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Pitfalls in creation of left atrial pressure-area relationships with automated border detection.

Creation of pressure-area relationships (loops) with automated border detection (ABD) involves correction for the variable inherent delay in the ABD signal relative to the pressure recording. This article summarizes (1) the results of in vitro experiments performed to define the range of, and factors that might influence, the ABD delay; (2) the difficulties encountered in evaluating a thin-walled structure like the left atrium in the dog model; and (3) the solutions to some of the difficulties found. The in vitro experiments showed that the ABD delay relative to high-fidelity pressure recordings ranges from 20 to 34 msec and 35 to 57 msec at echocardiographic frame rates of 60/sec and 33/sec, respectively. The delay was not influenced significantly by the type of transducer used, distance from the target area, or size of the target area. The delay in the ABD signal, relative to the echocardiographic image, ranges from nil to less than one frame duration, whereas it is delayed one to two frame durations relative to the electrocardiogram processed by the imaging system. In the dog model, inclusion of even small areas outside the left atrium rendered curves with apparent physiologic contour but inappropriately long delays of 90 to 130 msec. To exclude areas outside the left atrial cavity, time-gain compensation and lateral gain compensation were used much more extensively than during left ventricular ABD recording. By changing the type of sonomicrometers used in our experiments, we were able to record simultaneously ABD and ultrasonic crystal data. However, both spontaneous contrast originating from a right-sided heart bypass pump and electronic noise from the eletrocautery severely interferred with ABD recording.

Animals↗

Influence of left atrial pressure on left atrial appendage flow velocity patterns in patients in sinus rhythm.

To examine changes in left atrial appendage flow velocity patterns in relation to left atrial pressures during sinus rhythm, transesophageal echocardiography and cardiac catheterization were performed in 31 patients with myocardial diseases in sinus rhythm and 20 control subjects without cardiovascular disease. The 31 patients were divided into two groups according to mean pulmonary capillary wedge pressure: the group with high wedge pressure (19.9 +/- 5.8 mmHg) and the group with low wedge pressure (8.6 +/- 2.9 mmHg). The left atrial appendage peak early emptying velocity was decreased significantly in the groups with both high and low wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity was significantly greater in the group with low wedge pressure compared with the control group, whereas it was decreased significantly in the group, with high wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity had a significant negative correlation with wedge pressure. The maximum left atrial appendage area at end systole in the group with high wedge pressure was significantly greater than that in both the group with low wedge pressure and the control group. There was a significant positive correlation between the maximum left atrial appendage area and the wedge pressure, as well as a significant negative correlation between the left atrial appendage ejection fraction during atrial contraction and the wedge pressure. In the group with high wedge pressure, one patient had evidence of left atrial appendage thrombi and two had spontaneous echo contrast. These results suggest that even in patients in sinus rhythm, a marked elevation in the left atrial pressure is likely to reduce the left atrial appendage peak early and late emptying velocities. These changes may be accompanied by an increased incidence of thrombus formation in the left atrial appendage compared with individuals with normal or only slightly elevated left atrial pressures.

Atrial Function↗

Endogenous muscarinic activity attenuates adrenergic inotropic effects in field stimulated atrial myocardium from children with congenital heart defects.

To analyse the possible influence of endogenous muscarinic activity on the inotropic effects of endogenously released noradrenaline in field stimulated myocardial preparations from atria of children with congenital heart defects, we studied the maximal effect of the muscarinic antagonist atropine (1.5 micromol L(-1)). Maximal force of contraction increased by 12.8 +/- 2.0% (SEM), while the maximal rate of development of the force increased by 16.7 +/- 2.7% (SEM). Time to half maximal developed force was 57 +/- 5 s (SEM). Time to peak force, time to relax to the 20% level and relaxation time all decreased significantly after atropine. Compared with endogenous adrenoceptor stimulation alone, the combined effects of partial muscarinic and adrenergic receptor stimulation thus were moderate reductions of the maximal force of contraction and maximal rate of development of the force and increased time to peak force, time to relax to the 20% level and relaxation time. The main effect of the endogenous muscarinic activity probably was to attenuate the effect of the beta-adrenoceptor stimulation. The endogenous muscarinic activity in field stimulated atrial preparations from children is significant, and has to be taken into account in experimental set-ups.

Acetylcholine↗

Intracellular acidosis modulates the stretch-induced changes in E-C coupling of the rat atrium.

By inducing a small reduction of the intracellular pH (0.18 units) with 20 mmol L-1 propionate we demonstrated that acidification changed the responses of isolated rat atria to stretch. Stretch (increase of the intra-atrial pressure) in normal pH increased the Ca2+ transients' amplitude (Indo-1 fluorescence) from 0.26 +/- 0.09 in 1 mmHg to 0.36 +/- 0.13 in 4 mmHg (P < 0.05, n=6), without affecting the diastolic [Ca2+]i level (n.s. n=6). The changes in Ca2+ balance during stretch were accompanied by a biphasic increase in the contraction force. Five minutes of continuous stretch increased the action potential duration (APD90%, P < 0.01, n=13) and decreased the APD15% (P < 0.001, n=13). During acidosis, the stretch-induced increase of the Ca2+ transient amplitude (0.4 +/- 0. 13 vs. 0.3 +/- 0.08, P < 0.05, n=6) was accompanied by the increase of the diastolic [Ca2+]i (1.16 +/- 0.07, P < 0.05, n=6) compared with non-acidotic control (1.06 +/- 0.06, n=6). Acidic intracellular pH also inhibited the stretch-induced changes in the action potentials (n=10) and slowed down the development of the contractile force during stretch. The results showed that acidosis modulates the mechanotransduction. It does this by interfering with the intracellular Ca2+ balance, inhibiting the Ca2+ extrusion mechanisms and reducing the Ca2+-buffering power of the cells. The physiological and pathological processes associated with stretch are therefore modulated by intracellular pH owing to its concerted effects on intracellular Ca2+ handling caused by a competitive inhibition of various Ca2+-binding molecules.

Acidosis↗

Noninvasive right and left heart catheterization: taking the echo lab beyond an image-only laboratory.

The assessment of cardiovascular hemodynamics is an extremely important component of managing patients with cardiac diseases. For years, this has been accomplished primarily through the use of right and left heart catheters placed within the cardiac chambers. Since this is an invasive technique, it should only be used when necessary; patient discomfort, infections, and overall risks for physicians would be reduced if noninvasive methods were utilized when available. Echocardiography (echo) provides the greatest ability to determine cardiovascular hemodynamics noninvasively, but requires the utmost precision and care to avoid misinterpretation. When used correctly, echocardiographic modalities provide an even greater assessment of the cardiac patient than invasive techniques. A safer and more comprehensive interpretation is available, and thus, echo should be considered the modality of choice-the new gold standard.

Atrial Function↗

Pulmonary venous flow pattern studied by transoesophageal pulsed Doppler echocardiography in mitral stenosis in sinus rhythm: effect of atrial systole.

In 13 patients with isolated mitral stenosis in sinus rhythm the pulmonary venous flow was evaluated by transoesophageal pulsed Doppler echocardiography. The patients were divided into two groups according to their mitral valve area (MVA); Group I (MVA < 1.5 cm2, n = 7 patients); and Group II (MVA > 1.5 cm2, n = 6). The patients in group I with haemodynamically significant mitral stenosis had lower velocities of systolic (S), diastolic (D) and atrial retrograde (A) waves of pulmonary venous flow (PVF) compared to milder stenosis (P < 0.05). The peak velocity of pulmonary retrograde venous flow at atrial contraction (A) primarily depends on the relative amplitude of the atrial transmitral wave (RA), which is measured from the onset of atrial systole to its peak velocity. We found a highly positive correlation between RA of mitral valve flow (MVF) and A wave of PVF (r = 0.87, P < 0.0001). There was also a highly negative correlation (r = 0.80, P < 0.001) between A of PVF and ratio of early (PE) to late (PA) velocities of MVF. Therefore, the retrograde A wave of PVF is related to the pressure generated in the left atrium during atrial systole. Use of pulmonary vein velocities in conjunction with mitral flow velocities can increase our understanding of the haemodynamics of mitral stenosis and provide a new insight into left atrial performance.

Adult↗

Some observations on the mechanism of pressure related atrial fibrillation.

In order to investigate the effect of atrial pressure on the propensity of the atria to fibrillate and the mechanism of this association, the right atrial pressure was changed acutely by transfusion-bleeding in 12 anaesthetized open-chest dogs. Under various atrial pressures the conduction time was measured between two pairs of hook electrodes positioned on the two atrial appendages respectively. The effective refractory period was measured by continuous pacing of the right atrium at a 250 ms cycle length at double threshold intensity and interpolating a progressively earlier stimulus after each eighth paced beat. The propensity of fibrillation was studied by rapid (450 min-1) pacing of the atria at double threshold intensity for 10 s at different atrial pressures. At a high (> or = 14 mmHg) atrial pressure the conduction time (45.7 +/- 14.2 ms) was significantly (P < 0.01) longer, the effective refractory period (157.9 +/- 15.2 ms) significantly (P < 0.01) longer and the atrial fibrillation (11/19 or 57.9%) significantly (chi 2 = 9.95, P < 0.001) more common than at a low (< or = 10 mmHg) pressure (35.2 +/- 11.6, 146.2 +/- 12.4, 3/24 or 12.5%, respectively). Analysis of variance showed that the probability of atrial fibrillation was significantly affected by the atrial pressure but not by either the conduction time or the effective refractory period. The findings suggest that an increase in right atrial pressure by acute volume overload prolongs the inter-atrial conduction time and right atrial refractoriness and increases the propensity of the atria to fibrillate by rapid atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Characterization of the 5-HT4 receptor mediating tachycardia in piglet isolated right atrium.

1. In order to explore whether 5-HT4 receptor subtypes exist, we have characterized further the 5-HT4 receptor that mediates tachycardia in the piglet isolated right atrium. All experiments were carried out in the presence of propranolol (400 nM) and cocaine (6 microM). We used tryptamine derivatives, substituted benzamides and benzimidazolone derivatives as pharmacological tools. 2. Tachycardia responses to 5-hydroxytryptamine (5-HT) were mimicked by other tryptamine derivatives with the following order of potency: 5-HT > 5-methoxytryptamine alpha-methyl-5-HT = bufotenine bufotenine > 5-carboxamidotryptamine = tryptamine (after treatment with pargyline) > 5-methoxy-N,N-dimethyltryptamine > 2-methyl-5-HT. 3. The substituted benzamides were all partial agonists relative to 5-HT except (-)-zacopride which was a full agonist. The stimulant potency order was renzapride > cisapride = (-)-zacopride > metoclopramide > (+)-zacopride. 4. The benzimidazolone derivatives had contrasting effects. BIMU 8 (endo-N-(8-methyl-8-azabicyclo[3.2.1]oct-3-yl)-2,3-dihydro-(1-methyl(eth yl- 2-oxo-1H-benzimidazole-1-carboxamide hydrochloride) was a full agonist relative to 5-HT whilst BIMU 1 (endo-N-(8-methyl-8-azabicyclo[3.2.1]oct-3-yl)-2,3-dihydro-3-ethyl-2-oxo - 1H-benzimidazole-1-carboxamide hydrochloride) was a partial agonist with low intrinsic activity compared to 5-HT but had similar potency. We estimated a pKB of 7.9 for BIMU 1 antagonism of 5-HT-induced tachycardia. DAU 6215 (N-endo-8-methyl-8-azabicyclo[3.2.1]-oct-3-yl)-2,3-dihydro-2-oxo-lH-benzimidazole-l-carboxamide, hydrochloride) had no chronotropic activity and was found to be a simple competitive antagonist with a pKB of 7.15.SB 203186 (1-piperidinyl)ethyl lH-indole 3-carboxylate) was a potent antagonist with a pKB of 8.3.The affinity of SB 203186 was approximately 20 times higher than that of tropisetron (ICS 205-930;pKB= 6.9) and DAU 6215 (pKB= 7.0). GR1 13808 (([1-[2-[methylsulphonyl amino]ethyl]-4-piperidinyl]methyl 1-methyl-1H-indole-3-carboxylate) and SDZ 205-557 ((2-diethylaminoethyl)2-methoxy-4-amino-5-chloro-benzoate) also antagonized 5-HT-induced tachycardia but not by simple competitive blockade.6. The sinoatrial 5-HT4 receptor in the piglet has a pharmacological profile that correlates well with 5-HT4 receptors characterized in rat oesophagus, guinea-pig ileum and colon, mouse embryonic colliculi neurones and human atrium.

Animals↗

Effect of pacing site on the atrial electrogram at target sites for slow pathway ablation in patients with atrioventricular nodal reentrant tachycardia.

Atrial electrograms recorded from target sites during radiofrequency catheter ablation of the slow atrioventricular (AV) nodal pathway are often fractionated and may be associated with a late, high frequency component (the slow pathway potential). The purpose of the current study was to assess the effects of slow pathway ablation on the morphology of the atrial electrogram and to determine whether target site electrograms display direction dependent changes in morphology during atrial pacing maneuvers. Twenty-six patients with typical AV nodal reentry had electrograms recorded from target sites before and after successful ablation of the slow AV nodal pathway and during pacing from the high right atrium and distal coronary sinus at cycle lengths of 500 and 300 msec. There was no significant change in the duration or degree of fractionation of the atrial electrogram as the result of slow pathway ablation. In contrast, the duration and degree of fractionation were less when pacing from the coronary sinus compared with sinus rhythms or right atrial pacing. Pacing rate did not affect electrogram morphology. These data suggest that the morphology of the slow pathway target site electrogram is dependent on the direction of atrial activation and that the "slow pathway potential" does not represent activation of an anatomically discrete pathway.

Adult↗

Adverse pacemaker hemodynamics evaluated by pulmonary venous flow monitoring.

The pacemaker syndrome refers to symptoms and signs in the pacemaker patient caused by an inadequate timing of atrial and ventricular contractions. The lack of normal atrioventricular synchrony may result in a decreased cardiac output and venous cannon A waves. The objective of this study was to define the left atrial and pulmonary venous flow response to ventricular pacing in a group of 14 unselected consecutive patients with total heart block and sinus rhythm. Pulmonary venous flow was assessed by transesophageal pulsed Doppler echocardiography in the VVI and DDD pacing modes. An inappropriate atrial timing caused a marked augmentation of the normally small pulmonary venous z wave in all patients ("negative atrial kick," peak z wave in DDD pacing 14.5 +/- 4.6 cm/s, VVI pacing 51.8 +/- 15.0 cm/s). Restoration of AV synchrony (DDD pacing, AV interval 100 ms) abolished these "cannon z waves" in all patients, and a normal pattern of pulmonary venous flow was achieved. Abnormal pulmonary venous flow characteristics were observed in 2 of 14 patients during DDD pacing with short AV intervals (100 ms). The Doppler pattern was similar to the findings seen in VVI pacing. Assessment of pulmonary venous flow by transesophageal pulsed Doppler echocardiography may provide a simple, sensitive, and relatively noninvasive technique to evaluate patients with suspected pacing induced adverse hemodynamics.

Aged↗

Three dimensional flow in the human left atrium.

BACKGROUND: Abnormal flow patterns in the left atrium in atrial fibrillation or mitral stenosis are associated with an increased risk of thrombosis and systemic embolisation; the characteristics of normal atrial flow that avoid stasis have not been well defined. OBJECTIVES: To present a three dimensional particle trace visualisation of normal left atrial flow in vivo, constructed from flow velocities in three dimensional space. METHODS: Particle trace visualisation of time resolved three dimensional magnetic resonance imaging velocity measurements was used to provide a display of intracardiac flow without the limitations of angle sensitivity or restriction to imaging planes. Global flow patterns of the left atrium were studied in 11 healthy volunteers. RESULTS: In all subjects vortical flow was observed in the atrium during systole and diastolic diastasis (mean (SD) duration of systolic vortex, 280 (77) ms; and of diastolic vortex, 256 (118) ms). The volume incorporated and recirculated within the vortices originated predominantly from the left pulmonary veins. Inflow from the right veins passed along the vortex periphery, constrained between the vortex and the atrial wall. CONCLUSIONS: Global left atrial flow in the normal human heart comprises consistent patterns specific to the phase of the cardiac cycle. Separate paths of left and right pulmonary venous inflow and vortex formation may have beneficial effects in avoiding left atrial stasis in the normal subject in sinus rhythm.

Adult↗

Atrial and arterial baroreceptor influences on the circulatory response to acute changes in renal perfusion.

We have recently reported a neurally mediated reflex increase in hindlimb vascular resistance associated with an acute decrease in renal perfusion pressure in the chloralose-urethane-anesthetized rabbit. The present study was designed to investigate the influence of this reflex in the body's integrated response to circulatory disturbances by investigating the influence of carotid baroreceptor and left atrial receptors on this reflex and assessing the effect of acute changes in renal perfusion on the heart. Interaction of the renal-generated reflex with carotid baroreceptors was investigated by independent perfusion of the carotid sinus region. Responses in hindlimb perfusion pressure, at constant flow, to changes in renal perfusion were greatest with the carotid sinus perfusion pressure (CSP) low (27 +/- 4 mmHg (1 mmHg = 133.3 Pa) increase in hindlimb pressure at low CSP vs. 19 +/- 3 mmHg increase at normal CSP) and were inhibited with maximum carotid stimulation. Partial mitral obstruction, resulting in left atrial distension and atrial receptor stimulation, attenuated the hindlimb vascular response. The increase in hindlimb pressure under control conditions was 34 +/- 10 mmHg compared with 20 +/- 5 mmHg during atrial receptor stimulation. However, acute reduction of renal perfusion pressure did not result in any changes in heart rate, cardiac output, or inotropic state. It appears that both atrial and arterial baroreflexes modify the reflex change in hindlimb vascular resistance associated with acute alterations of renal perfusion.

Animals↗

Differential influence of various calcium-modulating compounds on ouabain intoxication in isolated rat left atria.

Various calcium-modulating compounds were tested with respect to their protective action against cardiac glycoside toxicity. At the concentrations applied, control force of contraction was reduced by nifedipine and verapamil and slightly attenuated by flunarizine, R 56865, and cimetidine, while it was strongly enhanced by Bay K 8644. The positive inotropic response to ouabain (stimulation rate: 1 Hz) was impaired by nifedipine and verapamil. The increment in contractile force induced by Bay K 8644 was not enhanced by ouabain. The increase in diastolic tension during toxic conditions of ouabain (stimulation rate: 3 Hz) was attenuated by nifedipine, verapamil, bepridil, flunarizine, cimetidine, phenytoin, and R 56865 but not by diltiazem, amiodarone, and amiloride. K loss was prevented by nifedipine, verapamil, diltiazem, bepridil, flunarizine, cimetidine, phenytoin, and R 56865. The increase in cellular Na content was inhibited by R 56865 only. Ca gain was prevented by verapamil, bepridil, flunarizine, R 56865, and cimetidine but not by nifedipine, diltiazem, phenytoin, amiodarone, and amiloride. Ionic deterioration was enhanced by Bay K 8644. These results suggest that pretreatment with various calcium-modulating compounds protects against mechanical and ionic changes during ouabain intoxication induced by Na-Ca overload through different mechanisms.

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

Orthodromic capture of the atrial electrogram during transient entrainment of atrioventricular nodal reentrant tachycardia.

BACKGROUND: The reentry circuit of atrioventricular nodal reentrant tachycardia (AVNRT) has not been fully demonstrated. We hypothesized that if an upper common pathway was present, the atrial electrogram could not be captured orthodromically during transient entrainment of AVNRT by rapid atrial pacing. Based on this hypothesis, the presence of an upper common pathway was investigated. METHODS AND RESULTS: The atrial electrogram at the recording site of the His bundle potential was identified during induced AVNRT in 9 patients. To entrain AVNRT transiently, rapid pacing from the high right atrium and coronary sinus was applied at a cycle length 10 milliseconds shorter than that of AVNRT and repeated after a decrement of the paced cycle length in steps of 5 milliseconds until AVNRT was interrupted. In 5 of 7 patients, orthodromic capture of the atrial electrogram at the recording site of the His bundle potential was observed during transient entrainment of AVNRT by coronary sinus pacing, ie, the first postpacing interval of the atrial electrogram at the recording site of the His bundle potential was the same as the paced cycle length. In these 5 patients, the mean minimum paced cycle length capable of orthodromic atrial capture was 349 milliseconds, and the mean difference from the cycle length of AVNRT was only 16 milliseconds. During transient entrainment of AVNRT by high right atrial pacing, the atrial electrogram could not be captured orthodromically. CONCLUSIONS: Observation of orthodromic capture of the atrial electrogram at the recording site of the His bundle potential by coronary sinus pacing ruled out the presence of an upper common pathway in AVNRT, and the concept that perinodal atrial tissue is involved in the reentry circuit of AVNRT was supported.

Atrial Function↗

Site-dependent intra-atrial conduction delay. Relationship to initiation of atrial fibrillation.

BACKGROUND: Atrial dysrhythmia patients have exaggerated intra-atrial conduction delays and prolonged relative refractoriness in response to atrial premature depolarizations (APDs). Furthermore, atrial fibrillation (AF) is more readily inducible by APDs from the high right atrium (HRA) than the coronary sinus (CS). In this study, we postulated that site-specific intra-atrial conduction delays can explain why AF is initiated more from the HRA than from the CS. METHODS AND RESULTS: We examined 17 patients (age, 49 +/- 22 years) without a history of atrial flutter, AF, or structural heart disease. Programmed stimulation was carried out from the HRA and distal CS, and bipolar recordings were made at the HRA, His bundle, posterior triangle of Koch, and CS. More prolongations in conduction and relative refractoriness in all intra-atrial sites were observed during HRA than CS APDs. AF was induced in 8 patients after HRA and not CS stimulation. During HRA stimulation, patients with AF inducibility exhibited significant prolongation of conduction to the posterior triangle of Koch and marked broadening of the posterior triangle of Koch electrogram compared with CS stimulation. In patients without AF inducibility, the posterior triangle of Koch electrogram width was the same during HRA and CS stimulation. CONCLUSIONS: The existence of site-dependent intra-atrial conduction delays and site-dependent dispersion of refractoriness appears to be a common property of the atrial myocardium and does not necessarily forecast AF inducibility. However, the presence of nonuniform anisotropic characteristics of the posterior triangle of Koch may be critical for AF induction.

Adult↗

Regional differences in the recovery course of tachycardia-induced changes of atrial electrophysiological properties.

BACKGROUND: Regional differences in recovery of tachycardia-induced changes of atrial electrophysiological properties have not been well studied. METHODS AND RESULTS: In the control group (5 dogs), atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) were assessed before and every 4 hours for 48 hours after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. In experimental group 1 (15 dogs), AERP and inducibility of AF were assessed before and after complete AVJ ablation with 8-week rapid right atrial (RA) pacing (780 bpm) and VVI pacing. In experimental group 2 (7 dogs), AERP and inducibility of AF were assessed before and after 8-week rapid left atrial (LA) pacing and VVI pacing. AERP and inducibility and duration of AF were obtained from 7 epicardial sites. In the control group, atrial electrophysiological properties obtained immediately and during 48-hour measurements after pacing did not show any change. In the 2 experimental groups, recovery of atrial electrophysiological properties included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease of duration and episodes of reinduced AF. However, recovery of shortening and maladaptation of AERP and inducibility of AF was slower at the LA than at the RA and Bachmann's bundle. CONCLUSIONS: The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF.

Animals↗

Electrophysiological effects of sodium channel blockers on guinea pig left atrium.

The electrophysiological effects of five sodium channel blockers (mexiletine, lidocaine, disopyramide, aprindine and flecainide) on the guinea pig left atrium were investigated by recording the action potential and its maximum rate of rise (Vmax). The onset and offset kinetics of use-dependent block of Vmax were analyzed. Lidocaine, aprindine and flecainide were classified clearly as fast, intermediate and slow, respectively. Mexiletine and disopyramide had two components in onset and offset of use-dependent block. Mexiletine showed fast and intermediate kinetics, whereas disopyramide showed intermediate and slow kinetics. Action potential duration at 90% repolarization (APD) was prolonged by disopyramide and mexiletine. The other drugs did not change the action potential duration. Effective refractory period was prolonged by all drugs with relative potency in the following order: disopyramide greater than mexiletine greater than lidocaine greater than aprindine = flecainide. In conclusion, the modes of actions of sodium channel blockers on the atrium were disclosed to be different from those on the ventricle. The pharmacological therapy for atrial arrhythmias should be based on the electrophysiological effects of the drugs on the atrium, not on the ventricle.

Action Potentials↗

Effect of acute haemodilution on right atrial type-A receptor activity and right atrial pressure in anaesthetized cats.

To determine the effects of acute haemodilution on right atrial pressure and right atrial type-A receptor activity, experiments were conducted in nine anaesthetized cats. Haemodilution was induced by replacement of blood by same volume of dextran (molecular weight-150000). Arterial blood pressure, right atrial pressure and right atrial type-A receptor activity were recorded. Hematocrit, arterial blood pO2, pCO2, and pH were measured. Mean arterial blood pressure, pO2, pCO2, and pH were not altered by haemodilution which extended to a hematocrit level of about 13%. Mean right atrial pressure, 'a' wave pressure showed significant changes after 2nd and 3rd exchange. Heart rate and 'a' wave amplitude changed significantly (P < 0.05) after 3rd exchange. The amplitude of the 'a' wave was increased from 3.57 +/- 0.93 to 5.79 +/- 1.46 cm H2O, heart rate was increased from 163.89 +/- 5.36 to 169.22 +/- 4.84 beats/min, mean right atrial pressure was increased from 2.85 +/- 0.31 to 4.61 +/- 0.27 cm H2O, initial 'a' wave pressure was increased from 1.78 +/- 0.09 to 5.06 +/- 0.44 cm H2O. The data indicate that under present experimental conditions, the activity of the type-A receptor did not show any significant change (P > 0.05) on acute haemodilution. Significant increase (P < 0.05) in the amplitude of 'a' wave, mean right atrial pressure and initial 'a' wave pressure could be attributed to increased myocardial contractility.

Animals↗