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Biomedical subjects

H Bjørnstad

Publications and source records attributed to H Bjørnstad.

At least 19 recordsLinked to original sources
PubMed1995

Diltiazem does not increase ventricular fibrillation threshold during hypothermia.

This study was designed to investigate whether the calcium channel blocker diltiazem affects the threshold for ventricular fibrillation during hypothermia in dogs. Ten dogs were cooled from 37 to 25 degrees C and rewarmed to 37 degrees C. The threshold for ventricular fibrillation was determined at body temperatures 37, 34, 31, 28 and 25 degrees C by programmed electrical stimulation using a stimulation protocol which involved application of maximal five extrastimuli. At 25 degrees C, six dogs were given an i.v. bolus dose of 100 micrograms.kg-1 followed by a continuous infusion of 100 micrograms.kg-1.h-1 of diltiazem hydrochloride. The other four dogs, were given no drugs at 25 degrees C and served as a control group. The dogs were rewarmed, and the stimulus protocol was performed at the same temperatures as during cooling. Cooling from 37 to 25 degrees C reduced the threshold for ventricular fibrillation in both groups. Heart rate were reduced, monophasic action potential duration at the apex and base of the heart increased from 167 +/- 5 ms to 469 +/- 17 ms and from 164 +/- 5 ms to 466 +/- 17 ms, respectively, when the temperature was reduced. The ventricular effective refractory period increased from 176 +/- 9 ms at 37 degrees C to 472 +/- 15 ms at 25 degrees C. Cooling increased QRS time on the ECG from 55 +/- 4 ms to 138 +/- 13 ms. Addition of diltiazem at 25 degrees C did not affect the threshold for ventricular fibrillation during rewarming. Further, diltiazem at 25 degrees C did not affect the heart rate or refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1994

Effect of bretylium tosylate on ventricular fibrillation threshold during hypothermia in dogs.

How bretylium tosylate affected the ventricular fibrillation threshold, electrophysiological parameters, and plasma catecholamine levels during hypothermia in dogs was studied. Threshold for ventricular fibrillation was determined by programmed electrical stimulation using a stimulation protocol that involved applying a maximum of five extrastimuli at body temperatures 37, 34, 31, 28, and 25 degrees C, and at the same temperatures during rewarming. Electrocardiogram, epicardial monophasic action potentials (MAP), and electrograms were recorded, and ventricular effective refractory period (VERP) was determined at each of the above temperatures. In one group (n = 7), a bolus dosage of bretylium tosylate (BT), 6 mg/kg body wt, was administered at 25 degrees C before rewarming. Another group (n = 4) was exposed to cooling and rewarming without addition of BT. Cooling to 25 degrees C reduced ventricular fibrillation threshold linearly, reduced heart rate, increased VERP and MAP, and slowed myocardial conduction velocity in both groups. There was no overall increase in plasma catecholamine levels during cooling. Addition of BT at 25 degrees C increased ventricular fibrillation threshold during rewarming compared with cooling. Addition of BT at 25 degrees C increased VERP by +/- 32 milliseconds and the corrected JT time by 0.06 +/- 0.02 seconds. VERP and JTc increased during rewarming with BT compared with cooling with no drug. BT had no effect on conduction velocity, and plasma catecholamine levels were not reduced. The antiarrhythmic effect of BT during hypothermia was attributed to an increased wavelength of refractoriness by its increase in the refractory period. This increased wavelength of refractoriness may prevent excitable gaps or increase circuit pathway in the setting of reentry arrhythmias.

Action Potentials↗
PubMed1994

Prevention of some hypothermia induced electromechanical changes by calcium channel blockade.

OBJECTIVE: Cooling induces electromechanical changes in the heart. The aim of the study was to examine how the calcium channel blocker, nisoldipine (NIS), altered these changes compared to those induced by other drugs that shorten action potential duration such as tetrodotoxin and nicorandil. METHODS: Guinea pig papillary muscle action potentials and developed force were recorded using the conventional microelectrode technique and a force transducer. Restitution of action potential duration was determined by introducing extrastimuli at progressively longer diastolic intervals from 40 to 9000 ms. Preparations were divided into four groups: (1) no drug (control); (2) 1 microM tetrodotoxin, a sodium channel blocker; (3) 1 mM nicorandil, an ATP sensitive potassium channel activator; and (4) 1 microM nisoldipine (n = 6 in each group). Action potential duration and developed force were recorded after addition of drug at 37 degrees C, and at each 1 degree C change in temperature during cooling to 27 degrees C. The restitution protocol was performed at 37 degrees C and 27 degrees C. RESULTS: Tetrodotoxin had no effect on action potential duration at 90% of repolarisation (APD90) while nisoldipine and nicorandil greatly shortened APD90. Cooling from 37 degrees to 27 degrees C with nisoldipine produced less hypothermia induced lengthening in APD90 than in the other group. Developed force did not increase with reduction in temperature in the presence of nisoldipine. The range of premature action potential durations was defined as the difference in APD90 at diastolic interval of 40 and 100 ms. This range decreased with nisoldipine in contrast to the marked increases that occurred in the other groups during cooling. CONCLUSIONS: Increased intracellular Ca2+ might be responsible for the hypothermia induced increase in APD90, developed force, and range of premature action potential durations, since calcium channel blockade, which prevents an increase in intracellular Ca2+, greatly reduced these changes. The reduced range of premature action potential durations may reduce dispersion of ventricular refractoriness, and hence be expected to decrease hypothermia induced arrhythmias.

Action Potentials↗
PubMed1994

Ambulatory electrocardiographic findings in top athletes, athletic students and control subjects.

Aim of the present study was to evaluate 24 h electrocardiographic recording in 30 top athletes, 30 athletic students and 30 sedentary control subjects. Each group consisted of 15 males and 15 females and were matched for age (about 24 years). Training was not allowed during the recording. Top athletes had the lowest diurnal and nocturnal heart rate, but the difference between top athletes and athletic students was far less pronounced than between athletic students and controls. This may indicate that bradycardia reaches a lower limit with moderate degrees of training. Atrioventricular (AV) block II was found in 3 top athletes and 4 athletic students and in none of the subjects, the longest pause being 2.4 s in both athletic groups. Most episodes occurred during night and nearly all were Mobitz type I. In all cases of AV block II the QRS complexes were narrow and AV block III did not occur. SA block was found in 3 top athletes, 1 athletic student and 1 control subject, the longest pause being 3.1, 2.9 and 1.9 s, respectively. Ventricular premature beats were rare in all groups and complex ventricular arrhythmias were not found. Half of the subjects were in Lown class 0, the other half in Lown class 1. Supraventricular premature beats were also scarce and most frequent in top athletes, followed by athletic students and sedentary controls (2.0, 1.0, 0.7 beats/h, respectively).

Adult↗
PubMed1994

Electrocardiographic findings of repolarization in athletic students and control subjects.

We have investigated resting electrocardiograms in 1,299 athletic students and 151 sedentary control subjects. ST elevations were more frequent and pronounced in athletes compared to controls, whereas there was no difference in ST depressions. Athletes with ST elevation above 2 mm were characterized by lower heart rate, increased PQ duration, increased indices of left, right and septal hypertrophy and T wave amplitude. Negative T waves in 3 of 6 precordial leads, V3-6, were found in 1.5% of athletes and 0.7% of controls, and in V5-6 in 0.4% of athletes and none of controls, the differences not being significant. Athletes had significantly more often a T wave axis between +30 and -180 degrees and less often a frontal T wave axis between +30 and +180 degrees. The mean QRS-T angle was significantly greater in athletes, and U waves were more prominent. Analyzing athletes with QTc below and above 0.430 s, we found an increased heart rate, QRS duration, ST depression and a more pronounced left QRS axis in the group with QTc above 0.430 s. There was a positive correlation between QTc and heart rate which indicates that the use of Bazett's formula leads to an underestimation of QTc at lower heart rates and to an overestimation at higher heart rates. Bazett's formula does not provide an adequate correction for heart rate and should be used with caution. Our finding of a prolonged QTc in athletes compared to control subjects in spite of lower heart rate in the athletic group demonstrates that a real QTc prolongation exists in athletes.

Adult↗
PubMed1994

Left ventricular mass and cardiovascular reactivity in young men.

The relation between left ventricular wall thickness and mass, arterial plasma catecholamines, and blood pressure at rest and during a mental arithmetic challenge and a cold pressor test was examined in 69 healthy men 19 years of age. The subjects were recruited from the 1st (n = 21), 50th (n = 26), and 99th (n = 22) percentiles in mean blood pressure. All underwent echocardiography to determine mean wall thickness and left ventricular mass. Continuous intra-arterial blood pressure, electrocardiogram, and arterial sampling of plasma catecholamines were performed after 30 minutes of supine rest, during a 5-minute mental arithmetic challenge, and during a 1-minute cold pressor test. Stepwise multiple-regression analyses considering mean wall thickness and left ventricular mass as the dependent variables were applied. Intra-arterial systolic blood pressure (r = .54, P < .0001) and arterial plasma epinephrine (r = .31, P = .009) after 30 minutes of supine rest were the only independent explanatory variables of mean wall thickness (multiple R2 = .33, P < .0001). Blood pressure at screening and during mental stress and cold pressor tests were not independent explanatory variables. The present study suggests that resting arterial blood pressure and plasma epinephrine may be of importance for development of left ventricular hypertrophy.

Adult↗
PubMed1993

Effects of temperature on cycle length dependent changes and restitution of action potential duration in guinea pig ventricular muscle.

OBJECTIVE: The aim was to investigate the effects of temperature on cycle length dependent changes of action potential duration and on restitution of action potential duration. METHODS: Guinea pig papillary muscle action potentials were recorded using conventional microelectrode techniques. Action potential duration was measured at cycle lengths ranging from 500 to 2000 ms at both 27 degrees C and 37 degrees C. Restitution of action potential duration was determined by introducing an extra stimulus at progressively longer diastolic intervals from 40 to 9000 ms at pacing cycle lengths of 500, 1000, and 2000 ms. RESULTS: At 37 degrees C, action potential duration measured at 90% of repolarisation (APD90) during continuous pacing and the maximum value of APD90 achieved during restitution (APD90pl) decreased by 18(SEM 6) ms (n = 7) and 24(7) ms (n = 6), respectively, when pacing cycle length was reduced from 2000 to 500 ms. At 27 degrees C, the magnitude of the shortening of APD90 and APD90pl observed when pacing cycle length was similarly reduced was greater than at 37 degrees C, ie, 143(21) ms (n = 6) and 115(11) ms (n = 6), respectively. Thus the relation for restitution of action potential duration shifted downwards with reduction in pacing cycle length, and the magnitude of this shift was greater at 27 degrees C than at 37 degrees C. The difference between APD90 at the shortest diastolic interval (40 ms) and at diastolic interval of 100 ms (range of premature action potential durations) was much greater at 27 degrees C than at 37 degrees C at all three pacing cycle lengths. CONCLUSIONS: Reduction in temperature magnifies the cycle length dependent changes in action potential duration both during abrupt changes in cycle length, as with an extra stimulus, and during changes of steady state cycle length. This may indicate a greater dispersion of premature action potential durations during hypothermia, and hence predispose to hypothermia induced arrhythmias.

Action Potentials↗
PubMed1993

Mechanisms for hypothermia-induced increase in contractile force studied by mechanical restitution and post-rest contractions in guinea-pig papillary muscle.

Lowering myocardial temperature increases contractile force, presumably by increasing intracellular calcium content. To study the mechanisms behind this, we compared the effects of some known inotropic interventions with hypothermia on mechanical restitution and post-rest contractile force in isolated guinea-pig papillary muscles. In four groups (n = 6 per group), the effects of: (1) reducing the ability for Na/Ca exchange to extrude Ca2+ (a) by increasing [Na+]i with ouabain or (b) by increasing [Ca2+]o; and (2) activation of calcium channels with Bay-K 8644, were compared with lowering temperature from 37 to 27 degrees C. Normally (at 37 degrees C and 2 mM CaCl2), mechanical restitution could be described by a rapid recovery phase with a time constant between 180 and 220 ms, followed by a slowly decaying phase with a time constant between 5000 and 8000 ms and post-rest contractions (1-10 min rest) were markedly depressed compared to steady-state contractions. Steady-state developed force was markedly increased at 27 degrees C, after 1 microM ouabain, 6 mM CaCl2 or 0.1 microM Bay-K 8644. At 27 degrees C the rapid recovery phase of restitution was delayed while the slowly decaying phase was not affected. Ouabain and increased [Ca2+]o caused elevation of the slowly decaying phase of restitution and markedly attenuated the post-rest depression of developed force, which may be attributed to a reduced diastolic extrusion of Ca2+ via the Na/Ca exchanger. Hypothermia and Bay-K 8644 on the other hand, augmented this post-rest depression. Hence, this study suggests that increased Ca2+ influx due to delayed inactivation of calcium channels may account for the increased developed force during hypothermia rather than reduced diastolic extrusion of Ca2+ via the Na/Ca exchanger.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Electrocardiographic findings of heart rate and conduction times in athletic students and sedentary control subjects.

We have investigated resting electrocardiograms in 1,299 athletic students and 151 sedentary control subjects. Bradycardia was significantly more common in athletes. The athletic group was divided according to a heart rate < 50, 50-100, and above 100 beats/min. Atrioventricular conduction time, prevalence of ectopic beats and other rhythms, parameters of right and left ventricular hypertrophy, ST elevation, and T wave amplitude were increased in the sinus bradycardia group. A significant negative correlation was found between heart rate and PQ duration in athletes. In the sinus tachycardia group, the PQ duration was shorter and the ST depression more prominent than in the other groups. The subjects were also divided according to PQ > or = 0.22, 0.21-0.12, and < 0.12 s. Parameters of left ventricular hypertrophy were markedly increased in athletes with PQ > or = 0.22 s, while the heart rate was only slightly decreased, suggesting an association between prolonged atrioventricular conduction time and left ventricular hypertrophy. Incomplete right bundle branch block was associated with a lower heart rate, increased duration of QRS and QTC, voltage of precordial Q waves, indices of right ventricular hypertrophy, and negative T waves. These findings are typical of right ventricular hypertrophy, indicating a close relation of incomplete right bundle branch block to right ventricular hypertrophy.

Adaptation, Physiological↗
PubMed1993

Electrocardiographic findings according to level of fitness and sport activity.

We have investigated 52 ECG parameters in 1,299 athletes and 151 control subjects. Data on fitness were available in 840 athletes. They were split in three groups according to level of fitness and compared with each other and the control group with regard to the ECG findings. The most marked findings with increasing fitness were lower heart rate, increased prevalence of bradycardia, increased precordial ST segment elevation, and increased T wave amplitudes. Only slightly increased parameters of right and left ventricular hypertrophy were found. A highly significant correlation was found between fitness and heart rate, while no such correlation was found between fitness and the Sokolow index. The athletes were subdivided according to sports activity, and ECG parameters were compared in endurance athletes, ball players, strength athletes, gymnasts, and controls. Apart from a lower heart rate in endurance athletes and ball players as compared with strength athletes and gymnasts, few differences were found between the athletic groups. The heart rate is the most important parameter reflecting level of fitness and sports activity. The differences in ECG findings are relatively minor and do not distinguish type of sport activity.

Adaptation, Physiological↗
PubMed1991

[Antiarrhythmic agents. Receptor hypothesis explains mechanisms of action].

Antiarrhythmic drugs are usually classified according to Vaughan Williams' classification I-IV. Class I includes the membrane stabilizers, class II includes the beta-blockers, drugs in class III lengthen the cardiac action potential and refractory period and class IV includes the calcium blockers. The effect of most antiarrhythmic drugs changes with heart rate and the level of myocardial depolarization, and these changes in effect can be explained by the modulated receptor hypothesis. Most class I antiarrhythmic drugs have greatest antiarrhythmic effect during periods of fast heart rate and in depolarized ischemic myocardium, and this might be attributed to greater affinity of the drugs for open or inactivated sodium channels. Most class III antiarrhythmic drugs have greatest effect during periods of slow heart rates, which may be attributed to greater affinity for closed potassium channels.

Anti-Arrhythmia Agents↗
PubMed1991

Class III antiarrhythmic action of d-sotalol during hypothermia.

To investigate whether changes in temperature influence the electrophysiologic effects of the class III antiarrhythmic agent d-sotalol, we studied its effects on propranolol-pretreated guinea pig papillary muscles at temperatures ranging from 37 degrees to 27 degrees C by means of conventional microelectrode techniques. We also examined the rate-dependent effect of d-sotalol at 37 degrees and 27 degrees C. Before the addition of d-sotalol, reducing the temperature from 37 degrees to 27 degrees C increased the action potential duration recorded at 50% repolarization (APD50) from 112 +/- 7 msec to 271 +/- 15 msec and action potential duration recorded at 90% repolarization (APD90) from 136 +/- 7 msec to 325 +/- 10 msec. d-Sotalol (50 mumol/L) lengthened APD50 and APD90 to a greater degree at low temperatures. Thus at 37 degrees C d-sotalol lengthened APD50 and APD90 by 12 +/- 6 msec and 19 +/- 5 msec, and at 27 degrees C by 37 +/- 5 msec and 52 +/- 7 msec, respectively. d-Sotalol produced its greatest effect on APD at long pacing cycle lengths, thus demonstrating reverse dependence. This rate-dependent effect was more marked at 27 degrees C than at 37 degrees C. The greater effect of d-sotalol on APD at long pacing cycle lengths may be explained by the modulated receptor hypothesis, assuming that the drug has a higher affinity for closed potassium channels. Such a mechanism may also explain the accentuated class III antiarrhythmic action of d-sotalol observed during hypothermia.

Action Potentials↗
PubMed1991

Electrocardiographic findings according to sex in athletes and controls.

We have previously compared the electrocardiogram of 1,299 male and female students of physical education and sports with 151 age- and sex-matched sedentary controls and found that the former had lower heart rate, longer conduction times and increased voltages. The same material of 1,450 young adult subjects was split according to sex into 617 females and 833 males in order to analyze the influence of gender on the resting 12-lead electrocardiogram. We found that females had a significant higher heart rate, shortened conduction times (PQ, Q, ventricular activation time and QRS) and a prolonged repolarization time (QTc), decreased P, Q and T amplitudes as well as indices of right, septal and left hypertrophy, and ST elevation in precordial leads were lower in females than in males. These differences were highly significant with p values less than 0.0001 for almost all parameters. Sinus bradycardia was more common in men and sinus tachycardia in women. The prevalence of other rhythms and supraventricular and ventricular premature beats was low in both sexes. AV block grade I was found in 1% of females and 3% of males (p less than 0.02). Notching of R/S in V1-V2 and incomplete right bundle branch block were less common in females (p less than 0.0001). The differences in ECG parameters between the two sexes in the total material persisted also when the athletic and control groups were investigated separately. Gender seems to be highly important for most ECG parameters in the resting ECG. This points to the necessity of discussing different upper normal limits for ECG parameters according to gender.

Adult↗
PubMed1991

Electrocardiographic findings in athletic students and sedentary controls.

We have investigated resting electrocardiograms from 1,299 athletic students taken in the same laboratory during the years 1973-1982 and compared them with electrocardiograms recorded in 151 age- and sex-matched sedentary controls. Fifty-two parameters were recorded for each electrocardiogram and computerized. We found that athletic students had a significant lower heart rate, longer PQ time and a prolonged QTc compared to control subjects. Athletes had higher maximal Q amplitudes in precordial leads, higher R in V1, and higher indices of right ventricular hypertrophy (RV1 + SV5) and left ventricular hypertrophy (Sokolow-Lyon and Grant indices). Furthermore, the athletes had higher maximal ST elevation and higher maximal T wave amplitudes in precordial leads. Sinus bradycardia was more frequent in athletes. All control subjects were in sinus rhythm whereas 0.9% of the athletes had other rhythms (nodal, coronary sinus or wandering pacemaker). Athletes and control subjects did not differ significantly with regard to premature beats, atrioventricular block, bundle branch block or the Wolff-Parkinson-White pattern. We conclude that training induces significant changes in heart rate, conduction times, ST elevation. QRS and T voltage, slow rhythm disturbances and atrioventricular and sinoatrial block were infrequent in the resting electrocardiogram taken in the supine position and disappeared immediately on sitting and during exercise. Training-induced electrocardiographic changes may partly be due to alterations in autonomic tone and partly to structural changes in the myocardium. Different normal criteria for left ventricular hypertrophy may be warranted in athletes.

Adolescent↗
PubMed1991

Cardiac electrophysiology during hypothermia. Implications for medical treatment.

Reduction in body temperature induces characteristic electrophysiological and mechanical alterations of the heart. The heart rate is markedly reduced. Myocardial conduction is slowed, partly due to reduced rate of depolarization of the action potential, and is reflected by widening of the QRS-complex in the ECG. There is also a fall in resting membrane potential. Action potential duration and refractory period are markedly lengthened during hypothermia, attributed to delayed repolarization. This is reflected by increased QT-time in the ECG. Since action potential duration changes significantly even after as small temperature changes as 1 to 2 degrees C, nonuniform cooling or rewarming of the heart may cause significant dispersion of conduction, action potential duration and refractoriness in the myocardium. This dispersion may cause unidirectional block, hence creating a substrate for reentry atrial and ventricular arrhythmias, and may be an important mechanism for explaining the hypothermia-associated arrhythmias. Class III antiarrhythmic drugs such as d-sotalol lengthen long action potentials at low temperatures to a greater extent than the shorter action potentials at higher temperatures. This may further increase dispersion and thereby the tendency towards arrhythmias. Sotalol as an example, shows that some antiarrhythmic drugs may have increased arrhythmogenic effect and should probably be contraindicated during hypothermia.

Electrocardiography↗
PubMed1990

Rate-dependent class III antiarrhythmic action, negative chronotropy, and positive inotropy of a novel Ik blocking drug, UK-68,798: potent in guinea pig but no effect in rat myocardium.

The electromechanical effects of UK-68,798 (UK), a novel class III antiarrhythmic drug, were studied in guinea pig and rat papillary muscles (PMs) and atria in vitro using conventional microelectrode technique. UK (10(-8)-10(-6) M) prolonged the action potential duration (APD) by 21-58% and effective refractory period in parallel, without affecting the resting potential or maximum rate of depolarization in guinea pig PM stimulated at 1 Hz. UK increased the contractile force without prolonging the time to peak force or relaxation. In comparison, 5 x 10(-5) M d-sotalol was needed to induce the same electrophysiological effects as 10(-8) M UK. UK prolonged the APD significantly less at 2 Hz than at 1 and 0.5 Hz. Early afterdepolarizations (EADs) developed in 2 of 11 preparations after 10(-6) M at 0.5 Hz. No reversal of drug effect was seen after up to 2 h washout. UK (10(-9)-10(-5) M) reduced the spontaneous heart rate and prolonged the sinus node recovery time of guinea pig right atria. No effects on rat PM or atria, even after 10(-5) M, indicate a selective action of UK on the delayed rectifying outward potassium current, Ik. These results indicate a potent and selective, rate-dependent class III antiarrhythmic action of UK-68,798 linked with positive inotropy. Increased APD, bradycardia, and induction of EADs, however, represent a potential arrhythmogenic combination.

Action Potentials↗