Ultrafast electron dynamics at Cu(111): Response of an electron gas to optical excitation.
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Journal Article↗
Biomedical subjects
G Ertl
Publications and source records attributed to G Ertl.
Magnetization exchange in capillaries by microcirculation affects diffusion-controlled spin-relaxation: a model which describes the effect of perfusion on relaxation enhancement by intravascular contrast agents.
The effect of perfusion on relaxation time in tissue has only been considered for first-pass kinetics of NMR-signal after application of contrast agents. The importance of perfusion on relaxation has not yet been studied for steady state conditions, i.e., when the intravascular relaxation rate is constant in time. The aim of this study is to develop a model in which T1 relaxation is derived as a function of perfusion and intracapillary volume fraction (regional blood volume). Tissue is considered to be two-compartment system, which consists of intracapillary and extravascular space. Intracapillary relaxation differs from relaxation in the arterial system due to diffusion-exchange of magnetization from extravascular to intracapillary space. Perfusion tends to attenuate this difference and thus counteracts the effect on intracapillary relaxation. Relaxation in the extravascular and intracapillary magnetization are linked by diffusion. This dependence is presented in analytical form and a generic equation is derived. AT1 experiment is considered in which all spins of tissue and blood are inverted at the beginning. Calculations are performed for the fast exchange model of tissue. Perfusion increases relaxation enhancement of intravascular contrast agents. This effect is considerable in highly perfused tissue like myocardium. The dependence of relaxation on perfusion implies an overestimation of the regional blood volume when the calculation of the latter is based on tissue models that neglect perfusion. The model presented here is applied to predict the effect of perfusion on T1 imaging with FLASH-pulse sequences because this technique has been proven to be a powerful method to obtain T1 maps within a short time interval. For the fast exchange model, two algorithms are suggested that determine perfusion and regional blood volume from T1 imaging in the presence and absence of intravascular contrast agents.
Blood Volume↗
Alterations of performance and oxygen utilization in chronically infarcted rat hearts.
Progressive dilatation of left ventricle has been demonstrated in hearts post-infarction. However, the relationship of performance and energy consumption in chronically infarcted heart has not been clarified. To address this problem, we measured left ventricular pressure and oxygen consumption (MVO2) during stepwise increases in left ventricular filling volume in isolated isovolumic buffer-perfused rat hearts 8 weeks after let coronary artery ligation or sham-operation. Systolic pressure-volume area (PVA) was calculated as an estimate of total mechanical energy consumed by the heart. The MVO2-PVA relation was analysed to define the economy of the contractile machinery in surviving myocardium. Structural dilatation and reduced pressure generation in infarcted hearts were indicated by a rightward shift of pressure-volume curves and a reduced maximal developed pressure of the left ventricle (80 +/- 5 v 119 +/- 4 mmHg, P < 0.01) which was obtained at substantially higher left ventricular volume compared to control hearts (0.79 +/- 0.02 v 0.39 +/- 0.01 ml, P < 0.01). The slope of the MVO2-PVA relation was significantly lower in the infarcted compared to the control groups (1.02 +/- 0.16 v 1.44 +/- 0.10 10(-5) mlO2/mmHg/ml, P < 0.05), reflecting an increased efficiency of chemomechanical energy transduction in surviving myocardium. However, at the similar MVO2 ventricular pressure development was significantly lower in infarcted hearts due to the unfavorable geometry resulting from ventricular dilatation.
Animals↗
In vivo colored microspheres in the isolated rat heart for use in NMR.
Myocardial perfusion measurement with colored microspheres may become an alternative for radioactive microsphere techniques. We use and validate a spectrophotometric method that has been previously established for large animals in the isolated perfused rat heart. The perfusion system was adapted for use in a NMR microscope. Hearts were perfused with constant coronary flow that was adjusted to a coronary perfusion pressure of 100 mmHg. Homogeneous coronary inflow of microspheres was represented by equal distribution of microspheres of two different colors after simultaneous injection. Mean regional myocardial blood flow was 17.76 +/- 5.01 ml/min/g, mean wet heart weight was 1.13 +/- 0.34 g and mean global flow was 20.06 +/- 0.60 ml/min. Heart rate was 296 +/- 8.9 beats/min and left ventricular pressure was similar 5 min before (149.1 +/- 14.27 mmHg) and after (147.1 +/- 13.49 mmHg) microsphere injection. Microspheres of four colors that were injected sequentially, at various coronary flows, demonstrated linearity and reproducibility of the technique. A cumulative use of less than 90 000 microspheres showed no effect on hemodynamics especially on left ventricular pressure.
Animals↗
Regional biochemical remodeling in non-infarcted tissue of rat heart post-myocardial infarction.
Changes in the capacities of ATP-synthesizing reactions were analysed in residual non-infarcted myocardium following myocardial infarction. Rats were subjected to left coronary artery ligation (MI; n = 11) or to sham operation (sham; n = 18). Two months later, hearts were excised, rinsed and buffer-perfused isovolumically. In vitro pressure-volume relationships were recorded. After separation into left and right ventricles (LV, RV) and atria (LA, RA), samples were analysed for citrate synthase, glycolytic enzymes (phosphofructokinase, glyceraldehyde-3-phosphate-dehydrogenase, lactate dehydrogenase (LDH) and its isoforms) and the creatine kinase (CK) system [total CK, CK isoenzymes (CKBB, CKMB, CKMM and CKmito) and total creatine]. In residual intact heart, citrate synthase activity and activities of most glycolytic enzymes were unchanged, but LDH activity and anaerobic LDH isoenzymes increased significantly. Total creatine kinae activity (6.5 +/- 0.2 IU/mg protein in sham LV) was decreased by chronic myocardial infarction in LV (5.4 +/- 0.3, with P < 0.05 sham v MI) but not in RV (6.2 +/- 0.2). Significant CK isoenzyme shifts occurred in both ventricles "adult" CKmito (32.5 +/- 1.4% in sham LV) was reduced in LV (22.1 +/- 2.1% with P < 0.05 sham v MI) and in RV (19.2 +/- 2.9%, with P < 0.05 sham v MI), "fetal" CKBB and CKMB increased. Total creatine content was reduced by up to 35% in both ventricles. In sham hearts atria had lower total and mitochondrial CK activity, lower total creatine content and higher CKMB and CKBB activity compared to ventricles; however, myocardial infarction induced changes directionally comparable to the changes observed in ventricles. Thus, 2 months after myocardial infarction changes of the capacities of ATP synthesizing reactions are comparable for all heart chambers, with the exception of total CK activity decreasing only in left ventricular tissue.
Animals↗
Angiotensin II type 1 receptor induced signal-transduction pathways as new targets for pharmacological treatment of the renin-angiotensin system.
The peptide hormone angiotensin II is the main effector of the renin angiotensin system and may be involved in the pathogenesis of several cardiovascular disease such as congestive heart failure and hypertension. Drugs developed to inhibit angiotensin II effects such as angiotensin-converting enzyme (ACE) inhibitors or receptor antagonists helped to detect the cardiovascular and cellular mechanisms of angiotensin II effects. ACE inhibitor effects are complex and include indirect as well as direct mechanisms. Indirect effects are mediated by unloading the heart via prevention of aldosterone release and modulation of sympathetic nervous system activity. Direct actions include the inhibition of cardiac fibroblast proliferation and collagen synthesis as well as hypertrophy of cardiomyocytes. Recent work has focused on uncovering the biochemical and molecular mechanisms of angiotensin II induced cell growth.
Angiotensin Receptor Antagonists↗
Long-term beta-blocker treatment prevents chronic creatine kinase and lactate dehydrogenase system changes in rat hearts after myocardial infarction.
OBJECTIVES: We tested the hypothesis that long-term beta-blocker treatment with bisoprolol prevents creatine kinase (CK) and lactate dehydrogenase system changes that occur after chronic myocardial infarction. BACKGROUND: The mechanism of the beneficial effect of beta-blocker therapy is still unclear. METHODS: Six groups of rats were studied. Sham operated (sham) and hearts with ligated left anterior descending coronary artery (myocardial infarction) were untreated, treated early (beginning 30 min after infarction) or treated late (beginning 14 days after infarction). After 8 weeks, hearts were isolated and buffer perfused isovolumetrically. With a left ventricular balloon, mechanical function was recorded at an end-diastolic pressure of 10 mm Hg. Biopsy samples of noninfarcted left ventricular tissue were taken. Enzyme activities were measured spectrophotometrically; isoenzymes were separated by agar gel electrophoresis; and total creatine levels were measured with high performance liquid chromatography. RESULTS: The decrease in left ventricular developed pressure in untreated hearts (120 +/- 9 vs. 104 +/- 5 mm Hg [mean +/- SE], p < 0.05, sham vs. myocardial infarction) after myocardial infarction was prevented by early treatment (118 +/- 9 vs. 113 +/- 4 mm Hg). Late treatment failed to improve mechanical function. Reduction of CK activity occurring in untreated infarcted hearts (6.4 +/- 0.3 vs. 5.1 +/- 0.3 IU/mg protein, p < 0.05, sham vs. myocardial infarction) was prevented by early beta-blocker therapy. The increase in CK isoenzyme BB and MB levels, decrease in mitochondrial CK isoenzyme levels and increase in anaerobic lactate dehydrogenase isoenzyme levels in untreated infarcted hearts did not occur during bisoprolol treatment. The decrease in total creatine levels after myocardial infarction (74.2 +/- 4.9 vs. 54.9 +/- 3.3 nmol/mg protein, p < 0.05, sham vs. myocardial infarction) was prevented by bisoprolol treatment. Early treatment was more effective than late therapy in preventing CK and lactate dehydrogenase system changes. In addition, in sham hearts, a 40% increase of creatine levels above normal levels was detected. CONCLUSIONS: Bisoprolol prevented changes in CK and lactate dehydrogenase system that occur after myocardial infarction. These observations may be related to the beneficial effects of long-term beta-blocker treatment in patients with chronic myocardial infarction.
Adrenergic beta-Antagonists↗
Sunny days, healthy ways: evaluation of a skin cancer prevention curriculum for elementary school-aged children.
BACKGROUND: Primary prevention of skin cancer must start early in life to reduce total life-time sun exposure and severe overexposure in childhood. Childhood is an excellent time to form life-long prevention habits. A school-based curriculum can be an effective prevention strategy. OBJECTIVE: Our purpose was to determine the effectiveness of a skin cancer prevention curriculum at increasing knowledge and attitudes supporting prevention and decreasing sun exposure by children in grades four, five, and six. METHODS: Twenty-four classes (N = 447 students) from four public elementary schools in southern Arizona participated. Half received a pretest, half were tested at the conclusion of the 5-week curriculum in early spring, and half were tested 8 weeks later in late spring. Objective measures of suntanning were obtained. RESULTS: The curriculum increased knowledge about skin cancer prevention and attitudes supporting prevention and decreased suntanning. Self-reported preventive behavior was inconsistent and only weakly associated with measures of suntanning. CONCLUSION: The curriculum was effective at increasing skin cancer prevention. Resulting reduction in sun exposure was superior to that achieved with previous prevention curricula. Change in attitude needed time to emerge, appearing after 8 weeks. Self-reported preventive behavior by children in elementary school may lack validity. Pretesting did not alter effectiveness. Sixth-graders may be ready for more advanced content, but the curriculum is probably too advanced for kindergarten through third grade.
Attitude to Health↗
Preservation of left ventricular mechanical function and energy metabolism in rats after myocardial infarction by the angiotensin-converting enzyme inhibitor quinapril.
We tested whether angiotensin-converting enzyme (ACE) inhibitor therapy with quinapril prevents the deterioration of mechanical function and high-energy phosphate metabolism that occurs in chronically infarcted heart. Rats were subjected to ligation of the left anterior descending coronary artery (LAD) or sham operation. Four groups were studied: sham-operated rats (n = 10), rats with myocardial infarction (MI, n = 9), sham-operated quinapril-treated rats (n = 8), and infarcted quinapril-treated (n = 13) rats. Treated rats received 6 mg/kg/day of the ACE inhibitor quinapril orally, initiated 1 h after MI or sham operation. Eight weeks after LAD ligation or sham operation, hearts were isolated and buffer-perfused isovolumically. High-energy phosphate metabolism and intracellular pH were continuously recorded with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hearts were subjected to 15-min control, 30-min hypoxia (95% N2/5% CO2, and 30-min reoxygenation. Left ventricular developed pressure (LVDP) was reduced in infarcted hearts (58 +/- 10 vs. 98 +/- 9 mm Hg in sham, p < 0.05), and this reduction was partially prevented by quinapril (78 +/- 8 mm Hg). ATP content of residual intact myocardium after sham operation or MI was unchanged. Creatine phosphate was reduced in infarcted hearts (107 +/- 10 vs. 138 +/- 5% of control ATP, p < 0.05), and quinapril prevented this decrease (131 +/- 8%). Therefore, quinapril preserved both function and high-energy phosphate metabolism in the chronically infarcted heart. However, when hearts were subjected to acute hypoxia, susceptibility to acute metabolic stress was substantially increased in both quinapril-treated groups: ATP content at end-hypoxia was reduced to 31 +/- 7 and 37 +/- 6% in sham and infarcted quinapril-treated groups, whereas ATP in untreated sham and infarcted hearts was 66 +/- 6 and 66 +/- 3% of baseline values (p < 0.05 untreated vs. quinapril treated). Likewise, recovery of LVDP during reoxygenation was impaired by quinapril treatment (15 +/- 7 and 15 +/- 4 mm Hg in quinapril-treated sham and MI vs. 73 +/- 9 and 46 +/- 9 mm Hg in untreated sham and MI groups, p < 0.05 untreated vs. quinapril treated). The most likely explanation for the unexpected finding of increased susceptibility to acute metabolic stress in the quinapril-treated groups is reduced wall thickness leading to increased wall stress. The preservation of high-energy phosphate content in residual intact hearts after MI may contribute to the beneficial effects of ACE inhibitors after MI.
Adenosine Triphosphate↗
Protective effect of the specific endothelin-1 antagonist BQ610 on mechanical function and energy metabolism during ischemia/reperfusion injury in isolated perfused rat hearts.
Endothelin-1 (ET-1) has been suggested to be involved in the pathophysiology of ischemia/reperfusion injury, but direct proof for this is still sparse. We tested whether protection of high-energy phosphate metabolism contributes to the beneficial effects of ETA receptor antagonists during ischemia/reperfusion. In isolated, buffer-perfused rat hearts, isovolumic function was measured by a left ventricular (LV) balloon, and 31P nuclear magnetic resonance spectra were continuously recorded. Two protocols were performed: (a) 15-min control, 30-min total, global ischemia, and 15-min reperfusion; and (b) 15-min control, 15-min total, global ischemia, and 30-min reperfusion. Treatment with BQ610 (1.75 micrograms/min) or saline was started during control and continued throughout the protocol. BQ610 did not affect function or energy metabolism under control conditions. In BQ610-treated hearts subjected to 30-min ischemia, time to ischemic contracture was significantly delayed (treated 10.6 +/- 0.4 min; untreated 8.1 +/- 0.7 min), and end-diastolic pressure (EDP) remained lower (after 30-min ischemia 26 +/- 2 vs. 35 +/- 2 mm Hg). In addition, recovery of mechanical function in BQ610-treated hearts was accelerated during reperfusion. BQ610 did not affect ATP but significantly accelerated and increased creatine phosphate (51 +/- 7 vs. 37 +/- 3%) recovery on reperfusion after 30-min ischemia. BQ610-treated hearts subjected to 15-min ischemia also showed lower EDP during ischemia and accelerated recovery of mechanical function during reperfusion. However, in this case, there were no differences in high-energy phosphate concentrations between treated and untreated hearts. We conclude that the protective action of BQ610 on mechanical function during ischemia/reperfusion injury can be but is not consistently associated with beneficial effects on cardiac high-energy phosphate metabolism.
Adenosine Triphosphate↗
Influence of cardiac dysfunction on fast sodium current regulation by Forskolin.
There are several reports of an altered beta-adrenergic pathway in heart failure. Since the fast cardiac sodium current (INa+) is also subject to beta-receptor dependent regulation, we investigated its regulation in a model of cardiac dysfunction. Adenylyl cyclase was stimulated directly with forskolin as one step in the beta-adrenergic pathway. Twelve-week-old Wistar rats were infarcted by ligation of the left anterior descending coronary artery. Eight weeks later, the induced hemodynamic changes were evaluated. The left ventricular end-diastolic pressure (LVEDP) was used as a measure of the hemodynamic effects of the myocardial infarction. With the loose patch clamp technique, INa+ was measured in intact papillary muscles at an external sodium concentration of 150 mmol/L. Potential dependent availability was tested with pulses to 0 mV from various conditioning potentials. In animals with minor infarction (n = 7, LVEDP = 7.7 +/- 0.9 mmHg), forskolin (3 mumol/L) increased the maximal available INa+ to 109% +/- 13% of baseline values. This increase was nearly the same in the group with significant infarctions (n = 7, LVEDP = 15.7 +/- 1.6 mmHg) to 113% +/- 6%. Thus, although we previously observed a reduction of the isoproterenol induced increase of INa+ in rats with significant myocardial infarctions, this increase remains the same when adenylyl cyclase is stimulated directly. This is consistent with a direct beta-receptor down-regulation or desensitization.
Action Potentials↗
The renin-angiotensin system and coronary vasomotion.
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Angiotensin I↗
Changes of atrial natriuretic peptide in brain areas of rats with chronic myocardial infarction.
We measured immunoreactive atrial natriuretic peptide (ANP) in 18 selected, microdissected brain areas. Rats were studied 8 wk after coronary ligation or sham operation or as nonoperated control animals. In separate animals, hemodynamic and plasma parameters were measured. Rats with myocardial infarction had marked elevated right atrial and left ventricular end-diastolic pressure (2.6 +/- 0.6 and 16.2 +/- 3.1 mmHg, respectively; n = 15) vs. sham-operated rats (1.3 +/- 1.0 and 5.5 +/- 1.2 mmHg, n = 14; P < 0.05) and depressed maximal rate of pressure development (9,613 +/- 980 vs. 15,600 +/- 2,027 mmHg/s; P < 0.05) but similar arterial pressure (126 +/- 4 vs. 124 +/- 3 mmHg; P > 0.05). After myocardial infarction (n = 10), plasma ANP, renin activity, and angiotensin (ANG) II were elevated (53.1 +/- 16.2 pg/ml, 10.7 +/- 2.5 ng ANG I ml-1 h-1, and 219.6 +/- 11.0 fmol/ml, respectively) vs. sham rats (12.0 +/- 2.2 pg/ml, 5.7 +/- 0.7 ng ANG I ml-1, h-1, and 142.9 +/- 9.4 fmol/ml; n = 10; P < 0.05), whereas vasopressin and aldosterone levels remained unchanged among groups. In rats with myocardial infarction, a substantial decrease of ANP was found in the medial preoptic nucleus, the supraoptic nucleus, the subfornical organ, the paraventricular nucleus, and the locus ceruleus. These nuclei are involved in electrolyte, and fluid homeostasis, blood pressure regulation, and modulation of neuroendocrine systems. The mechanism of this reduction and the consequences for systemic adaption or decompensation remain unclear. However, the data suggest that myocardial infarction and chronic left ventricular dysfunction may induce changes of a neurotransmitter in brain.
Animals↗
[Effect of the cardiac renin-angiotensin system on hypertrophy].
The existence of a cardiac renin-angiotensin-system is confirmed. An influence of AII on growth and mitosis of various cells contributing to cardiac hypertrophy has been shown. Prove for a clinical role would be prevention of hypertrophy and of its complications in patients by specific AII-receptor antagonists in a state of a not-activated systemic renin-angiotensin-system and in absence of mechanical effects. This prove is difficult to obtain.
Angiotensin Receptor Antagonists↗
Anisotropic thermal displacements of adsorbed atoms and molecules on surfaces studied by low-energy electron diffraction.
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Journal Article↗
Observation of front bifurcations in controlled geometries: From one to two dimensions.
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Journal Article↗
Incommensurate structures and epitaxial growth of Li on Ru(0001): A quantitative low-energy electron-diffraction study.
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Journal Article↗
Reconstructive adsorption of Na on Al(111) studied by scanning tunneling microscopy.
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Journal Article↗