Search PubMed⌕ Search

Biomedical subjects

M J Janse

Publications and source records attributed to M J Janse.

At least 127 records · Page 7Linked to original sources
PubMed1987

Myocardial metabolism, catecholamine balance, and left ventricular function during coronary artery surgery: effects of nitroprusside and nifedipine.

The effects of nitroprusside and nifedipine on myocardial oxygen consumption (MVO2), catecholamine release, and left ventricular (LV) function (using 2D transesophageal echocardiography) were compared. Thirty-seven patients undergoing coronary artery surgery, anesthetized with fentanyl, 100 micrograms/kg, were studied. All had good LV function and had been receiving long-term oral beta-blocking therapy. Patients were randomly allocated to one of three groups. Group C (n = 12) received no vasodilator and served as control. Group S (n = 13) received nitroprusside at an initial rate of 1 microgram/kg/min. Group N (n = 12) received nifedipine at an initial rate of 0.7 microgram/kg/min. Baseline measurements were obtained ten minutes after intubation. Vasodilator therapy was then started in groups S and N. Infusion rates were adjusted to maintain systolic blood pressure (SBP) between 80% and 120% of baseline values. Additional measurements were made ten minutes after the start of the infusion, ie, before surgery (in group C immediately before surgery), and after sternotomy when the pericardium was opened. The mean (+/- SD) total dose requirements were 1.9 +/- 0.5 micrograms/kg/min for nitroprusside and 1.1 +/- 0.2 micrograms/kg/min for nifedipine. The mean (+/- SD) total infusion time was 31 +/- 5 minutes for nitroprusside and 32 +/- 11 minutes for nifedipine. After sternotomy, heart rate increased in all groups. At this time arterial blood pressure and systemic vascular resistance (SVR) increased in group C. SVR was decreased after the first ten minutes of nitroprusside infusion and after sternotomy in group S. Coronary sinus blood flow, MVO2, and myocardial norepinephrine release increased in group N, but not in groups C or S. After sternotomy, LV percentage area reduction increased in groups S and N, but not in group C. In group N there was a significant correlation (r = 0.65; P less than .05) between the increases in MVO2 and LV percentage area reduction, an estimate of myocardial function. Lactate production occurred in two patients in group C after sternotomy. This was not associated with ECG changes, but in one patient regional wall motion abnormalities developed. No evidence of myocardial ischemia was observed in groups S and N. However, in contrast to nitroprusside, the use of nifedipine was associated with increases in MVO2, myocardial norepinephrine release, and inotropy.

Blood Pressure↗
PubMed1987

Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle.

Extracellular and intracellular longitudinal resistances (ro and ri), transmembrane potentials, and conduction velocity were determined in arterially blood-perfused rabbit papillary muscles. Cable analysis was made possible by placing the muscle in a H2O-saturated gaseous environment, which acted as an electrical insulator. Ischemia was produced by exchanging the O2 in the atmosphere by N2 (94% N2-6% CO2) in addition to arresting coronary flow. The first 10-15 minutes of ischemia were characterized by an increase in ro, while ri remained constant. The early part of the increase in ro coincided with the drop in perfusion pressure and was probably due to the diminution of intravascular volume. Rapid electrical uncoupling, reflected by an increase in ri (threefold within 5 minutes), occurred thereafter. The dissociation between the early increase in ro and the delayed increase in ri produced an initial increase in the ratio ro:ri, which subsequently decreased. The decrease in conduction velocity was less than observed in intact hearts with ischemia. This difference is explained by the relatively small changes in resting membrane potential and action potential amplitude in the preparation used. Our results suggest that in the early, reversible phase of ischemia, the increase in ro contributes to a small but significant extent to the slowing of conduction. After 15-20 minutes, the rapid cellular uncoupling, which was most likely coincident with breakdown of cellular homeostasis, may contribute to the occurrence of arrhythmias during this phase of ischemia. Moreover, the early change in the ratio ro:ri will influence the amplitude of the extracellular electrograms following coronary occlusion (TQ-segment and ST-segment shifts).

Action Potentials↗
PubMed1986

Electrophysiological basis for arrhythmias caused by acute ischemia. Role of the subendocardium.

The major electrophysiological changes during the first 10 min of myocardial ischemia caused by complete obstruction of a coronary artery are a reduction in membrane potential, a decrease in action potential amplitude and upstroke velocity, and a prolongation of recovery of excitability following an action potential. Conduction velocity in the direction parallel to the long axis of myocardial fibers (VL) and in the transverse direction (VT) in normal myocardium are in the order of 40 cm/s and 20 cm/s respectively. During ischemia, conduction velocity decreases and lowest values for VL are in the order of 20 cm/s, for VT around 10 cm/s, before the ischemic tissue becomes inexcitable. Calculated dimensions of a possible re-entrant circuit in acutely ischemic myocardium (the product of refractory period and conduction velocity) are in the order of 7 to 8 cm. Re-entrant circuits of such dimensions were indeed demonstrated by simultaneous recording of 125 extracellular potentials from the epicardial surface of the ventricles during spontaneously occurring ventricular arrhythmias after coronary occlusion. Previous studies provided evidence that premature ventricular depolarization which initiate re-entry originated in the subendocardium, and the present experiments confirmed this. Destruction of the subendocardium of isolated, Langendorff perfused canine hearts, including the Purkinje system, by intracavitary application of phenol, did not, however, abolish ectopic activity during either ischemia or reperfusion, although the nature of the arrhythmias during ischemia was different from those in intact hearts. Coupling intervals of ectopic beats were longer in phenol-treated hearts than in intact hearts, but the site of origin of initial ectopic beats leading to ventricular tachycardia could not be determined. Re-entrant circuits with revolution times in the order of 340 to 400 ms accounted for the slow tachycardias observed in phenol-treated hearts. In contrast to intact hearts, these tachycardias never degenerated into ventricular fibrillation, indicating that an intact Purkinje system may be a necessary requirement for ventricular fibrillation to occur during acute, regional myocardial ischemia.

Animals↗
PubMed1986

Changes in conduction velocity during acute ischemia in ventricular myocardium of the isolated porcine heart.

Conduction velocities along longitudinal (vL) and transverse (vT) fiber axes were determined in isolated porcine hearts from subepicardial activation patterns that were produced by local stimulation and measured with a multiterminal electrode. In some of the experiments extracellular [K+] ([K+]o) and transmembrane potentials were recorded. During normal perfusion vL and vT were (cm/sec) 50.08 +/- 2.13, (SE) and 21.08 +/- 0.97. After 3 to 5 min of global ischemia, vL and vT decreased to approximately 30 and 13 cm/sec. Before the occurrence of total inexcitability propagation became time dependent 2: 1 block developed and centrifugal spread from the stimulus site was partially blocked at short intervals and was normal at long intervals. This suggested that slowed conduction was dependent on spatial nonuniformities of recovery from excitability. Slowing of conduction during ischemia was not explained by accumulation of [K+]o alone, because vL and vT at a given [K+]o were lower during ischemia than during perfusion with elevated K+. In hearts perfused at 20 mM [K+]o "slow responses" were produced by addition of epinephrine (2.5 X 10(-5)M). Resting membrane potentials of slow responses were significantly lower than of depressed action potentials during ischemia. The values vL and vT of slow responses (10 and 5 cm/sec) were much lower than the lowest values during ischemia (20 and 10 cm/sec). This indicates that slow conduction in ischemia is associated with depressed action potentials initiated by a partially inactivated rapid Na+ inward current. The time dependence of nonuniform propagation and the relatively high conduction velocities explain two major characteristics of reentrant tachycardias in acute ischemia: the large diameters of reentrant circuits and the beat-to-beat changes in localization of conduction block.

Action Potentials↗
PubMed1986

The subendocardial border zone during acute ischemia of the rabbit heart: an electrophysiologic, metabolic, and morphologic correlative study.

Isolated preparations of rabbit interventricular septum were perfused through the coronary arteries with oxygenated Tyrode's solution and placed in a tissue bath where they were superfused as well. Transmembrane potentials were simultaneously recorded from the subendocardium with two flexibly mounted microelectrodes, one from a superficial cell, and the other from a deep cell. Ischemia was produced by stopping coronary flow while superfusion with oxygenated Tyrode's solution was maintained. After a 7 to 12 min ischemic period, the preparation was fixed by coronary perfusion with fixative while the microelectrodes remained in place. After fixation, the microelectrodes were withdrawn. Appropriate tissue blocks were cut in 4 micron serial sections and the microelectrode track was followed until the tip position was identified. Transmembrane potentials during ischemia were divided into two categories: "border zone" potentials (resting membrane potential [RMP] 73 +/- 3 mVe, action potential amplitude [APA] 81 +/- 13 mV, action potential duration [APD] 116 +/- 48 msec, n = 12) and "ischemic" potentials (RMP 53 +/- 4 mV, APA 44 +/- 11 mV, APD 102 +/- 42 msec, n = 8). Ischemic potentials were recorded from cells at depths greater than 560 micron below the endocardial surface and border zone potentials were recorded in a layer at between 130 and 650 micron below the surface. In a separate series of experiments, extracellular concentrations of K+ and pH were measured with ion-sensitive electrodes at different depths and, after a 10 min period of ischemia, part of the septum was placed in liquid nitrogen to allow determination of phosphocreatine (PC) levels in successive 50 to 100 micron layers. After 10 min of ischemia, extracellular K+ gradually increased from 4 to 9 mM in endocardium to a depth of 600 micron, pH fell from 7.4 to 6.6 over the same distance, and PC decreased to very low, stable levels at only 800 micron. It is concluded that in the first 10 min of acute ischemia, an endocardial border zone exists of 40 to 60 cell layers in which transmembrane potentials are affected relatively little by ischemia. Within this electrophysiologic border zone extracellular K+ was lower than 9 mM, pH was higher than 6.6, and tissue content of PC was not lower than 40% of normal. In layers deeper than 600 micron, with further development of a metabolic gradient, action potentials became markedly depressed. This electrophysiologic inhomogeneity within the ischemic subendocardium could be a factor in arrhythmogenesis during the first minutes of ischemia.

Action Potentials↗
PubMed1986

Electrophysiological effects of myocardial ischaemia. Relationship with early ventricular arrhythmias.

Transmembrane potentials and local extracellular electrograms were recorded from isolated Langendorff perfused canine and porcine hearts. Experiments were also performed on hearts in open-chested anaesthetized animals. Following occlusion of a major coronary artery, resting membrane potential decreased, resulting in depression of the TQ segment. Action potential amplitude and upstroke velocity decreased, leading to ST elevation and delayed activation. At resting membrane potentials around -60 mV, ischaemic cells became inexcitable. Arguments are presented that action potentials during the first 10 min of ischaemia, when malignant ventricular arrhythmias frequently occur, are not 'slow responses' but are instead 'depressed fast responses' where inward current is carried by Na+ ions through partially inactivated fast channels. Mapping experiments, in which 60 to 98 electrograms were simultaneously recorded during spontaneous ventricular arrhythmias demonstrated that ventricular tachycardia is due to macro-re-entry with the re-entrant pathway having a wavelength of the order of 6 cm. No evidence was found for macro-re-entry being the cause of ventricular premature depolarizations. A hypothesis is put forward, whereby the experimental findings of a 'focal' origin are explained on the basis of electrotonic transmission through a small inexcitable zone close to the ischaemic border.

Action Potentials↗
PubMed1986

Electrophysiology and electrocardiology of acute myocardial ischemia.

Transmembrane potentials and local direct current extracellular electrograms were simultaneously recorded from intact, isolated porcine and canine hearts, perfused according to the Langendorff technique with a 1:1 mixture of blood and Tyrode solution. Regional ischemia was produced by clamping the left anterior descending coronary artery. The first change produced by ischemia was a loss of resting membrane potential, resulting in a depression of the TQ-segment in the local electrogram. Later, action potential amplitude decreased, leading to true ST-segment elevation. Action potential shortening of ischemic cells caused positive T waves, provided activation delay was not marked. When activation of ischemic cells was considerably delayed, and repolarization in the ischemic area occurred later than in non-ischemic myocardium, local T waves became negative. Changes in TQ- and ST-segments and in T waves of local electrograms can qualitatively be explained by local current circuits, resulting from intracellular potential differences between ischemic and normal cells in the different phases of the cardiac cycle. ST-segment elevation, as recorded with conventional, condenser-coupled, alternating current amplifiers, can be caused by a diastolic current of injury (due to depolarization of resting membrane potential), or to a combination of diastolic and systolic current of injury (due to a reduction of action potential amplitude).

Angina Pectoris↗
PubMed1985

Variability of recovery of excitability in the normal canine and the ischaemic porcine heart.

Normal hearts: Refractory periods were determined at 12 to 15 intramural sites of the normal canine left ventricle during steady state regularly driven rates, after each of a series of four early premature beats, and after a long pause following a series of three premature beats. The dispersion in recovery of excitability, defined as the standard deviation of the mean refractory periods, was in absolute terms the same for all three situations. However, since mean refractory periods shortened after premature beats, in relative terms, dispersion of recovery of excitability was greatest after a series of four premature beats. The refractory periods of the specialized conducting system determined during the initial beats of a new, faster rate, showed that in subsequent beats, the refractory periods of the bundle branches are alternatively shorter and longer than the refractory period of the ventricular myocardium. An example of 'concealed bundle branch re-entry' is shown. It is concluded that normal hearts are well protected from sustained arrhythmias induced by changes in rate and rhythm. Ischaemic hearts: In isolated, Langendorff perfused porcine hearts, regional ischaemia was produced by clamping the left anterior descending coronary artery. The transmembrane potentials then were recorded within a distance of less than 1 mm from a stimulating electrode in the ischaemic zone. Refractory periods in the central ischaemic zone lengthened, those in the border zone shortened. Recovery of excitability in an ischaemic myocardium cannot be expressed in terms of intervals between stimuli alone: the quality of the premature response must also be taken into account. Typically, responses elicited well after completion of repolarization have markedly reduced amplitudes and upstroke velocities. Thresholds for stimulation increase in an ischaemic myocardium, and the use of strong test stimuli leads to artefactual results: evidence is presented that strong premature stimuli excite less injured cells far away from the stimulus site. Premature stimuli often induced arrhythmias. Presence of local responses in central ischaemic cells suggest regions of unidirectional block, creating circumstances where re-entry may occur. After a long pause, alternation in action potential amplitude and duration became more pronounced: possibly, a premature impulse elicited after a long pause encounters more regions of unidirectional block so that re-entry is facilitated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Effects of unilateral stellate ganglion stimulation and ablation on electrophysiologic changes induced by acute myocardial ischemia in dogs.

We recorded direct-current extracellular electrograms simultaneously from 60 left ventricular epicardial sites in 38 alpha-chloralose-anesthetized dogs during repeated, 5 min coronary arterial occlusions. In each dog recordings made during control occlusions were compared with those made in occlusions after, or during, the following interventions on the sympathetic nervous system: left stellate ganglion stimulation, left stellectomy, right stellectomy, and clamping the abdominal aorta with intact sympathetic nerves to induce a rise of blood pressure equal to that present during left stellate stimulation. Heart rate was kept constant. Measurements included determination of TQ segment potentials and times of local activation. After 2 min of ischemia, the degree of TQ segment depression was increased by left stellate ganglion stimulation and was decreased by both left stellectomy and clamping the aorta. Also, the area showing negative TQ potentials, indicating decreased resting membrane potentials, was enlarged by both left stellate stimulation and right stellectomy and reduced by left stellectomy. No differences were found in the results of experiments in which the left anterior descending coronary artery was occluded and those in which the circumflex branch was occluded. Left stellate stimulation significantly improved conduction within the ischemic zone. No evidence was found to suggest that the arrhythmogenic effects of left stellate stimulation and of right stellectomy, confirmed in the present study, resulted from an increased likelihood for reentry in the subepicardium of the ischemic zone.

Animals↗
PubMed1984

On sudden death.

Explore the source record for details and available documents.

Death, Sudden↗
PubMed1984

Combined effects of hypoxia, hyperkalemia and acidosis on membrane action potential and excitability of guinea-pig ventricular muscle.

The effects of hypoxia (with and without acidosis) on membrane action potentials and recovery kinetics of their upstroke velocity (Vmax) were studied in isolated guinea-pig papillary muscles at various extracellular K+ concentrations. At 5 mM [K+]0, hypoxia (hypoxic and glucose-free perfusate) at pH 7.4 caused a progressive shortening of action potential duration and a slight decrease in Vmax and resting potential. The recovery kinetics of Vmax assessed by premature stimuli were not affected by hypoxia. At high [K+]0 of 10 or 12 mM, hypoxia caused a marked decrease in Vmax, while the shortening of the action potential and the decrease in resting potential were similar to those at 5 mM [K+]0. However, the recovery kinetics of Vmax were markedly slowed by hypoxia. When hypoxia was added in the presence of mild acidosis (pH 6.8), the shortening of the action potential due to hypoxia was appreciably less. However, other hypoxia-induced changes in action potential and in recovery kinetics of Vmax under normal and high [K+]0 were not influenced by the concomitant acidosis. These results show that the depressant effect of hypoxia on the action potential upstroke and on the recovery of excitability of ventricular myocardium is increased when the muscles are partly depolarized at high K+. Slight differences in extracellular K+ in the presence of hypoxia have a marked effect on the time course of recovery of excitability. This inhomogeneity in refractoriness could be important for the occurrence of re-entrant arrhythmias in ischemic myocardium.

Acidosis↗
PubMed1984

Sudden death during longterm ambulatory monitoring.

Ten instances of sudden cardiac death documented with longterm ambulatory electrocardiography are described. All had coronary artery disease. The lethal arrhythmia was ventricular fibrillation in seven, bradyarrhythmia ending in asystole in two, and electromechanical dissociation in one. There was no specific arrhythmia pattern in the preceding hour of the terminal event and no predictable electrical trigger for the lethal arrhythmia. The literature on the subject has been reviewed. It appears from the information available that larger series of documented sudden death cases are needed if one wishes to define subgroups with a preventable case of sudden cardiac death.

Adult↗