The role of calcium in the enhanced myocardial contractility of the hyperthyroid rat heart

Summary The hyperthyroid rat myocardium exhibits enhanced contractility. There is evidence that altered calcium handling by the myocardium may be responsible for this enhanced state. To investigate this, isolated hyperthyroid and cuthyroid hearts were perfused in the working mode and exposed to alterations in external calcium concentration. Heart rate was not significantly different in either group of hearts, nor was it altered by the change in calcium. The concentration of calcium needed to elicit half-maximal contractility (dP/dt_max) was lower in the hyperthyroid (0.81±0.07 mM) than in the cuthyroid hearts (1.12±0.09 mM, p<0.05). This increase in calcium sensitivity was unlikely to be at the site of the sarcolemma as verapamil exerted equal negative inotropic effects on both groups of hearts. Dantrolene, which blocks calcium release from the sarcoplasmic reticulum, exerted a significantly greater (p<0.01) depression in dP/dt_max after 12 min in the hyperthyroid (50±7%) than in the cuthyroid heart (15±2%). We conclude from our results that the enhanced contractile state of the hyperthyroid rat heart is likely to involve an altered mechanical response to calcium which is possibly at the level of enhanced calcium release from the sarcoplasmic reticulum.     

Alterations in heart and serum lysosomal activities in streptozotocin-induced diabetes

Summary Alterations in the cardiac tissue and serum acid hydrolase activities were studied in chronic streptozotocin-induced diabetes in rats. No changes were observed in total cardiac tissue homogenate lysosomal enzyme activities at 4 weeks of diabetes but there were significant alterations in the distribution of selected enzymes. Significant decreases in nonsedimentable -N-acetylglucosaminidase (NAG) and -galactosidase (Gal) activities were observed at 4 weeks of diabetes. At 8 weeks of the disease, decreased activities of NAG and Gal were observed in heart homogenates but no changes were apparent in -mannosidase (Man) or acid phosphatase activities. Nonsedimentable activities of NAG and both sedimentable and nonsedimentable activities of Gal were decreased at 8 weeks. At 16 weeks of the diabetic condition, increased activities of NAG, Gal and acid phosphatase were observed. This increase at 16 weeks of the disease was due to an increase in sedimentable enzyme activity. At all times of diabetes, serum enzyme activities were significantly increased. Insulin treatment reversed all of the observed changes in tissue homogenates, but serum levels were not completely reversed. These results suggest that cardiac lysosomal hydrolases are probably only involved in the later stages of the diabetic cardiomyopathy when extensive ultrastructural derangements are evident. The present evidence also suggests that the heart may be a source of serum hydrolase activities.     

Effect of verapamil on contractile function of the isolated perfused rat heart during postnatal ontogeny

Summary The negative inotropic effect of the calcium antagonist, verapamil, was compared in isolated hearts from 15-, 30-, 45-, 60-, and 90-day-old rats. Electrically paced hearts were perfused in vitro according to Langendorff, either under constant pressure or under constant flow conditions. An intraventricular-pressure curve was measured isovolumetrically and analyzed on-line using a microcomputer. Changes in pressure amplitude and maximum rate of pressure development were evaluated during a stepwise increase of the verapamil concentration in the perfusion solution (10^–9–3.3×10^–7 mol·l^–1). It was found that the sensitivity of cardiac contractile function to verapamil declines gradually in the course of postnatal ontogeny. The higher sensitivity of the developing heart to calcium channel blockade is probably a consequence of a higher functional dependence of the immature myocardium on trans-sarcolemmal calcium influx.     

Acute treatment with vitamin E does not protect the regionally ischemic,reperfused porcine heart

Summary Thirty pigs were randomly assigned to a blind treatment with vitamin E or placebo. Ten animals each received 0.5g d-alpha tocopherol intravenously before ischemia (group 1) or before reperfusion (group 2). Ten control pigs were treated with a lipid emulsion as placebo. The left anterior descending coronary artery was distally ligated for 45 min followed by 3 days of reperfusion. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Myocardial and plasma concentrations of vitamin E were determined by high-performance liquid chromatography. Global hemodynamic parameters and estimated left ventricular oxygen consumption did not differ among the three groups. Intravenous treatment with vitamin E raised the plasma levels of this vitamin from 1 ± 0.3 mg/l (control group) to 21 ± 6 mg/l before ischemia, to 4 ± 2 mg/l before reperfusion and to 2 ± 0.6 mg/l at the end of the experiments in group 1. In group 2, vitamin E plasma levels increased from 1 ± 0.3 mg/l to 24 ± 13 mg/l before reperfusion and to 2 ± 0.6 mg/l after 3 days of reperfusion. At the end of the experiments, myocardial vitamin E concentrations amounted to 4.2 ± 0.7 ng/mg fresh weight (control group), 9.7 ± 2.1 ng/mg (group 1), and to 8.7 ± 1.4 ng/mg (group 2). The increase in vitamin E plasma concentration was not associated with a cardioprotective effect. Infarct sizes of the three groups (group 1: 68 ± 12%, group 2: 66 ± 15%, control group: 69 ± 8%) were almost identical. Furthermore, recovery of systolic shortening was not improved by the acute vitamin E treatment. Mean systolic shortening of the reperfused segment amounted to 4% in the two treatment groups and 3% in the control group after 3 days of reperfusion. These results suggest that an acute increase in vitamin E plasma concentration before ischemia or during the early phase of reperfusion does not protect the ischemic, reperfused porcine heart.This study was supported by a grant from the Deutsche Forschungsgemeinschaft, KL 724     

Spontaneous oscillation of systemic arterial pressure during cardiopulmonary bypass in the dog

Summary Cardiopulmonary bypass and an open-heart operation were carried out on four beagle dogs kept under ketamine anesthesia. Oscillation of systemic arterial pressure during this maneuver was observed in three dogs and oscillation of pulmonary arterial pressure in two dogs. Mean amplitude of the oscillation in systemic arterial pressure was 6 to 7 mm Hg and that in pulmonary arterial pressure about 1 mm Hg. The duration of an oscillatory wave was about 20 s. Systemic arterial pressure was 130 to 150 mm Hg. The oscillation disappeared in two dogs when weaning from the bypass. These oscillations resemble those observed in humans during cardiopulmonary bypass and also those observed in experimental animals without bypass conditions.     

Halothane anesthesia reduces inducibility of ventricular tachyarrhythmias in chronic canine myocardial infarction

Summary This study examined the effects of 2% halothane general anesthesia on ventricular electrophysiological properties and inducibility of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF). Dogs with chronic anterior infarction and control dogs (no infarction) were studied before and after anesthesia using chronically implanted ventricular epicardial electrodes. PQ interval was increased by 15% with halothane, but QRS duration, QT interval, QTc, and sinus rhythm cycle length were unaffected by anesthesia. Diastolic threshold was unchanged by halothane. Halothane caused significant increases of 10–30% in ventricular effective refractory period (ERP) both in control and in infarct animals. VT and VF were not inducible in any of the nine control animals either before or after anesthesia. In infarct animals 34 of 75 (45%) had inducible VT or VF prior to halothane, but the incidence of inducible arrhythmias was significantly lower at 29% (22 of 75 animals) after halothane (p<0.01). In 75% of animals in which halothane suppressed inducibility of tachyarrhythmias, halothane-induced increases in ERP prevented achievement of the short extrastimulus coupling intervals at which the arrhythmias were induced before anesthesia. In conclusion: halothane anesthesia reduces the incidence of inducible sustained ventricular tachyarrhythmias in chronic canine myocardial infarction.A preliminary report of this study was given to the American Heart Association, Dallas, Texas, USA, November 1986.     

Arrhythmias and infarction in the ischemic pig heart are not mediated by xanthine oxidase-derived free oxygen radicals

Summary Xanthine oxidase activities of pig myocardium and blood during and following myocardial ischemia were measured using HPLC, and electrochemical detection of hypoxanthine, xanthine and uric acid. Myocardial ischemia was produced by occluding the anterior descending coronary artery two-thirds of the way from its origin. There was no accumulation of either xanthine orurate in the ischemic pig myocardium during occlusion periods of 90 min, but there was a substantial accumulation of hypoxanthine. Similarly, there was no increase in myocardial xanthine or urate during the 30 min reperfusion following coronary artery occlusion periods of 15, 30, 60 or 90 min. Following in vitro incubation at pH 8 of myocardial homogenates or blood with either hypoxanthine or xanthine and NAD, no urate production was detectable. In contrast, significant amounts of xanthine and/or urate were produced, following addition of xanthine oxidase to the reaction mixtures. Additional in vitro experiments showed that the following pig tissues were lacking xanthine oxidase activity: left and right atrial appendage, left and right ventricle, interventricular septum, anterior descending and circumflex coronary arteries, ascending aorta, lung, and blood. Large amounts of xanthine oxidase (9.3±1.8 SEM mU/g wet weight, n=7) were found in pig liver. In the ischemic pig heart, transmural infarction developed within 60 min of ischemia. Ventricular arrhythmias and fibrillation occured most frequently within 45 min of ischemia and within seconds after reperfusion. These results showed that the pig heart and blood were xanthine oxidase deficient, suggesting that xanthine oxidase-derived free oxygen radicals were not involved in the cytotoxic and arrhythmogenic effects brought about by myocardial ischemia and/or reperfusion in the pig.This work was supported by grant Po 252/1-1 from the Deutsche Forschungsgemeinschaft.     

Open chest and open pericardium affect the distribution of myocardial blood flow in the right ventricle

Summary We have investigated the effects of open chest and open pericardium on the distribution of myocardial blood flow assessed with the radioactive microsphere technique (15 m). Five dogs with intact thorax served as controls (group I) and six dogs were studied after a right-sided thoracotomy and pericardiotomy (group II). Global myocardial blood flow (mean±S.D.) was 0.73±0.17 ml·min^–1·g^–1 in group I and 1.22±0.09 ml·min^–1·g^–1 in group II (p<0.05). Analysis of transmural blood flow distribution revealed that flow was 44% higher in the right and 60% higher in the left ventricular endocardial layers in the open-chest animals, whereas epicardial flow increased by 105% and 90%, respectively. As a result of the preferential blood flow to the epicardial layers of the right ventricle, the endo/epi ratio was reduced from 1.30±0.26 in group I to 0.86±0.11 in the open-chest group (p<0.05). Left ventricular endo/epi ratio was 1.27±0.16 and 1.06±0.11 (n.s.), respectively. External work and diastolic filling pressure of the right ventricle did not differ between the two groups and therefore cannot account for the redistribution of myocardial blood flow. It is concluded that the distribution of myocardial blood flow, particularly in the RV, is severely disturbed by thoracotomy and pericardiotomy. This is an important aspect for the planning and evaluation of studies under open-chest/open-pericardium conditions.Supported by Deutsche Forschungsgemeinschaft grant SFB 320     

Determination of rat heart morphology and function in vivo in two models of cardiac hypertrophy by means of magnetic resonance imaging

Summary Quantitative magnetic resonance imaging (MRI) was applied to assess structural and functional parameters of the rat heart in vivo. Using ECG and respiratory triggering, MR images were obtained at different time points during the cardiac cycle. This allowed accurate determinations of the left ventricular (LV) mass, wall thickness, LV end-systolic and end-diastolic volumes, stroke volume, and ejection fraction. LV mass determined by MRI showed an excellent linear correlation with post mortem gravimetric determination of LV weight. MRI was then used to examine the pathophysiological changes in two models of LV hypertrophy. In one group of animals the aortic arch was banded to an outer diameter of 1.0 mm to elicit a pressure overload on the LV. A second group was subjected to a volume overload due to graded disruption of the aortic valve. Although both models exhibited a similar degree of LV hypertrophy as shown by the LV weight/body weight ratio, important functional and structural differences were revealed by MRI. Aortic stenosis resulted in an increase in wall thickness, whereas stroke volume and ejection fraction did not differ compared to control animals. In contrast, aortic valve insufficiency did not affect LV wall thickness, however, LV chamber volume as well as stroke volume were markedly increased. Ejection fraction was significantly reduced in these animals. In conclusion, MRI allows the reliable in vivo determination of important structural and functional parameters of hearts in small rodents.     

Binding of calcium to myoplasmic buffers contributes to the frequency-dependent inotropy in heart ventricular cells

Summary In guinea-pig ventricular cells, the Ca²⁺ buffer capacity of the myoplasm was estimated from the ratio of ionized calcium (from Indo-1 fluorescence) through total calcium (ionized plus bound calcium, fron x-ray microprobe analysis). During post-rest potentiation (1 Hz paired-pulses in voltage-clamp), where diastolic sarcomere length remained nearly constant, Ca²⁺ buffer capacity slowly fell from 55001 to 7001 suggesting that slow Ca²⁺ binding sites became saturated. We discuss that frequency-inotropy depends not only on the replenishment of intracellular stores with Ca²⁺, but also on binding of Ca²⁺ to these slow sites; the slow Ca²⁺ sites could complete with the fast activator sites on troponin C for systolic Ca²⁺, or they could enhance the Ca²⁺ affinity of the fast Ca²⁺ sites on troponin C by cooperative interaction.     

Different responses of left ventricular systolic function to changes in right ventricular volume and shortening —comparison between aorto-femoral vein and aorto-left atrium shunts in dog hearts

Summary It has been reported that left ventricular end-systolic volume decreases during arteriovenous shunt and increases during subclavian artery-left atrium shunt at a constant end-systolic pressure. The mechanism of the opposing changes in end-systolic volume during the two types of shunt is not clear. One possible cause is that left ventricular pump function with enhanced right ventricular ejection differs from that without enhancement. To investigate this hypothesis, we studied the two types of shunt (Aorto-femoral vein shunt, AoFV; aorto-left atrium shunt, AoLA) with matched reduction of systemic vascular resistance in open-chest dogs with -blockade. Both right and left ventricular volumes and shortenings were assessed from short-axis views by two-dimensional (2D)-echocardiogram. Left ventricular end-systolic short-axis area decreased from 76 ± 3 to 62 ± 3% in AoFV shunt (p < 0.05), but tended to increase in AoLA shunt (76 ± 4 in control state vs 81 ± 5% in AoLA, NS) in spite of a similar reduction in left ventricular end-systolic pressure. There was no difference in left ventricular shortening, but significant differences were observed in right ventricular shortening (50 ± 8 in AoFV vs 24 ± 7% in AoLA, p < 0.05) and right ventricular short-axis area at end-diastole (142 ± 6 in AoFV vs 96 ± 3% in AoLA, p < 0.01), and at end-systole (92 ± 8 in AoFV vs 73 ± 7% in AoLA, p < 0.05) between the two types of shunt. We conclude that the different changes in left ventricular end-systolic short-axis area found in the two shunts are not caused by the different left ventricular shortenings, but by the different right ventricular mechanical actions. These findings suggest that left ventricular pumping action in the high output state changes, depending on whether it is accompanied by augmented ejection of the right ventricle or not.     

Cardiovascular reactions and respiratory events during platelet activating factor-induced shock

Summary The platelet activating factor (PAF), a low molecular phospholipid, plays an important role in inflammation, anaphylaxis, and shock state development. In the isolated perfused guinea pig heart, PAF induces a decrease in coronary flow and cardiac contractility and atrioventricular conduction disturbances. Furthermore, PAF mediates a powerful bronchoconstrictory action causing a severe impairment in respiratory function. In the present study an attempt was made to separate cardiac from respiratory events during PAF-induced shock in vivo. PAF was injected intravenously (0.1–10 g/kg) into anesthetized guinea pigs ventilated with room air or 100% oxygen. Administration of 10 g/kg PAF was uniformly lethal: already within 2 min, cardiac output decreased by 60% and end-diastolic left ventricular pressure increased markedly indicating cardiac failure. ECG recordings showed signs of acute myocardial ischemia. Arrhythmias occurred in terms of atrioventricular conduction delay. Blood pressure initially increased, then declined continuously to below baseline within 10 min. All animals died within 25 min. Ventilation with room air was paralleled by development of severe hypoxia. However, under ventilation with 100% oxygen a dissociation between PAF-mediated cardiac and respiratory effects occurred. It is concluded that the PAF-induced shock is primarily based on direct cardiac damage. Furthermore, the ECG signs of ischemia are most likely due to coronary spasms.     

Changes in heart rate by verapamil during carotid sinus stimulation in patients with hyperparathyroidism,pre- and postoperatively

Summary It has been investigated whether calcium- and verapamil-dependent sensitivities of carotis baroreceptors also exist in man. To answer this question, we pre- and postoperatively measured changes in heart rate during carotid sinus stimulation before and after intravenous administration of 5 mg verapamil in 23 patients with primary hyperparathyroidism. Findings during hypercalcemia were as expected: a more pronounced reduction of heart rate at comparatively low calcium levels. During normocalcemia, we found an opposite effect: a more pronounced reduction at relatively high calcium levels, which was statistically significant. This fact could be explained according to our interpretation. In previous reports, local effects on baroreceptors were examined, whereas we measured the combined effect of several calcium actions. As expected, verapamil attenuated the decrease in heart rate which, however, was not statistically significant.     

Effects of riboflavin analogues and diuretics on the spontaneously hypertensive rat heart

Summary The chronic treatment of spontaneously hypertensive rats (SHR) with 7,8-dimethyl-10-(3-chlorobenzyl) isoalloxazine [CBI], 7,8-diethyl-10-aminol isoalloxazine [DEAI], enduron (methyclothiazide) and amiloride were studied for their effects on blood pressure and cardiac contractile protein ATPasc activities. After 35 weeks of treatment all the above antihypertensive agents showed a decrease in blood pressure in the SHR (p<0.01). Chronic treatment with CBI, DEAI, enduron, and amiloride significantly improved the myofibrillar ATPasc activity at all pCa²⁺ concentrations (p<0.01). Furthermore, CBI, DEAI, enduron, and amiloride drug treatments enhanced actin-activated myosin ATPase activity (p<0.01). The Ca²⁺-activated myosin ATPase activity was significantly elevated after treating with CBI and DEAI (p<0.01). These results suggest that the antihypertensive agents used in this study helped in reducing the blood pressure with a subsequent increase in myocardial contractile protein ATPase activity.     

Less peri- and postoperative inotropic support in open-heart patients with vasomotor waves during cardiopulmonary bypass?

Summary Although vasomotor waves (VMW) (Mayer waves) were recognized more than one century ago their physiological role is still under discussion. During cardiopulmonary bypass (CPB) the appearance of VMW is random. The clinical significance of the phenomenon was studied by comparing open-heart patients with (n=33) or without (n=33) VMW of arterial pressure during CPB. The patients with VMW had higher perfusion pressure (p<0.05) and vascular resistance (p<0.01) during bypass and higher mean arterial pressure before and after CPB. During CPB the need for vasoconstrictors was of lesser magnitude (p<0.01) but the need for vasodilators was of greater magnitude (p<0.001) in patients with VMW and they also less frequently needed inotropic support at weaning from CPB (p<0.05) or after CPB (p<0.01). The use of inotropics was also shorter (p<0.01) during intensive care in the patients with VMW. Based on the present results the open-heart patients who had VMW during CPB appeared to have higher arterial blood pressure and to need less pharmacological cardiovascular support during the intraoperative and the immediate postoperative period.     

Preconditioning of the heart by repeated stunning: attenuation of post-ischemic dysfunction

Summary The effect of repetitive brief periods of coronary occlusion on subsequent prolonged ischemic insult was studied using a swine heart model. Four 5-min episodes of left anterior descending coronary artery (LAD) occlusion, each separated by 10 min of reperfusion, did not affect any of the regional or global myocardial functions examined, except that the level of adenosine triphosphate (ATP) dropped to some extent. Sixty minutes of LAD occlusion following four repeated stunnings further reduced the ATP level, but this reduction was significantly lower compared to nonstunned control. Myocardial global functions were not affected significantly by prolonged ischemic insult. Segment shortening (SS) was reduced comparably in both control and stunned groups. However, SS improved significantly during subsequent reperfusion in the stunned group compared to control. The experimental group also demonstrated reduced infarct size and an area of risk compared to nonstunned control. These results indicate that repeated stunning prior to irreversible ischemic insult can attenuate ischemic injury and post-ischemic dysfunction.     

Comparison of cardiac and hemodynamic effects of plateletactivating factor-acether and leukotriene D4 in anesthetized dogs

Summary In anesthetized dogs, platelet-activating factor-acether (PAF; 0.2–1.6 g/kg) and leukotriene (LT) D₄ (0.5, 1, and 3 g/kg) were injected into the left circumflex (LCX) coronary artery. Cardiac and systemic hemodynamics, and the ECG were continuously recorded.PAF reduced cardiac performance and affected hemodynamics in a dose-dependent manner: At 7±3s, LCX flow initially increased by 40%–172% followed by a reduction of 43%–100%, and coronary diameter (measured with ultrasonic techniques) decreased by 4%–10%. Total and late coronary resistance increased. Left ventricular (LV) systolic pressure fell by 22%–48% and LV filling pressure decreased by 5 mm Hg after 0.8 g/kg PAF. The LVdP/dt_max diminished by 38%–47%. Peak blood pressure reduction (35%) occurred 60s after PAF application and lasted for 1.4 min. Heart rate decreased by 10%–17% at peak PAF actions. LTD ₄ reduced LCX flow by 38%–87%, and coronary diameter by 5%–12%, returning to control value within 3.4 min. Blood pressure, LV pressure, and LVdP/dt_max decreased while heart rate and LV filling pressure increased. ST segments and R-wave voltage of the ECG in lead II elevated after either compound although the effects were more pronounced after LTD₄.Indomethacin (5 mg/kg i.v.) pretreatment did not affect LTD₄ actions on cardiohemodynamics, but the putative leukotriene antagonist FPL 55712 (1 mg/kg i.v.) blocked LTD₄ actions on the heart and circulation. PAF influences on LCX flow were modified by indomethacin: initial flow rose by 250%, and coronary diameter fell by 12%, followed by sustained flow and diameter reduction during the second phase on PAF action. FPL 55712 did not affect the early flow increase after PAF but attenuated the later flow reduction, which was blocked by indomethacin.Thus, PAF and LTD₄ may have effects on canine conduit arterics besides their effects on the coronary resistance vessels. The circulatory derangement after PAF may be aggravated by additional eicosanoid release. PAF and LTD₄ may be involved in coronary blood flow variations and negative inotropy accompanying anaphylactic disease state.     

Sarcolemmal integrity during ischaemia and reperfusion of the isolated rat heart

Summary The effects of ischaemia and reperfusion on sarcolemmal permeability were studied in the isolated rat heart using an ionic lanthanum probe technique. Detection of increased permeability after exposure to short periods of ischaemia without accompanying reperfusion effects was achieved by employing a substrate-free, low calcium saline solution as vehicle for ionic lanthanum. Quantifiable results showed a rapid increase in sarcolemmal permeability in the subendocardium after 15 min of ischaemia, with the subepicardium showing similar alterations after longer periods. Reperfusion after 15 min of ischaemia led to recovery of normal permeability characteristics, correlating well with ultrastructural and functional recovery. Reperfusion after 25 min of ischaemia did not allow recovery of sarcolemmal permeability, ultrastructure, or function. These results show a clear correlation between the development of irreversible myocardial damage and increased sarcolemmal membrane permeability.     

Signal transduction by cGMP in heart

Summary Early studies in whole heart indicated that cGMP antagonized the positive inotropic effects of catecholamines and cAMP. However, the regulation of cGMP levels by a variety of agents was not always consistent with their effects on contractility. It is now clear that at least two major cell types in whole heart, cardiac myocytes and vascular smooth muscle cells, differ markedly in their mechanisms of cGMP regulation and response to cGMP. Furthermore, experiments on isolated cardiac myocytes indicate that the mechanism of cGMP action even in this single cell type can be multifaceted. Cyclic GMP inhibits the L-type calcium channel current (I_Ca), which is the major source of Ca⁺⁺ entry into heart cells, and which plays a predominant role in the initiation and regulation of cardiac electrical and contractile activities. Patch-clamp measurements of I_Ca indicate that in isolated frog myocytes cGMP inhibits I_Ca by stimulation of cAMP phosphodiesterase (cGS-PDE), whereas in purified rat ventricular myocytes, cGMP predominantly inhibits I_Ca via a mechanism involving cGMP-dependent protein kinase (cGMP-PK). Under certain conditions, cGMP can also inhibit a cGMP-inhibited cAMP phosphodiesterase (cGI-PDE) and thereby produce a stimulatory effect on I_Ca. Biochemical characterization of the endogenous PDEs and cGMP-PK in purified cardiac myocytes provided further evidence in support of these mechanisms of cGMP action on I_Ca.     

Detection and continuous monitoring of intracardiac low-level potentials from the surface of the Langendorff-perfused heart

Summary By appropriate placement of two electrodes on the epicardiac surface of Langendorff-perfused hearts, His-bundle and preatrial signals can be recorded by the surface electrogram (S-ECG). These signals are difficult to detect because of their low amplitude of a few microvolts. To improve the monitoring of these low-level potentials we studied the His-bundle spike as detected by intracardiac electrodes and by epicardial records (S-ECG) and compared these signals in the time and frequency domain. The frequency spectra of these cardiograms were used to develop appropriate filters and high-gain amplifiers for a continuous monitoring of the His-bundle signal from the epicardiac surface. By means of such a monitoring system, high-frequency components of preatrial activities could be resolved also. The time coincidence of these spikes to the simultaneously recorded intraatrial electrogram from electrodes positioned near the sinus node and near the His-bundle is demonstrated. Hence, the early atrial signals likely yield information about sinoatrial conduction. Application examples of monitoring His-bundle signals and preatrial signals in a beat-to-beat manner are described also for various conduction blocks or arrhythmias. With this monitor the evaluation of characteristic parameters of the conduction system of the heart like HV-, AH- and A'H-time, and likely, SACT can easily be performed for every heartbeat on a digital oscilloscope with low resolution or a two-channel chart recorder. Small and intact hearts can be used with this system to detect intracardiac low-level potentials during the heart beat.Preliminary results have been published at the III Simposion Internacional de Ingeneria Biomedica, Madrid 1987 and at the World Congress on Medical Physics and Biomedical Engineering, San Antonio, Texas 1988.Supported by a grant of the Austrian Research Fund (FFW, project number P7141).