No abstract available.
Myocardium*

No abstract available.
Myocardium

Hypertrophic cardiomyopathy is characterized by inappropriate hypertrophy of the myocardium and is associated with various clinical presentations ranging from complete absence of symptoms to sudden, unexpected death. These are caused by dynamic obstruction of the left ventricular outflow tract and surgical approaches were initiated. But, the complete resection of hypertrophied midventricular septum is impossible by standard, transaortic approach, because of narrow vision and limited approach. And it leads to inadequate excision, will leave residual left vetnricular outflow tract obstruction or systolic anterior motion of mitral leaflet, and limit symptomatic improvement and patient's survival. We report a case of extended septal myectomy for hypertrophic cardiomyopathy of mid-septum in a child. The extended septal myectomy was performed by aortotomy and left ventricular apical incision, and made possible the complete resection of mid-ventricular septum, abnormal papillary muscles and chordae. The patient's symptom was improved and the postoperative course was uneventful.
Cardiomyopathy, Hypertrophic* ; Child ; Heart Septum ; Humans ; Hypertrophy ; Myocardium ; Papillary Muscles

The influences of osmolarity on the cardiac muscle contraction were investigated in cat papillary muscles. The muscle was immersed in the modified Krebs-Ringer-bicarbonate solutions containing various Ca ion concentrations and osmolarities and the resultant changes in maximum developed tension, rate of development of tension and time to maximum tension were analyzed. Following are the results. 1) Mean length of papillary muscle used was 9.3+/-0.60mm, end mean cross-sectional area was l. 73+/-0.07 mm2. Normal contraction amplitude at 5 mM Ca ion-K-R-B solution was 2. 46+/-0. 1 gram/mm. 2) Within the range of 2.5-10.0 mM Ca ion concentration, the contraction amplitude increased along with the increment of Ca concentration. 3) Osmolarity exerted dual effects on contraction; within the range of 300-400 mosm/I solution, the hypertonic solution exported a positive inotropic effect while 500 mOsm/1 solution exerted a negative inotropic effect upon papillary muscle. 4) Maximum rate of tension development increased in 350 mOsm/1 solution, but decreased in 400 mOsm/1 or more hypertonic solution. The time to maximum tension did not change within the range of 300 400 mOsm/1 osmolarity and in 500 mOsm/1 solution. 5) The difference in maxium developed tension between single and paired stimulation was 1. 99 gram/mm' at 300 mOsm/1 solution and was negligible in 450 mOsm/1 or more hypertonic solutions.
Animals ; Cats ; Hypertonic Solutions ; Myocardium ; Osmolar Concentration ; Papillary Muscles

BACKGROUND: The synthetic narcotic sufentanil has been used in clinical practice for anesthetic induction and maintenance. But there is little information concerning its direct effects on heart. The purpose of this study is to evaluate the direct effects of sufentanil on contracture of ventricular myocardium. METHODS: Isometric contraction of isolated right ventricular papillary muscle of rabbit was measured under 0.2 Hz electrical stimulation in Krebs solution. Peak developed force(F), maximum rate of rise of developed force(+dF/dt(max)), maximum rate of fall of developed force(-dF/dt(max)) were analyzed. RESULTS: There were no statistically significant differences in frequency of isometric contraction from the 100% baseline value in time-matched control group. Sufentanil, in concentration of 0.01-0.1 mM, increased F, and -dF/dt(max) was decreased especially in concentration of 0.1 mM but not +dF/dt(max) Fo +dF/dt(max) and -dF/dt(max) were statistically different from time-matched control group in concentration of 0.1 mM. CONCLUSIONS: We conclude that sufentanil has mild contracture effect on ventricular muscle of rabbit directly.
Analgesics ; Contracture ; Electric Stimulation ; Heart ; Isometric Contraction ; Myocardium ; Papillary Muscles ; Rabbits* ; Sufentanil*

BACKGROUND: The effects of various concentration (20, 50, 100? M) of mepivacaine were studied in isolated guinea pig and rat right ventricular papillary muscles by measuring the effects on myocardial contractility and electrophysiological parameters. METHODS: Isometric force of isolated guinea pig ventricular papillary muscle was studied in modified normal and 26 mM K+ Tyrode's solution. Rat papillary muscle was used to evaluate the effect on Ca2+ release from the sarcoplasmic reticulum (SR) at low stimulation rates. Normal and slow action potentials (APs) were evaluated by using conventional microelectrode technique. Rapid cooling contractures (RCCs), an index of SR Ca2+ content, which are known to be activated by Ca2+ released from the SR were performed. RESULTS: Mepivacaine caused dose-dependent depression of peak force from 0.5 to 3 Hz stimulation rates in guinea pig papillary muscles. Conduction block was frequently noted especially at higher stimulation rates (2 and 3 Hz) at all concentration ranges. In rat, ~20% depression of peak force was shown at rested state contraction. Shortening of AP duration and rate-dependent depression of dV/dt max could be observed at 100 M mepivacaine. In 26 mM K+ Tyrode's solution, 50 and 100 M mepivacaine caused dose-dependent depression of early and late force development. In slow APs, neither shortening of AP duration nor changes of dV/dtmax were not shown at 100 M mepivacaine. ~30% depression of RCC after 2 Hz stimulation rate was shown at 100 M mepivacaine. CONCLUSION: It may be concluded that the direct myocardial depressant effects of mepivacaine may partly be related to inhibition of Ca2+ release from the SR. Shortening of AP duration in normal APs seems to be partly related by blockade of TTX-sensitive ""window"" Na+ current.
Action Potentials ; Anesthetics ; Animals ; Contracture ; Depression* ; Guinea Pigs ; Mepivacaine* ; Microelectrodes ; Myocardium* ; Papillary Muscles ; Rats ; Sarcoplasmic Reticulum

BACKGROUND: The effects of various concentration (20, 50, 100 micrometer) of meperidine were studied in isolated guinea pig and rat ventricular papillary muscles. METHODS: Isometric force of guinea pig ventricular papillary muscle was examined in normal and 26 mM K+ Tyrode's solution. Experiments using rat and guinea pig papillary muscle under normal and low Na+ (40 mM), respectively, were performed to evaluate the effect on Ca2+ release from the sarcoplasmic reticulum (SR). Normal and slow action potentials (APs) were evaluated by using conventional microelectrode technique. Rapid cooling contractures were performed. RESULTS: Meperidine caused dose-dependent depression of peak force from rested-state (RS) to 3 Hz stimulation rates in guinea pig papillary muscles. Conduction block was frequently noted at high stimulation rates (2 and 3 Hz) at 150 micrometer meperidine. ~40% depression of peak force was shown at RS contraction under low Na+ Tyrode's solution, although contractile depression was not shown at RS and low stimulation rates in rat papillary muscles. 100 micrometer naloxone did not reverse the contractile depression caused by 100 micrometer meperidine. Either depression of dV/dt-max from 0.1 to 3 Hz stimulation rates or rate-dependent depression among 1, 2 and 3 Hz could be observed at 150 micrometer meperidine. In 26 mM K+ Tyrode's solution, 50 and 100 micrometer meperidine caused dose-dependent depression of early and late force development. In slow APs, changes of dV/dt-max were not shown at 100 micrometer meperidine. ~40% depression of contracture induced by rapid cooling following 2 Hz stimulation rates was shown at 100 micrometer meperidine. CONCLUSION: The direct myocardial depressant effect of meperidine seems likely to be caused by local anesthetic properties of meperidine, not by the opioid action. Inhibition of SR Ca2+ release, and decreased intracellular Ca2+ secondary to Na+ channel blocking action of meperidine may at least in part be related to direct myocardial depression.
Action Potentials ; Anesthetics* ; Animals ; Contracture ; Depression* ; Guinea Pigs ; Meperidine* ; Microelectrodes ; Myocardium* ; Naloxone ; Papillary Muscles ; Rats ; Sarcoplasmic Reticulum

BACKGROUND: The purpose of this study is to examine the effect of Desflurane on myocardial contractility and cellular electrophysiologic behabior in isolated guinea pig and rat right ventricular papillary muscle. METHODS: The isometric force of a guinea pig ventricular papillary muscle was studied in normal and 26 mM Tyrode's solution at various stimulation rates. Experiments using rat papillary muscles under normal Tyrode's solution at resting-state (RS) and using guinea pig papillary muscles under low Na Tyrode's solution (25 mM) were performed to evaluate the effect on Ca2+ release from the sarcoplasmic reticulum (SR). Normal and slow action potentials (APs) were evaluated by using a conventional microelectrode technique. Effects of desflurane on SR function in situ were examined by its effect on rapid colling contractures (RCCs). 1 MAC (end-tidal concentration: 6%) and 2 MAC desflurane were applied. RESULTS: Desflurane equivalent to 6% and 12% depressed guinea pig myocardial contractions in the control to -70% and -40% from RS to 3 Hz stimulation rates. Contractile force after rest in rat and guinea pig myocardium under low Na Tyrode's solution showed modest depression. In the partially depolarized, beta-adrenergically stimulated myocardium, 6% and 12% desflurane caused marked depression of late force (6%: -60%, 12%: -80%) with moderate changes of early peak force (6%: -20%, 12%: -40%). RCCs were abolished at 6% concentration. CONCLUSIONS: The direct myocardial depressant effects of desflurane is slightly greater to those seen with isoflurane. The rapid initial release of Ca2+ from the SR by depolarization seems to be modestly depressed, although certain release pathways induced by rapid colling appear to be markedly depressed.
Action Potentials ; Animals ; Contracture ; Depression ; Guinea Pigs ; Isoflurane ; Microelectrodes ; Myocardial Contraction ; Myocardium ; Papillary Muscles ; Rats ; Sarcoplasmic Reticulum*

BACKGROUND: Low dose dobutamine echocardiography has recently been introduced for use in identification of viable myocardium in patients with acute myocardial infarction and prediction of the response of dysfunctioning myocardial segments to coronary angioplasty. The aim of this study was to evaluate wheter tihs test could be used to predict the early response of dysfunctioning myocardial segements to coronary artery bypass grafting(CABG). METHODS: We studied in 23 patients with multi-vessel disease during CABG. Myocardial segments were monitored by intraoperative transesophageal echocardiography(TEE) in the transgastric short-axis view at papillary muscle level. The left ventricle was divided into five segments and sixty eight myocardial segments in 23 patients were analyzed. Percentage of systolic wall thickening(PSWT) was calculated in each segment for three times: at basline(early after pericardiectomy);before bypass during dobutamine infusion(3-5ug/kg/min);and after seperation from cardiopulmonary bypass. Segments showing baseline PSWT >_30% were considered normal and those < 30% were dysfunctional. Segments showing an increase in PSWT >_10% during dobutamine infusion were considered responders and those < 10% nonresponders. RESULTS: AT baseline, 24%(36%) of 68 segments had PSWT > 30%(normal) and 44(68%) had PSWT < 30%(dysfuctioning segments). During dobutamine infusion, 21(47.7%) among 44 dysfunctional segments showed increase in PSWT >_10%(from 12.3+/-7.2% to 33.5+/-11.8%, p<0.01 ; responder segments), and 23(52.3%) showed increase in PSWT < 10%(from 14.7+/-6.5% to 17.4+/-7.4%, p=NS ; nonresponder segments). After CABG, responder segments showed a significant increase in PSWT in comparison with baseline values(from 12.3+/-7.2% to 32.1 +/-11.0%,p<0.01). Segments not responded to dobutamine showed no significant changes in PSWT after CABG(from 14.7+/-6.5% to 16.0+/-8.2%, p=NS). Twenty-four normal segments (PSWT 41.9+/-6.2%) showed a slight but significant reduction in PSWT both during dobutamine infusion(38.7+/-6.9%;p<0.05) and after CABG(38.9+/-6.3%, p<0.05), suggesting that compensatory hyperfunction was present at baseline. Estimation of clinical accruacy of low dose dobutamine TEE yieded to 69% sensitivity, 93.9% specificity, 95.2% positive predictive value, 60.9% negavive predictive value, and 77.3% overall accuracy. In both responders and nonresponders of dysfunctioning segments, there was a correlation between PSWT during dobutamine infusion and that after CABG(r=0.61, r=0.63, respectively). CONCLUSION: Low dose dobutamine TEE test well predicts the early response of dysfunctioning myocardial segments to CABG.
Angioplasty ; Cardiopulmonary Bypass ; Coronary Artery Bypass* ; Coronary Vessels* ; Dobutamine* ; Echocardiography* ; Heart Ventricles ; Humans ; Myocardial Infarction ; Myocardium ; Papillary Muscles ; Sensitivity and Specificity

BACKGROUND: The effects of various concentrations (10, 25 micrometer) of azumolene, an analogue of dantrolene, were studied in isolated guinea pig ventricular papillary muscles by measuring the effects on myocardial contractility and electrophysiologic parameters. METHODS: Isometric forces were studied in normal and 26 mM K Tyrode's solution. Rapid cooling contracture, an index of SR Ca2 content, was performed. Normal and slow action potentials (APs) were evaluated by using conventional microelectrode technique. RESULTS: Ten and 25 micrometer azumolene depressed peak force and maximum rate of force development ( 30 40%). Dose-dependent depression was shown at 2 and 3 Hz stimulation rate. Rapid cooling contractures following 10 and 25 micrometer azumolene was not altered compared to control while peak force at 2 Hz stimulation rate just prior to cooling was depressed similarly to normal Tyrode's solution. In 26 mM K Tyrode's solution, 10 and 25 micrometer azumolene caused depression of early (10 micrometer: 20%) and late (10 micrometer: 50%) force development. In slow APs, shortening of AP duration at 20, 50, and 90% of the repolarization phase, as well as a small but significant reduction of dV/dt-max ( 20%) were shown at 0.25 Hz stimulation rate. There was no alteration in AP parameters in normal APs. CONCLUSIONS: The direct myocardial depressant action of azumolene seems to be at least in part caused by inhibition of Ca2 influx via the Ca2 channel in sarcolemma. It seems likely that azumolene does not alter the sarcoplasmic reticulum function such as Ca2 uptake and release in cardiac muscle.
Action Potentials ; Animals ; Contracture ; Dantrolene ; Depression ; Guinea Pigs ; Malignant Hyperthermia ; Microelectrodes ; Myocardium* ; Papillary Muscles ; Sarcolemma ; Sarcoplasmic Reticulum