRI: Toward direct quantification of myocardial oxygen consumptionMAGNETIC RESONANCE IN MEDICINE, Issue 6 2010Kyle S. McCommis Abstract A new 17O-labeled blood contrast agent was injected intravenously in control dogs. Electrocardiogram (ECG)-triggered myocardial T1, imaging was performed to obtain spin-locking T1,-weighted myocardial signals for the detection of resultant metabolite H217O water in the heart. Bolus and slow injection methods of various doses of the 17O-labeled and 16O-labeled agents were carried out in order to evaluate the sensitivity of this method and determine the optimal injection method. Bolus injection provided approximately 1% signal reduction, whereas slow injection with larger amount of agent yielded 11.9 ± 0.6% signal reduction. Myocardial oxygen consumption rate was determined by a technique to quantify cerebral oxygenation consumption rate previously developed in 17O brain studies. With either injection method, myocardial oxygen consumption rate at rest was 5.0 , 5.6 ,mol/g/min. Therefore, it appears feasible to detect metabolically generated HO water in vivo in the heart, using the 17O-labeled blood tracer. Myocardial oxygen consumption rate can then be quantified in vivo, which may open new doors for the assessment of myocardial metabolism. Magn Reson Med 63:1442,1447, 2010. © 2010 Wiley-Liss, Inc. [source] EPR oximetry in the beating heart: Myocardial oxygen consumption rate as an index of postischemic recoveryMAGNETIC RESONANCE IN MEDICINE, Issue 4 2004Govindasamy Ilangovan Abstract Oxygen plays a critical role in the pathophysiology of myocardial injury during both ischemia and subsequent reperfusion (I/R). Thus, oxygen concentration is an important variable to measure during I/R. In the present work, electron paramagnetic resonance (EPR)-based oximetry was used to measure the oxygen concentration during a series of I/R episodes and oxygenation levels were correlated with the contractile and hemodynamic functions of the heart. A custom-developed electronically tunable surface coil resonator working at 1.1 GHz was used to determine tissue pO2 in the beating heart. Microcrystalline particulate of lithium phthalocyanine was used as an EPR oximetry probe. Isolated and perfused rat hearts were subjected to 1 or 3 hr durations of preischemic perfusion, followed by 15-min I/R cycles. In hearts perfused for 3 hr prior to 15-min I/R cycles, the myocardial pO2 decreased gradually on subsequent reperfusions of three successive I/R cycles. However, in hearts perfused for 1 hr there was almost 100% recovery of myocardial pO2 in all three I/R cycles. The extent of oxygenation recovered in each reperfusion cycle correlated with the recovery of hemodynamic and contractile function. The results also showed that the oxygen consumption rate of the heart at the end of each I/R episode decreased in direct proportion to the functional recovery. In summary, it was observed that the amount of myocardial oxygen consumption during I/R could provide a reliable index of functional impairment in the heart. Magn Reson Med 51:835,842, 2004. © 2004 Wiley-Liss, Inc. [source] Proteomics of ischemia/reperfusion injury in rabbit myocardium reveals alterations to proteins of essential functional systemsPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2005Melanie Y. White Abstract Brief periods of myocardial ischemia prior to timely reperfusion result in prolonged, yet reversible, contractile dysfunction of the myocardium, or "myocardial stunning". It has been hypothesized that the delayed recovery of contractile function in stunned myocardium reflects damage to one or a few key sarcomeric proteins. However, damage to such proteins does not explain observed physiological alterations to myocardial oxygen consumption and ATP requirements observed following myocardial stunning, and therefore the impact of alterations to additional functional groups is unresolved. We utilized two-dimensional gel electrophoresis and mass spectrometry to identify changes to the protein profiles in whole cell, cytosolic- and myofilament-enriched subcellular fractions from isolated, perfused rabbit hearts following 15 min or 60 min low-flow (1 mL/min) ischemia. Comparative gel analysis revealed 53 protein spot differences (> 1.5-fold difference in visible abundance) in reperfused myocardium. The majority of changes were observed to proteins from four functional groups: (i) the sarcomere and cytoskeleton, notably myosin light chain-2 and troponin C; (ii) redox regulation, in particular several components of the NADH ubiquinone oxidoreductase complex; (iii) energy metabolism, encompassing creatine kinase; and (iv) the stress response. Protein differences appeared to be the result of isoelectric point shifts most probably resulting from chemical modifications, and molecular mass shifts resulting from proteolytic or physical fragmentation. This is consistent with our hypothesis that the time course for the onset of injury associated with myocardial stunning is too brief to be mediated by large changes to gene/protein expression, but rather that more subtle, rapid and potentially transient changes are occurring to the proteome. The physical manifestation of stunned myocardium is therefore the likely result of the summed functional impairment resulting from these multiple changes, rather than a result of damage to a single key protein. [source] Regulation of lactate production at the onset of ischaemia is independent of mitochondrial NADH/NAD+: insights from in silico studiesTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Lufang Zhou Ischaemia decreases mitochondrial NADH oxidation, activates glycolysis, increases the NADH/NAD+ ratio, and causes lactate production. The mechanisms that regulate anaerobic glycolysis and the NADH/NAD+ ratio during ischaemia are unclear. Although continuous measurements of metabolic fluxes and NADH/NAD+ in cytosol and mitochondria are not possible in vivo with current experimental techniques, computational models can be used to predict these variables by simulations with in silico experiments. Such predictions were obtained using a mathematical model of cellular metabolism in perfused myocardium. This model, which distinguishes cytosolic and mitochondrial domains, incorporates key metabolic species and processes associated with energy transfer. Simulation of metabolic responses to mild, moderate and severe ischaemia in large animals showed that mitochondrial NADH/NAD+ was rapidly reset to higher values in proportion to the reduced O2 delivery and myocardial oxygen consumption . Cytosolic NADH/NAD+, however, showed a biphasic response, with a sharp initial increase that was due to activation of glycogen breakdown and glycolysis, and corresponded with lactate production. Whereas the rate of glycolysis and the malate,aspartate shuttle had a significant effect on the cytosolic NADH/NAD+, their effects on the mitochondrial NADH/NAD+ were minimal. In summary, model simulations of the metabolic response to ischaemia showed that mitochondrial NADH/NAD+ is primarily determined by O2 consumption, while cytosolic NADH/NAD+ is largely a function of glycolytic flux during the initial phase, and is determined by mitochondrial NADH/NAD+ and the malate,aspartate shuttle during the steady state. [source] A Novel Subcutaneous Counterpulsation Device: Acute Hemodynamic Efficacy During Pharmacologically Induced Hypertension, Hypotension, and Heart FailureARTIFICIAL ORGANS, Issue 7 2010Carlo R. Bartoli Abstract The miniaturization of mechanical assist devices and less invasive implantation techniques may lead to earlier intervention in patients with heart failure. As such, we evaluated the effectiveness of a novel, minimally invasive, implantable counterpulsation device (CPD) in augmenting cardiac function during impaired hemodynamics. We compared the efficacy of a 32-mL stroke volume CPD with a standard 40-mL intra-aortic balloon pump (IABP) over a range of clinically relevant pathophysiological conditions. Male calves were instrumented via thoracotomy, the CPD was anastomosed to the left carotid artery, and the IABP was positioned in the descending aorta. Hemodynamic conditions of hypertension, hypotension, and heart failure were pharmacologically simulated and data were recorded during CPD and IABP support (off, 1:2, 1:1 modes) for each condition. In all three pathophysiological conditions, the CPD and IABP produced similar and statistically significant (P < 0.05) increases in coronary artery blood flow normalized to the left ventricular (LV) workload. During hypotension and heart failure conditions, however, the CPD produced significantly greater reductions in LV workload and myocardial oxygen consumption as compared with the IABP. A novel 32-mL CPD connected to a peripheral artery produced equivalent or greater hemodynamic benefits than a standard 40-mL IABP during pharmacologically induced hypertension, hypotension, and heart failure conditions. [source] Coronary Hemodynamics and Myocardial Oxygen Consumption During Support With Rotary Blood PumpsARTIFICIAL ORGANS, Issue 1 2009Peter Voitl Abstract Mechanical support offered by rotary pumps is increasingly used to assist the failing heart, although several questions concerning physiology remain. In this study, we sought to evaluate the effect of left-ventricular assist device (VAD) therapy on coronary hemodynamics, myocardial oxygen consumption, and pulmonary blood flow in sheep. We performed an acute experiment in 10 sheep to obtain invasively measured coronary perfusion data, as well as pressure and flow conditions under cardiovascular assistance. A DeBakey VAD (MicroMed Cardiovascular, Inc., Houston, TX, USA) was implanted, and systemic and coronary hemodynamic measurements were performed at defined baseline conditions and at five levels of assistance. Data were measured when the pump was clamped, as well as under minimum, maximum, and moderate levels of assistance, and in a pump-off condition where backflow occurs. Coronary flow at the different levels of support showed no significant impact of pump activity. The change from baseline ranged from ,10.8% to +4.6% (not significant [n.s.]). In the pulmonary artery, we observed a consistent increase in flow up to +4.5% (n.s.) and a decrease in the pulmonary artery pressure down to ,14.4% (P = 0.004). Myocardial oxygen consumption fell with increasing pump support down to ,34.6% (P = 0.008). Left-ventricular pressure fell about 52.2% (P = 0.016) as support was increased. These results show that blood flow in the coronary arteries is not affected by flow changes imposed by rotary blood pumps. An undiminished coronary perfusion at falling oxygen consumption might contribute to cardiac recovery. [source] Geomagnetic field effect on cardiovascular regulationBIOELECTROMAGNETICS, Issue 2 2004Juraj Gmitrov Abstract The goal of the present research was try to explain the physiological mechanism for the influence of the geomagnetic field (GMF) disturbance, reflected by the indices of the geomagnetic activity (K, Kp, Ak, and Ap indices), on cardiovascular regulation. One hundred forty three experimental runs (one daily) comprising 50 min hemodynamic monitoring sequences were carried out in rabbits sedated by pentobarbital infusion (5 mg/kg/h). We examined the arterial baroreflex effects on the short term blood pressure and heart rate (HR) variabilities reflected by the standard deviation (SD) of the average values of the mean femoral arterial blood pressure (MAP) and the HR. Baroreflex sensitivity (BRS) was estimated from blood pressure/HR response to intravenous (i.v.) bolus injections of vasoconstrictor (phenylephrine) and vasodilator (nitroprusside) drugs. We found a significant negative correlation of increasing GMF disturbance (Kp) with BRS (P,=,0.008), HR SD (P,=0.022), and MAP SD (P,=,0.002) signifying the involvement of the arterial baroreflex mechanism. The abrupt change in geomagnetic disturbance from low (K,=,0) to high (K,=,4,5) values was associated with a significant increase in MAP (83,±,5 vs. 99,±,5 mm Hg, P,=,0.045) and myocardial oxygen consumption, measured by MAP and HR product (24100,±,1800 vs. 31000,±,2500 mm Hg,·,bpm, P,=,0.034), comprising an additional cardiovascular risk. Most likely, GMF affects brainstem and higher neural cardiovascular regulatory centers modulating blood pressure and HR variabilities associated with the arterial baroreflex. Bioelectromagnetics 25:92,101, 2004. © 2004 Wiley-Liss, Inc. [source] Nicorandil Improves Myocardial High-Energy Phosphates In Postinfarction Porcine HeartsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2002Yo Murakami SUMMARY 1.,Nicorandil is a potent vasodilator combining the effects of a nitrate with an ATP-sensitive potassium channel (KATP) opener. Because the postinfarct remodelled heart has increased vulnerability to subendocardial hypoperfusion, it is possible that the vasodilator effects of nicorandil could cause transmural redistribution of blood flow away from the subendocardium. Alternatively, the KATP channel opening effects of nicorandil could exert a beneficial effect on mitochondrial respiration. Consequently, the present study was performed to examine the effect of nicorandil on energy metabolism in the postinfarct heart. 2.,Studies were performed in swine in which myocardial infarction produced by proximal left circumflex coronary artery ligation had resulted in left ventricular remodeling. [31P] nuclear magnetic resonance spectroscopy (MRS) was used to examine the myocardial energy supply/demand relationship across the left ventricular wall while the transmural distribution of blood flow was examined with radioactive microspheres. Data were obtained during baseline conditions and during infusion of nicorandil (100 ,g, i.v., followed an infusion of 25 ,g/kg per min). 3.,Nicorandil caused coronary vasodilation with a preferential increase in subepicardial flow; however, subendocardial flow also increased significantly. Nicorandil had no significant effect on the rate,pressure product or myocardial oxygen consumption. The ratio of phosphocreatine (PCr)/ATP determined with MRS was abnormally depressed in remodelled hearts (2.01 ± 0.11, 1.85 ± 0.10 and 1.59 ± 0.11 for subepicardium, midwall and subendocardium, respectively) compared with normal (2.22 ± 0.11, 2.01 ± 0.15 and 1.80 ± 0.09, respectively). Nicorandil had no effect on the high-energy phosphate content of normal hearts. However, nicorandil increased the PCr/ATP ratio in the subendocardium of remodelled hearts from 1.59 ± 0.11 to 1.87 ± 0.10 (P < 0.05). 4.,Although nicorandil caused modest redistribution of blood flow away from the subendocardium of the postinfarct left ventricle, this was associated with an increase of the PCr/ATP ratio towards normal. These results suggest that nicorandil exerts a beneficial effect on energy metabolism in the subendocardium of the postinfarct remodelled left ventricle. [source] | |||||||||||||