Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Airway edema has been described in heart failure, and, in animal experiments, airway narrowing was observed with elevated left atrial pressure (Pla). On the basis of double-indicator-dilution principles using helium and dimethylether, we were able to measure a water compartment of the tracheal mucosa (VH2O) in dogs. Hypervolemia with an attendant increase in Pla caused by infusion of 2 liters of dextran increased VH2O from 368 +/- 71 (SE) to 794 +/- 177 microliters (P < 0.01). Pulmonary arterial wedge and central venous pressures (Pcv) rose concomitantly. Increases in pulmonary arterial wedge and Pcv by a left atrial balloon catheter produced similar increases in VH2O, whereas increases in Pcv alone by a right atrial balloon did not increase VH2O. Increasing VH2O by dextran infusion was associated with an increase in pulmonary resistance from 1.16 +/- 0.19 to 2.15 +/- 0.24 cmH2O.l-1.s (P < 0.01). These observations show that fluid accumulation in the lung during pulmonary congestion also involves extraparenchymal airways and is related to Pla rather than right atrial pressure. This indicates that sufficient collateral drainage exists during right-sided but not left-sided pressure elevations.
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PMID:Tracheal mucosal edema in hydrostatic pulmonary edema. 796 Dec 56

Pharmacological support with inotropes and vasodilators to control decompensated hemodynamics requires strict monitoring of patient condition and frequent adjustments of drug infusion rates, which is difficult and time-consuming, especially in hemodynamically unstable patients. To overcome this difficulty, we have developed a novel automated drug delivery system for simultaneous control of systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (Pla). Previous systems attempted to directly control AP and CO by estimating their responses to drug infusions. This approach is inapplicable because of the difficulties to estimate simultaneous AP, CO, and Pla responses to the infusion of multiple drugs. The circulatory equilibrium framework developed previously (Uemura K, Sugimachi M, Kawada T, Kamiya A, Jin Y, Kashihara K, and Sunagawa K. Am J Physiol Heart Circ Physiol 286: H2376-H2385, 2004) indicates that AP, CO, and Pla are determined by an equilibrium of the pumping ability of the left heart (SL), stressed blood volume (V), and systemic arterial resistance (R). Our system directly controls SL with dobutamine, V with dextran/furosemide, and R with nitroprusside, thereby controlling the three variables. We evaluated the efficacy of our system in 12 anesthetized dogs with acute decompensated heart failure. Once activated, the system restored SL, V, and R within 30 min, resulting in the restoration of normal AP, CO, and Pla. Steady-state deviations from target values were small for AP [4.4 mmHg (SD 2.6)], CO [5.4 ml x min(-1) x kg(-1) (SD 2.4)] and Pla [0.8 mmHg (SD 0.6)]. In conclusion, by directly controlling the mechanical determinants of circulation, our system has enabled simultaneous control of AP, CO, and Pla with good accuracy and stability.
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PMID:Automated drug delivery system to control systemic arterial pressure, cardiac output, and left heart filling pressure in acute decompensated heart failure. 1637 47

Uncoupling protein 3 (UCP3), is primarily expressed in skeletal muscle mitochondria and has been suggested to be involved in mediating energy expenditure via uncoupling, hereby dissipating the mitochondrial proton gradient necessary for adenosine triphosphate (ATP) synthesis. Although some studies support a role for UCP3 in energy metabolism, other studies pointed towards a function in fatty acid metabolism. Thus, the protein is up regulated or high when fatty acid supply to the mitochondria exceeds the capacity to oxidize fatty acids and down regulated or low when oxidative capacity is high or improved. Irrespective of the exact operating mechanism, UCP3 seems to protect mitochondria against lipid-induced oxidative stress, which makes this protein a potential player in the development of type 2 diabetes mellitus. Next to skeletal muscle, UCP3 is also expressed in cardiac muscle where its role is relatively unexplored. Interestingly, energy deficiency in cardiac muscle is associated to heart failure and UCP3 might contribute to this energy deficiency. It has been suggested that UCP3 decreases energy status via uncoupling of mitochondrial respiration, but the available data does not provide a unified answer. In fact, the results obtained regarding cardiac UCP3 are very similar as in skeletal muscle, implying that its physiological function can be extrapolated. Therefore, cardiac UCP3 can just as well serve to protect the heart against lipid-induced oxidative stress, similar to the function described for skeletal muscle UCP3. The present review will deal with the available literature on both skeletal muscle- and cardiac UCP3 to elucidate its physiological function in these tissues.
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PMID:Mitochondrial uncoupling protein 3 and its role in cardiac- and skeletal muscle metabolism. 1819 Nov 61