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Biomedical subjects

F L Meijler

Publications and source records attributed to F L Meijler.

At least 19 recordsLinked to original sources
PubMed1992

Electrocardiogram of the humpback whale (Megaptera novaeangliae), with specific reference to atrioventricular transmission and ventricular excitation.

OBJECTIVES: The objective of the study was to record the electrocardiogram (ECG) of a large whale to obtain crucial data for comparative electrophysiologic analysis. BACKGROUND: The data were needed to establish the mismatch between heart size and PR interval and QRS duration in mammals. METHODS: In the waters off the coast of Newfoundland, in two humpback whales (Megaptera novaeangliae) with an estimated weight of 30,000 kg a 1-lead ECG was recorded, enabling reliable assessment of P waves and QRS complexes. RESULTS: It was found that both the PR interval (atrioventricular [AV] transmission time) and QRS duration (ventricular excitation) are extremely short for animals of this size. These findings are difficult, if not impossible, to explain on the basis of currently accepted electrophysiologic theories. However, the narrow QRS complex may be due to a very dense His-Purkinje network in the ventricular wall of whales. Alternative mechanisms that can explain the function of the mammalian AV node need to be considered and explored. CONCLUSIONS: The results of the study may be of value for the understanding of the ECG in humans.

Animals↗
PubMed1990

Post-extrasystolic potentiation without a compensatory pause in normal and diseased hearts.

Variables derived from left ventricular volume were used to study post-extrasystolic potentiation. Left ventriculograms were obtained from 11 healthy individuals and 49 patients with coronary heart disease (30 with a previous myocardial infarction and 19 without any signs of myocardial damage). Post-extrasystolic potentiation was induced by a regularly driven right atrial rhythm that was interrupted by one atrial extrasystole in such a way that the post-extrasystolic RR interval was kept equal to the basic RR interval. The left ventricular end diastolic volumes of the pre-extrasystolic and post-extrasystolic beats were equal. In all groups there was evidence of post-extrasystolic potentiation in one or more of the indices of left ventricular function (ejection fraction, mean normalised systolic ejection rate, and systolic volume, and stroke volume). Potentiation was especially evident in patients with left ventricular damage; this suggests that a compensating mechanism is an intrinsic property of the myocardium. The Frank-Starling mechanism does not contribute to the increased performance of the post-extrasystolic beat in normal individuals or in patients with coronary artery disease.

Action Potentials↗
PubMed1990

[Comparative pathophysiology of the atrioventricular node].

The apparent mismatch between size and electrical function of the mammalian heart can be exemplified by the relation between ventricular rate during atrial fibrillation in dog, human, and horse, and bodyweight. The same is true for the relation between atrioventricular transmission time and heart size. While heart size may increase with a factor of 10(8), PR interval (on the surface ECG) will only increase with a factor 30. The curve of the PR interval versus the third root of heart weight has an S-shape. This form of relation cannot easily be explained on the basis of current electrophysiological theories. The contribution of the AV nodal delay to AV transmission time probably diminishes with increasing heart size. The mechanism of AV nodal delay is therefore not clear. Right ventricular pacing with intervals twice as long as the shortest PR-intervals in patients with atrial fibrillation results in complete block of anterograde conduction. The AV node as an unprotected pacemaker, entrained during sinus rhythm and electrotonically modulated during atrial fibrillation, rather than a cable with conduction properties, may offer an explanation for the non-linear and non-conductive behaviour of the AV node. This may well have consequences for the treatment of patients with atrial fibrillation.

Animals↗
PubMed1989

Low Ca2+ reperfusion and enhanced susceptibility of the postischemic heart to the calcium paradox.

This study was designed to define the effect of postischemic low Ca2+ perfusion on recovery of high-energy phosphates, intracellular pH, and contractile function in isolated rat hearts. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intracellular inorganic phosphate, and intracellular pH during control perfusion (15 minutes), total ischemia (30 minutes), and reperfusion (30 minutes). In Group I the perfusate [Ca2+] was 1.3 mmol/l throughout the experiment, whereas in Group II the perfusate [Ca2+] was reduced to 0.05 mmol/l during the first 10 minutes of reperfusion. Hearts from Group III were not made ischemic but were subjected to 10 minutes of low Ca2+ perfusion followed by 20 minutes of normal Ca2+ perfusion. During low Ca2+ reperfusion (Group II) recovery of high-energy phosphates and pH was significantly better than in controls (Group I). However, after reexposure to normal Ca2+, metabolic recovery was largely abolished, coronary flow was suddenly impaired, and contracture developed without any rhythmic contractions. These observations indicated the occurrence of a calcium paradox rather than postponed ischemia-reperfusion damage. On the other hand, normoxic hearts (Group III) tolerated temporary perfusion with 0.05 mmol/l Ca2+ very well with respect to left ventricular developed pressure, coronary flow, and metabolic parameters. In conclusion, postischemic low Ca2+ (0.05 mmol/l) perfusion may reduce reperfusion damage, but at the same time ischemia appears to enhance the susceptibility of the heart to the calcium paradox.

Adenosine Triphosphate↗
PubMed1988

The presence and molecular forms of cardiodilatin immunoreactivity in the human and rat right atrium.

A sensitive and specific radioimmunoassay has been developed for cardiodilatin, the N-terminal peptide sequence of the atrial natriuretic peptide (ANP) prohormone. Cardiodilatin-immunoreactivity (-IR) concentrations in the human right atrial appendage were found to correlate with ANP-IR concentrations, determined by an established radioimmunoassay, (cardiodilatin-IR = 13.2 +/- 1.2 nmol/g, ANP-IR = 19.8 +/- 2.0 nmol/g, r = 0.80, p less than 0.001). Characterisation of the cardiodilatin-IR in the human and rat right atrium by gel permeation and fast protein liquid chromatography revealed only two cardiodilatin-IR molecular forms. The larger more hydrophobic form, the majority of the cardiodilatin-IR, contained in addition ANP-IR and therefore represents the prohormone. The smaller, less hydrophobic form, lacked ANP-IR and thus represents the cleaved N-terminal peptide sequence of the prohormone. These findings indicate that the prohormone is the major molecular form in the human and rat atrium. Furthermore, they demonstrate that a single large N-terminal peptide, cardiodilatin, derived from the prohormone, may exist as a distinct molecular form in the atrium of these species.

Animals↗
PubMed1988

Effect of right ventricular pacing on ventricular rhythm during atrial fibrillation.

In 13 patients with atrial fibrillation, the effect of right ventricular pacing at various rates on spontaneous RR intervals was studied. Five hundred consecutive RR intervals were recorded and measured before and during varying right ventricular pacing rates. As anticipated, all RR intervals longer than the right ventricular pacing intervals were abolished. However, RR intervals shorter than the right ventricular pacing intervals were also eliminated. It is difficult to explain the elimination of RR intervals shorter than the pacing intervals with the accepted concepts concerning the mechanisms governing the rate and rhythm of the ventricular response to atrial fibrillation. An alternative explanation may be that during atrial fibrillation the atrioventricular node behaves as a nonprotected pacemaker that is electrotonically modulated by the chaotic atrial electrical activity. The result is a random ventricular rhythm. With right ventricular pacing, the automatic focus is depolarized by the retrogradely concealed conducted ventricular impulses, the short RR intervals are not generated as a consequence and the rhythm becomes pacemaker dependent.

Aged↗
PubMed1988

Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: a phosphorus-31 nuclear magnetic resonance study.

To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was then isolated and perfused by the Langendorff technique. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor myocardial energy metabolism and intracellular pH during control perfusion and 30 min of total ischemia (37 degrees C), followed by 30 min of reperfusion. Pretreatment with anipamil altered neither left ventricular developed pressure under normoxic conditions nor the rate and extent of depletion of adenosine triphosphate (ATP) and creatine phosphate during ischemia. Intracellular acidification, however, was attenuated. On reperfusion, hearts from anipamil-pretreated animals recovered significantly better than untreated hearts with respect to replenishment of ATP and creatine phosphate stores, restitution of low levels of intracellular inorganic phosphate and recovery of left ventricular function and coronary flow. Intracellular pH recovered rapidly to preischemic levels, whereas in untreated hearts a complex intracellular inorganic phosphate peak indicated the existence of areas of different pH within the myocardium. It is concluded that anipamil pretreatment protects the heart against some of the deleterious effects of ischemia and reperfusion. Because this protection occurred in the absence of a negative inotropic effect during normoxia, it cannot be attributed to an energy-sparing effect during ischemia. Therefore, alternative mechanisms of action are to be considered.

Animals↗