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Biomedical subjects

L H Snoeckx

Publications and source records attributed to L H Snoeckx.

32 records · Page 2Linked to original sources
PubMed1991

Performance of the isolated, ejecting heart: effects of aortic impedance and exogenous substrates.

The workload of the isolated, left-ventricular ejecting heart (i.e. working heart) is determined by the left atrial filling pressure and the afterload imposed on the left ventricular outflow tract. In addition to the level of end-diastolic aortic pressure, afterload is highly determined by the aortic impedance. For the isolated, ejecting heart optimum matching of the left ventricle to its afterload requires the highest possible similarity between the impedance of the artificial aortic conduit and the natural aortic impedance. The present study shows that the haemodynamic performance of the ejecting rat heart preparation can be affected by the impedance of the aortic conduit. A proper choice of substrates in the perfusion fluid further improves the performance of the heart in the artificial set-up. The present paper also provides guidelines with respect to the design of the aortic cannula and compliance chamber. The occurrence of turbulence, which is related to the Bernoulli pressure drop, is a major determinant of the impedance of the aortic conduit. This effect is used to simulate the natural resistance component of the aortic impedance. Further, the applicability of the perfusion model can be extended by the so-called assisted-mode perfusion, which allows automatic adjustment from antegrade to retrograde perfusion if the heart is not able to generate sufficient pumping power to provide its own coronary perfusion.

Animals↗
PubMed1991

Expression and cellular distribution of heat-shock and nuclear oncogene proteins in rat hearts.

An early, transient accumulation of mRNAs of the protooncogenes c-fos and c-myc and the heat-shock protein HSP70 has been described in hypertrophying rat hearts. It is unclear 1) in which cardiac cell type-these gene activations occur and 2) whether the corresponding proteins are translated. We studied protein expression in rat hearts during ontogenic development and under stress conditions associated with pressure overload with the use of immunofluorescent techniques. During cardiac development no HSP70 could be detected. c-Fos was expressed consistently after birth but only in coronary smooth muscle cells, and c-Myc was found exclusively in adult coronary endothelium and myocardial nonmuscle cells. In adult rats, HSP70 and, to a lesser extent, c-Fos were induced in myocardial muscle and some nonmuscle cells within 3 h following methohexital sodium anesthesia. A similar, more intense immunolabeling of these peptides was observed after thoracotomy and/or aortic stenosis. The coronary c-Fos and c-Myc labeling remained unchanged in these conditions. Thus the expression in cardiac muscle and nonmuscle cells of the three peptides differs and depends on different triggers.

Aging↗
PubMed1990

The effects of global ischemia and reperfusion on compensated hypertrophied rat hearts.

Abdominal aorta constriction was performed in 10-week-old Lewis rats (Aoband). Ten weeks later the hearts were isolated and attached to a non-recirculating perfusion apparatus. The hearts could eject against a diastolic aortic pressure of either 60 or 100 mmHg. The functional recovery was compared with that of hearts of sham-operated (Sham) rats. After 45 min of global ischemia, Sham hearts regained cardiac output up to 75% and 70% of the pre-ischemic levels at 60 and 100 mmHg, respectively. At 60 mmHg Aoband hearts showed a minor recovery of ejection function. However, at 100 mmHg the recovery of Aoband hearts was completely comparable with that of Sham hearts. At 60 mmHg but not at 100 mmHg, the pre-ischemic and post-ischemic coronary flow was lower in Aoband than in Sham hearts (P less than or equal to 0.05). During the initial reperfusion phase Sham hearts, perfused at 60 mmHg, released more degradation products of adenine nucleotides and lactate dehydrogenase (LDH) than Aoband hearts (P less than or equal to 0.05), while the Aoband hearts lost more degradation products and LDH than the Sham hearts later during the reperfusion phase (P less than or equal to 0.05). In the groups perfused at 60 mmHg, higher tissue levels of ATP were found in Sham than in Aoband hearts at the end of the reperfusion period (P less than or equal to 0.05). However, at 100 mmHg comparable levels were found in the Sham and Aoband hearts. It is concluded that the height of the coronary perfusion pressure is of critical importance for the post-ischemic functional recovery of the compensated hypertrophied heart. At sufficiently high perfusion pressure levels, the functional and biochemical recovery of the hypertrophied heart is at least as good as in the non-hypertrophied heart. However, in the hypertrophied heart a coronary perfusion pressure which is too low leads to relative underperfusion during the initial reperfusion period which is associated with severely depressed cardiac performance and delayed wash-out of metabolites and intracellular enzymes.

Adenine Nucleotides↗
PubMed1989

Recovery of hypertrophied rat hearts after global ischemia and reperfusion at different perfusion pressures.

The ability to resist transient ischemia was studied in isolated hearts of 18 months old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Both types of hearts showed optimal performance during the preischemic period when perfused at a diastolic perfusion pressure of 8.0 (WKY) and 13.3 (SHR) kPa. Hemodynamic recovery of WKY hearts during reperfusion at 8.0 kPa, following 45 min global ischemia, was satisfactory. coronary perfusion completely normalized, contractility (dPlv/dtmax) was slightly depressed and cardiac output returned, on the average, to 40% of the preischemic values. In contrast, hemodynamic function of SHR hearts reperfused at 13.3 kPa was greatly depressed, as evidenced by almost complete abolition of cardiac output, severe reduction of dPlv/dtmax and persistent underperfusion of the endocardial layers. In addition, the postischemic release of lactate dehydrogenase was retarded and enhanced. The release patterns of degradation products of adenine nucleotides showed a shift to the endstage products xanthine and uric acid. The enhanced vulnerability of the hypertrophied heart to ischemia was even more expressed when the SHR hearts were reperfused at 8.0 kPa. Postischemic function was characterized by electrical instability, loss of contractility and cardiac output, and noreflow in the endocardial layers. Persistent accumulation of lactate and degradation products of adenine nucleotides in the postischemic hearts are in line with the lack of reperfusion. The present results indicate that a detailed mechanistic explanation for the reduced ability to withstand ischemia of SHR cannot be based on differences in ATP content or an altered anaerobic glycolitic activity prior and during ischemia. It is suggested that a defect on the circulatory level, probably caused by enhanced reactivity of the coronary vessels towards ischemia-elicited factors, is responsible for the higher vulnerability of hypertrophied heart to an ischemia insult.

Adenosine Triphosphate↗
PubMed1988

Effects of pyruvate on post-ischemic myocardial recovery at various workloads.

In the present study the hemodynamic and metabolic effects of pyruvate (5 mM), added as cosubstrate to glucose (11 mM) perfused, transiently ischemic, isolated working rat hearts, were evaluated. During 2 h of normoxic perfusion pyruvate improved functional stability, prevented depletion of glycogen and triacylglycerol stores, and increased non-esterified fatty acid (NEFA) levels, even at relatively high workloads. The elevated NEFA levels are in line with the notion that pyruvate competes with endogenously produced fatty acids for oxidative energy production. After 45 min of global ischemia pyruvate was found (a) to affect markedly the relative contribution of ATP, ADP and AMP to the total adenine nucleotide content and (b) to stimulate the degradation of glycogen and to enhance the accumulation of lactate, suggesting enhanced anaerobic ATP production. After restoration of flow pyruvate reduced the incidence of fibrillation and markedly improved recovery of cardiac output at both normal and high workload. Pyruvate did neither attenuate the release of lactate dehydrogenase, a marker for cell death, nor improve the conservation of the total adenine nucleotide and ATP content of hearts reperfused for 30 min. The latter findings indicate that hemodynamic recovery during reperfusion in the presence of pyruvate is neither related to the absolute tissue content of ATP nor to a reduction of irreversible cell damage, and suggest that pyruvate exerts its advantageous hemodynamic effects rather by improving the condition of reversibly damaged cells during reperfusion.

Animals↗
PubMed1986

A microcomputer system for haemodynamic measurements in isolated, working rat hearts.

This study describes the application of an Apple IIe microcomputer in combination with a pre-processor in the on-line calculation of haemodynamic variables of the isolated working rat heart and of relative rapid changes in these variables, induced by variations in left atrial filling pressure (preload) and end-diastolic aortic pressure (afterload). Variables such as heart rate, systolic and diastolic left ventricular pressure, the maximal positive and negative first derivative of the left ventricular pressure, systolic and diastolic aortic pressure and aortic flow were continuously calculated and printed at minimal intervals of 6 s. A newly designed procedure to detect the activation of the electrogram, which was necessary to start the detection of a new cardiac cycle, is described.

Animals↗
PubMed1986

Myocardial function in normal and spontaneously hypertensive rats during reperfusion after a period of global ischaemia.

Isolated working hearts of 16 month old spontaneously hypertensive rats (SHR, n = 8) and age matched Wistar-Kyoto (WKY, n = 8) rats were exposed to 30 min global normothermic ischaemia followed by 60 min reperfusion. The hearts were routinely perfused at an afterload level of 13.3 kPa and a preload level of 1.0 kPa. The control values of left ventricular pressure, its maximal positive first derivative (dP1v/dtmax), coronary flow per gram heart tissue, and release of lactate and enzymes such as lactate dehydrogenase and aspartate aminotransferase were comparable in both groups. WKY rat hearts ejected almost twice as much perfusate per gram heart weight as the SHR hearts. In pressure-flow curves, obtained during the control period in SHR hearts, cardiac output was independent of changes in afterload, varying between 10.7 and 18.7 kPa. In contrast, in WKY rat hearts increases in afterload resulted in a progressive decrease in cardiac output. Reperfusion of the SHR hearts after 30 min of global normothermic ischaemia resulted in a poor recovery of cardiac output (13% of the control values) and dP1v/dtmax (32%) compared with the values in the WKY rat hearts (66% and 91% of the control values respectively). Reactive hyperaemia was prominent in the WKY rat hearts but completely absent in the SHR hearts. During one hour reperfusion, SHR hearts lost 3.5 times more lactate dehydrogenase and 2.5 times more aspartate aminotransferase than the WKY rat hearts. Pressure-flow curves, obtained during the reperfusion period, showed modest recovery of myocardial function of the WKY rat hearts at the lowest afterload level tested but completely depressed myocardial function of the SHR hearts at all afterload levels. Heart tissue contents of adenosine triphosphate and creatine phosphate after one hour of reperfusion were lower in the SHR than in the WKY rats, but compared with native values a comparable percentage decrease was seen in both groups of rats.

Adenosine Triphosphate↗
PubMed1983

Cardiac dimensions in athletes in relation to variations in their training program.

The cardiac dimensions of male long-distance runners (LDR) and cycle racers (CR) were determined echocardiographically during four different training seasons, i.e., a preparation, a competitive, a slowing-down and a resting season, and were compared with those of control subjects (CS). Left ventricular hypertrophy (LVH) was also assessed from the electrocardiogram. The maximal aerobic performance was determined on a bicycle ergometer. In the athletes, left ventricular mass was significantly greater in all seasons than the values in the CS. This difference resulted from a thicker interventricular septum and left ventricular posterior wall as well as a larger left ventricular internal diameter. The existence of LVH was confirmed by the electrocardiographic findings. No differences were observed between the four different training seasons, despite considerable changes in the training program for weeks to months. The maximal aerobic performance test in LDR showed a significantly higher workload during the competitive than during the preparation season. The CR reached significantly lower values during the resting season than during the other seasons. The results indicate that the possible adaptation of the cardiac dimensions to variations in the heaviness of the training program is relatively slow.

Adolescent↗
PubMed1982

Effect of training specificity on maximal treadmill and bicycle ergometer exercise.

Sixteen competitive athletes in long-distance running (n = 8) and cycle racing (n = 8) performed three maximal exercise tests on the treadmill as well as on the bicycle ergometer. The test protocol for both ergometers was similar in work intensity and duration. The results obtained at the maximum work load were compared between and within the two groups of athletes. Comparing treadmill to bicycle exercise, the oxygen uptake was 14% higher on treadmill in the long-distance runners, but equal in the cycle racers. The work efficiency on both types of ergometers showed a clear relationship with the training activity: the cycle racers worked more efficiently on the bicycle ergometer while the results of the long-distance runners were better on the treadmill. Heart rate and minute ventilation reached similar values in the cycle racers on both ergometers, but treadmill exercise induced higher values in the long-distance runners as compared to cycling. Opposite results were found in the variables of the acid-base balance: lactate concentration and base excess reached similar values (13 and -14 mmol l-1, respectively) in the long-distance runners on both ergometers, but in the cycle racers bicycle exercise induced higher values than running. From these results it can be concluded that congruence between the mode of ergometer exercise and the sport activity improves the validity of the test result.

Acid-Base Equilibrium↗
PubMed1982

Echocardiographic dimensions in athletes in relation to their training programs.

The cardiac dimensions of long-distance runners (LDR), cycle racers (CR), and weight lifters (WL) were determined echocardiographically and were compared with those of control subjects (CS). Left ventricular hypertrophy (LVH) was also assessed from the electrocardiogram. Training information was obtained through a questionnaire. The maximal aerobic performance was assessed on a cycle ergometer. Comparison of the cardiac dimensions revealed that left ventricular mass (LVmass) was significantly increased in LDR and CR as compared to CS. This resulted from thickening of the interventricular septum and left ventricular posterior wall as well as from enlargement of the left ventricular internal diameter. The existence of LVH was confirmed by electrocardiographic investigation. Although the left ventricular wall was enlarged in WL, their LVmass was not significantly increased as compared with CS. These results are in agreement with the training program followed. Weight lifters almost exclusively performed strength training, while LDR and CR were mainly involved in endurance training. The LDR and CR reached significantly higher maximal aerobic performance levels than WL. The present results suggest a close relationship between the type of cardiac enlargement and the training program followed by the athletes.

Adolescent↗
PubMed1976

On-line computation of cardiac output with the thermodilution method, using a digital minicomputer.

In the present study, several techniques for calculating cardiac output were evaluated in order to find an accurate technique suitable for on-line digital computation. The thermodilution method was evaluated by different calculation techniques and by comparing these techniques with electromagnetic flowmeter values. Comparison of thermal dilution curves, manually calculated by the log-normal and the exponential assumption, showed a correlation coefficient of 0.978 between the two methods, the former values being 11% higher. The exponential method correlated very well with the technique, using a correction factor for injection errors (r = 0.999). Since the exponential technique correlated well with the electromagnetic values (r = 0.84) and since it was less complicated than the technique, using correction factors, this technique was chosen for automation. Comparison of exponential calculated thermodilution values with a digital computer and manually, showed a correlation coefficient of 0.991. Therefore, it was concluded that on-line computation of thermodilution curves improves the applicability of the termodilution techniques as a means of measuring cardiac output.

Animals↗
PubMed1975

Influence of guanethidine on the nicotinic effects of acetylcholine in atropinized dogs.

The influence of guanethidine on the nicotinic effects of acetylcholine was studied in anaesthetized atropinized dogs. Guanethidine (5 mg/kg i.v.) reversed the initial nicotinic pressor reaction, abolished the accompanying femoral vasoconstriction and reduced the increase of mean aortic flow. Therefore, nicotinic hypotension after guanethidine was due to a decrease of the peripheral vascular resistance. The height of the second pressor reaction was hardly affected by guanethidine. This drug inhibited the increases in mean aortic flow and heart rate but not the elevation of peripheral resistance, occurring at the secone nicotinic pressor phase. The present findings support the assumption that the initial hypertension is due to increased sympathetic outflow towards heart and vessels, whereas the second hypertension is due to adrenal medullary stimulation. The neurogenic femoral vasodilation at the onset of the second nicotinic pressor phase was blocked by guanethidine, which also inhibited the catecholamine-induced neurogenic vasodilation. These antagonisms may result from the interference of guanethidine with noradrenaline re-uptake.

Acetylcholine↗