: Longer‐term (>2 weeks) mechanical circulatory support will provide an improved quality of life for thousands of pediatric cardiac failure patients per year in the United States. These pediatric ...patients suffer from severe congenital or acquired heart disease complicated by congestive heart failure. There are currently very few mechanical circulatory support systems available in the United States as viable options for this population. For that reason, we have designed an axial flow pediatric ventricular assist device (PVAD) with an impeller that is fully suspended by magnetic bearings. As a geometrically similar, smaller scaled version of our axial flow pump for the adult population, the PVAD has a design point of 1.5 L/min at 65 mm Hg to meet the full physiologic needs of pediatric patients. Conventional axial pump design equations and a nondimensional scaling technique were used to estimate the PVAD's initial dimensions, which allowed for the creation of computational models for performance analysis. A computational fluid dynamic analysis of the axial flow PVAD, which measures approximately 65 mm in length by 35 mm in diameter, shows that the pump will produce 1.5 L/min at 65 mm Hg for 8000 rpm. Fluid forces (∼1 N) were also determined for the suspension and motor design, and scalar stress values remained below 350 Pa with maximum particle residence times of approximately 0.08 milliseconds in the pump. This initial design demonstrated acceptable performance, thereby encouraging prototype manufacturing for experimental validation.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UILJ, UKNU, UL, UM, UPUK
Adenosine levels in venous effluent and epicardial fluid of isovolumic guinea pig hearts were measured during graded underperfusion (8 min periods of perfusion at 11.0, 8.0, 6.0, 3.0, and 1.5 ...ml/min). Metabolism was monitored using ^^31 P-NMR spectroscopy. Left ventricular pressure and MVO_2 displayed linear relations with coronary perfusion rate. Venous adenosine production and epicardial adenosine did not change until hearts were perfused with ≦ 3.0 ml/min. Venous adenosine production displayed bi-phasic relationships with logATP/ADPPi and AMP, reaching maximal values as logATP/ADPPi decreased and AMP increased, then stabilizing. Epicardial adenosine increased in a hyperbolic manner as logATP/ADPPi declined, and AMP increased. Epicardial adenosine correlated significantly with the ratio of oxygen supply：MVO_2 under all conditions (r=0.75). Venous adenosine formation did not correlate with epicardial adenosine during underperfusion, whereas venous adenosine correlated exponentially (r=0.94). Thus, venous adenosine formation is not a consistent index of interstitial adenosine during graded underperfusion. Alternatively, venous adenosine is a reasonable index under these conditions. The relationships between epicardial adenosine, oxygen supply：MVO_2 , and cytosolic metabolism support a role for endogenous interstitial adenosine in the metabolic regulation of coronary flow.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Release of adenosine into coronary venous effluent and epicardial fluid of isovolumic guinea pig hearts was examined during control perfusion and norepinephrine infusion (30 nM). Changes in ...metabolism were monitored using ^^31 P-NMR spectroscopy. During control perfusion, (9.6±0.3 ml/min/g), epicardial and venous adenosine levels were 154±40 nM and 17±5 nM, respectively. The cytosolic phosphorylation potential (logATP/ADPPi) was 5.26±0.04. During infusion of norepinephrine, left ventricular pressure, heart rate, and MVO_2 increased by 21%, 70%, and 45%, respectively. LogATP/ADPPi declined to 4.57±0.06 (P<0.05). Epicardial and venous adenosine concentrations increased to 496±74 nM and 461±94 nM, respectively (P<0.05). The changes in epicardial adenosine concentration correlated significantly with logATP/ADPPi (r=0.92), and coronary resistance (r=0.85). Epicardial adenosine levels correlated linearly with cytosolic AMP (r=0.97). Venous adenosine concentrations displayed a significant exponential correlation with epicardial adenosine (r=0.81). These results indicate that： i) epicardial adenosine levels appear to be linked to changes in cytosolic metabolism, ii) epicardial adenosine may be responsible for regulating coronary resistance, and iii) while venous adenosine levels largely underestimate epicardial adenosine during control perfusion, venous adenosine closely approximates epicardial adenosine during norepinephrine stimulation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Previously we have shown myocardial adenosine A1 receptors are up-regulated during the newborn period. The timing of the increase or the mechanism of the changes are not known. The purpose of the ...present study was to (1) determine the time course of increased A1 adenosine receptors during fetal development and (2) determine if A1 adenosine receptor regulation is secondary to changes in A1 receptor mRNA levels. A1 adenosine receptor density was determined in whole hearts from fetal rats at 14 and 19 days' gestation and from newborn and adult rats using standard receptor-binding techniques. A quantitative PCR assay was developed to measure A1 adenosine receptor mRNA using total RNA samples from the above ages. A1 receptor density (fmol receptor/mg protein) increased during late gestation (79 +/- 14 and 122 +/- 7 in 14 and 19 days' gestation respectively) peaked during the newborn period (136 +/- 12) and decreased in the adult rat (36 +/- 5). A1 receptor message levels (fg message/microgram total RNA) changed in parallel to receptor density (7.2 +/ 1.7, 15.6 +/- 1.8, 19.9 +/- 4.3 and 9.9 +/- 1.3 in 14 and 19 days' gestation, newborn and adult respectively). These results provide evidence for transcriptional control of A1 receptor density and the increased receptor density in the newborn heart supports a possible role for the A1 receptor in the transition to the extrauterine circulation.
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