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At least 415 records · Page 23Linked to original sources
PubMed1997

Effects of wrapping tightness on acute cardiac function in dynamic cardiomyoplasty.

BACKGROUND: It has not been clarified how tightly the heart should be wrapped for maximal augmentation of cardiac function in cardiomyoplasty. METHODS: Hearts in acute failure induced by propranolol were wrapped with the left latissimus dorsi muscle, loosely (loose CMP), moderately (moderate CMP), and tightly (tight CMP) in each of 5 pigs. To measure the pressure between the latissimus dorsi muscle and the left ventricle (LV), a Millar pressure catheter with a latex balloon was placed on the anterior wall of the LV. Left ventricular wall tension was calculated according to Laplace's law, using the difference between the LV pressure and the balloon pressure. RESULTS: In the loose CMP, moderate CMP, and tight CMP groups, the mean balloon pressures during unassisted beats were 8.2, 10.4, and 13.2 mm Hg, respectively. During unassisted beats, the mean LV wall tension values were 38,683, 29,938 (p < 0.05 versus loose CMP), and 26,652 (p < 0.05 versus loose CMP) dynes/cm, respectively, the peak LV pressures were 76.8, 73.8, and 65 (p < 0.05 versus loose CMP) mm Hg, respectively, and the stroke volumes were 12.8, 9.2, and 8.5 (p < 0.05 versus loose CMP) mL, respectively. During assisted beats, the mean LV wall tension values were 20,059, 11,290, and 7,893 (p < 0.05 versus loose CMP) dynes/cm, respectively, the peak LV pressures were 94.1, 98.1, and 92.0 mm Hg, respectively, and the stroke volumes were 13.8, 11.6, and 9.4 (p < 0.05 versus loose CMP) mL, respectively. CONCLUSIONS: During unassisted beats, tight CMP (13 mm Hg) had the advantage of diminishing LV wall tension, but the disadvantage of diminishing LV pressure and stroke volume, compared with loose CMP (8 mm Hg). Moderate CMP (10 mm Hg), however, had the advantage of diminishing LV wall tension without a decrease in LV pressure and stroke volume.

Animals↗
PubMed1991

Pharmacologic interventions for the neonate with compromised cardiac function.

The developmental aspects of myocardial performance must be considered when pharmacologic agents are used to support the neonate with compromised cardiac function. Neonatal cardiovascular function is characterized by a limited preload reserve, decreased ventricular compliance, limited contractile reserve, and CO that is primarily dependent on the HR. Nurses caring for these neonates need a baseline understanding of normal cardiovascular physiology to evaluate the effectiveness of pharmacologic interventions to augment CO. Neonatal nurses play a pivotal role in the therapeutic management of pharmacologic interventions to provide safe, high quality care for the sick neonate.

Cardiovascular Agents↗
PubMed1986

The effects of burn injury and fluid resuscitation on cardiac function in vitro.

The effects of a 30% full-thickness total body surface area scald burn on in vitro mechanical cardiac function was studied in Sprague-Dawley rats. The findings were a 50% decrease in tension development and velocities of contraction and relaxation, when papillary muscle functions from sham and unresuscitated burned animals were compared. Fluid resuscitation synchronous with burning completely reversed the defects in papillary muscle function. This defect in function was partially transferable to normal muscles incubated in serum from burned rats.

Animals↗
PubMed1984

Disturbed cardiac function possibly associated with mianserin therapy.

Two patients, who were receiving therapy with mianserin for depressive disorders, developed signs of disturbed cardiac function which resolved after mianserin therapy was discontinued. One of the patients also developed hypokalaemia which was probably caused by the drug. It is felt that these side effects warrant further research.

Aged↗
PubMed1998

Effect of "living high-training low" on the cardiac functions at sea level.

Living high-training low (LHTL), living at high altitude and training at sea level, is reported to be beneficial in enhancing physical performance. Effect of LHTL on cardiac function which is one of major determinants in performance, however, was not examined. To address this issue, 21 well-trained triathletes divided into control (n = 10, living and training at sea level) and LHTL group (living at 1980 m altitude > or = 12 hrs/day and training at sea level) were Doppler echocardiographically examined before and at the end of the two-week program. Heart rate and blood pressure did not change in both groups. At end of the training, left ventricular endsystolic diameter of LHTL group was smaller than that of controls (32 vs 34 mm, P < 0.05). Shortening fraction and ejection fraction in LHTL group increased by 9% and 17 %, respectively, P < 0.05. Preejection period/ejection time was more greatly reduced in LHTL group (P < 0.05). Stroke volume and cardiac output in LHTL increased. Diastolic function was not significantly affected by LHTL. These results suggest that LHTL produced an improvement of systolic function underlined by incremented left ventricular contractility, which might be associated with increased beta-adrenergic receptor or an improved myocardial energy utilization.

Adult↗
PubMed1996

Myocardial signaling defects and impaired cardiac function of a human beta 2-adrenergic receptor polymorphism expressed in transgenic mice.

A threonine to isoleucine polymorphism at amino acid 164 in the fourth transmembrane spanning domain of the beta 2-adrenergic receptor (beta 2AR) is known to occur in the human population. The functional consequences of this polymorphism to catecholamine signaling in relevant cells or to end-organ responsiveness, however, are not known. To explore potential differences between the two receptors, site-directed mutagenesis was carried out to mimic the polymorphism. Transgenic FVB/N mice were then created overexpressing wild-type (wt) beta 2AR or the mutant Ile-164 receptor in a targeted manner in the heart using a murine alpha myosin heavy chain promoter. The functional properties of the two receptors were then assessed at the level of in vitro cardiac myocyte signaling and in vivo cardiac responses in intact animals. The expression levels of these receptors in the two lines chosen for study were approximately 1200 fmol/mg protein in cardiac membranes, which represents a approximately 45-fold increase in expression over endogenous beta AR. Myocyte membrane adenylyl cyclase activity in the basal state was significantly lower in the Ile-164 mice (19.5 +/- 2.7 pmol/min/mg) compared with wt beta 2AR mice (35.0 +/- 4.1 pmol/min/mg), as was the maximal isoproterenol-stimulated activity (49.8 +/- 7.8 versus 77.1 +/ 7.3 pmol/min/mg). In intact animals, resting heart rate (441 +/- 21 versus 534 +/- 17 bpm) and dP/dtmax (10,923 +/- 730 versus 15,308 +/- 471 mmHg/sec) were less in the Ile-164 mice as compared with wt beta 2AR mice. Similarly, the physiologic responses to infused isoproterenol were notably less in the mutant expressing mice. Indeed, these values, as well as other contractile parameters, were indistinguishable between Ile-164 mice and nontransgenic littermates. Taken together, these results demonstrate that the Ile-164 polymorphism is substantially dysfunctional in a relevant target tissue, as indicated by depressed receptor coupling to adenylyl cyclase in myocardial membranes and impaired receptor mediated cardiac function in vivo. Under normal homeostatic conditions or in circumstances where sympathetic responses are compromised due to diseased states, such as heart failure, this impairment may have important pathophysiologic consequences.

Adenylyl Cyclases↗
PubMed1987

Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children.

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1984

Evaluation of size and dynamics of the inferior vena cava as an index of right-sided cardiac function.

To define normal criteria of size and dynamics of the inferior vena cava (IVC) and its clinical value in assessing right-sided cardiac function, 2-dimensional (2-D) and M-mode echocardiography (echo) were performed in 175 subjects, who were classified into 3 groups: group 1-80 normal subjects; group IIA--65 patients with documented right-sided cardiac disease, and group IIB--30 patients with cardiac disease but no right-sided abnormality. The IVC was adequately imaged in 175 of 185 subjects (95%). There was good correlation between M-mode and 2-D echo (r = 0.84) and long- and short-axis (r = 0.88) measurements. The IVC diameter during expiration was: group 1-9 to 28 mm (mean 18.2 +/- 4.6); group IIA--15 to 40 mm (mean 23.1 +/- 4.8) and group IIB-8-24 mm (mean 15.6 +/- 3.7). Collapsibility index (inspiratory decrease in diameter) was: group I-37 to 100% (mean 55.8 +/- 15.9); group IIA--0 to 39% (mean 13.5 +/- 10.5); and group IIB--44 to 100% (mean 60.4 +/- 13.1). A and V waves could be measured in 120 of 151 cases (79%). Both A and V waves were less than 125% of its diameter in group I. The A wave was absent in 34 patients; 30 (88%) were in atrial fibrillation. Among 8 patients with tricuspid regurgitation, 5 (63%) had V waves greater than 125%. There was no correlation between diameter or collapsibility index and age, sex, rhythm or body surface area.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Augmentation of cardiac function by elevation of intrathoracic pressure.

We studied the cardiovascular effects of increasing intrathoracic pressure in an acute pentobarbital-anesthetized canine model of acute ventricular failure induced by large doses of propranolol. Left ventricular (LV) function curves were generated by volume loading from LV filling pressures of 5-20 Torr. The animals were ventilated by using intermittent positive-pressure ventilation with large tidal volumes (30 ml/kg). Chest and abdominal pneumatic binders were used to increase intrathoracic pressure. When compared with the control state, acute ventricular failure was associated with a decrease in the slope of the LV function curves (P less than 0.01). After binding the increase in intrathoracic pressure (1.1 +/- 1.6 to 12.1 +/- 2.4 Torr, P less than 0.01) was associated with an improvement in both right ventricular and LV function. Our study demonstrates that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function. We postulate that this observed improvement with increased intrathoracic pressure is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.

Acute Disease↗
PubMed1987

Cardiac function: evaluation with fast-echo MR imaging.

Magnetic resonance (MR) imaging of the heart has, to date, been limited in its ability to evaluate cardiac function. The authors have implemented a technique for functional assessment of the heart using shorter echo times than those generally used for conventional spin-echo imaging. With these short echo times, multiple images can be obtained in a multisection mode approximately within the isovolumetric phases of the cardiac cycle. This permits a pair of image stacks to be obtained, one in end systole and the other in end diastole. With the use of a modified Simpson rule, left ventricular volume and ejection fraction were calculated and compared with results obtained from contrast material-enhanced ventriculography. Preliminary results indicate that this method has promise for the evaluation of a variety of functional parameters in the heart. The short acquisition times for this functional study permit it to be combined with a tissue characterization study within the time constraints of a clinical MR imaging session.

Heart Function Tests↗
PubMed1995

Effects of short-term aminophylline administration on cardiac functional reserve in patients with syndrome X.

OBJECTIVES: This study sought to evaluate the effect of adenosine receptor blockade by aminophylline on cardiac functional reserve in patients with syndrome X. BACKGROUND: Aminophylline may have a potentially antiischemic effect through the inhibition of adenosine and, thus, the coronary steal phenomenon in patients with syndrome X. METHODS: A single-blind, placebo-controlled study of an intravenous infusion of aminophylline (6 mg/kg body weight over 15 min) or placebo (20 ml of saline solution over 15 min) was performed during continuous radionuclide monitoring of left ventricular ejection fraction in 12 patients performing supine bicycle ergometric exercise. RESULTS: Aminophylline increased exercise time (aminophylline 400 s vs. placebo 355 s, p < 0.01), decreased degree of ST segment depression (aminophylline 1.6 mm vs. placebo 2.4 mm, p < 0.01) and either abolished (seven patients) or diminished (five patients) chest pain during exercise. Aminophylline also increased left ventricular ejection fraction at rest (aminophylline 66.5% vs. placebo 62.3%, p < 0.05) but did not improve its deterioration at peak exercise (aminophylline 60.1% vs. placebo 56.6%, p = NS) or shorten the abnormally prolonged interval between the end of exercise and the overshoot (aminophylline 115 s vs. placebo 130 s, p = NS). CONCLUSIONS: Aminophylline infusion increases ischemic threshold and prolongs exercise duration in patients with syndrome X. It is hypothesized that aminophylline acts by inhibiting the coronary steal phenomenon through adenosine receptor blockade. It does not improve the deterioration in left ventricular function at peak exercise or the delayed response in ejection fraction in the recovery period, presumably because the beneficial effects of aminophylline that result from the redistribution of coronary blood flow are limited.

Aminophylline↗
PubMed1989

[Relationship between left atrial diameter and cardiac function in myocardial infarction--assessment of left ventricular end-diastolic pressure by the left atrial index].

To study the assessment of cardiac function in acute myocardial infarction (AMI), we measured left atrial diameter, left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), ejection fraction (EF) in 20 patients with acute myocardial infarction. Left atrial diameter was measured using echocardiography and was expressed as left atrial index (LAI, mm/m2) dividing by body surface area. LAI in AMI was 21.3 +/- 2.7 mm/m2 and significantly larger than LAI in normal subject (19.9 +/- 2.0 mm/m2) (p less than 0.05), In AMI, LVEDP was 13.3 +/- 3.4 mmHg, PCWP was 9.0 +/- 2.8 mmHg and EF was 52.3 +/- 14.8%, Relationship (r value) between LAI and LVEDP (r = 0.70, p less than 0.001, y = 0.87 x-5.4 x; LAI, y; LVEDP) was greater than PCWP and LVEDP (r = 0.60, p less than 0.01). LVEDP calculated from LAI using this method was directly measured LVEDP directly measured +/- 2.4 mmHg. In 9 patients, LAI was larger than 20.9 mm/m2, in 8 patients of them LVEDP was higher than 13 mmHg. In 11 patients LAI was smaller than 20.9 mmHg, only in 2 of them LVEDP was lower than 13 mmHg. It concluded that sensitivity was 88.9%, specificity was 81.8%, accuracy was 85.0%. Relationship between LAI and PCWP (r = 0.30), LAI and EF (r = -0.36) were not significant. We can measure LAI repeatedly in AMI non-invasively, and predict LVEDP. Thus, the measurement of LAI is useful in treatment of AMI.

Adult↗
PubMed1978

Effects of 5-([2-(diethylamino)-ethyl]amino)-3-phenyl-1,2,4-oxadiazole dihydrochloride (DEPO) on cardiac functions and myocardial metabolism of the dog.

Effects of 5-([2-(diethylamino)-ethyl]amino)-3-phenyl-1,2,4-oxadiazole (DEPO) on cardiac functions and myocardial metabolism were examined using the heart in vivo and the isolated perfused heart of dogs. In the heart in vivo DEPO i.v. produced dose-dependent decreases in coronary perfusion pressure (PP), heart rate (HR), left ventricular pressure (LVP), dP/dt max of LVP and coronary vascular resistance (VR). DEPO i.c. dose-dependently increased left circumflex coronary flow (LCCF) and decreased PP, LVP and dP/dt max of LVP, but did not change HR. In the isolated perfused heart, DEPO induced a marked increase in coronary blood flow (CBF) and depressed HR and myocardial contractile force. Myocardial oxygen consumption and myocardial redox potential were not significantly changed. DEPO could not modify the effects of isoproterenol, adenosine and reactive hyperaemia on the heart. The results suggest that DEPO may have a coronary vasodilating action and some direct inhibitory actions on the heart.

Adenosine↗
PubMed1981

Hepatic sequelae of congestive cardiac failure. Evidence for a liver lesion in patients in whom cardiac function has been restored to normal.

In order to test the hypothesis that clinical and biochemical features of liver disease due to cardiac failure regress upon relief of cardiac decompensation, 38 patients with constrictive pericarditis were studied before and after pericardiectomy for periods ranging from 1 week to 25 years. All patients were judged to be free of clinical evidence of heart failure. Hepatomegaly was present in 10 of the 38 patients studied. Of the patients studied 1-25 years after operation, 96% had elevated serum levels of total and conjugated bilirubin. The percentage Bromsulphalein (BSP) retention at 45 minutes was abnormal in all 29 patients studied 1 year or more after surgery. There was no significant correlation between the level of bilirubin or the percentage BSP retained when these were compared with the pre-operative height of jugular venous pressure, degree of pulsus paradoxus, duration of symptoms or degree of hepatic congestion. Our study reveals that the liver lesion of cardiac failure persists for up to 25 years after restoration of normal cardiac function.

Adolescent↗
PubMed1990

Cardiac function and morphology of Hanford miniature swine and Yucatan miniature and micro swine.

The use of miniature swine in biomedical research is increasing; however, a comparison of cardiac function and morphology between strains has yet to be characterized. The purpose of this project was to examine comprehensive hemodynamics and cardiac morphology of three groups of ten normal, 4 months old, age-matched Yucatan miniature (MINI) pigs, Yucatan micropigs (MICRO) and Hanford (HAN) miniature pigs, 5 males and five females per group. Closed chest cardiac catheterization under equivalent conditions was performed followed by post mortem cardiac morphometry. Mean arterial pressure was significantly greater in the Hanford group when compared to both the minipig and micropig pigs (HAN: 89 +/- 4; MINI: 48 +/- 3; MICRO: 53 +/- 2 mmHg). Pulmonary vascular resistance was significantly different between the three groups (HAN: 9 +/- 1; MINI: 60 +/- 12; MICRO: 111 +/- 29 dyne x sec/cm x m2). The Hanford strain had a significantly smaller heart weight to body weight ratio than the other two groups (HAN: 4.6 +/- 1.0; MINI: 5.7 +/- 0.1; MICRO: 5.5 +/- 1.0). Variations in cardiovascular parameters occur among these strains and should be considered when constructing experimental designs.

Animals↗
PubMed1995

Enhancement of cardiac function by cyclocreatine in models of cardiopulmonary bypass.

This study tests the hypothesis that the administration of cyclocreatine prior to global ischemia enhances recovery of cardiac function during reperfusion. Two models were used. First, in a Langendorff-working heart model of normothermic cardioplegic arrest, rats (n = 6 per group) were injected intravenously with saline or cyclocreatine (600, 300, or 150 mg/kg). After 30 min or 2 h, hearts were excised and perfused in the Langendorff mode for 5 min and then in the working heart mode for 20 min. Normothermic arrest was induced by infusing warm St. Thomas solution once; then hearts were kept at 37 degrees C for 40 min. Following arrest, hearts were reperfused in the Langendorff mode for 15 min and then in the working mode for 30 min. Cyclocreatine consistently produced significantly better recovery of aortic flow and cardiac output compared to that of saline hearts. Second, in an intact canine model of cold cardioplegic arrest, adult mongrel dogs (n = 3 to 6 per group) underwent aortic cross-clamping for 1 h, followed by reperfusion on bypass for 45 min and off bypass for 4 h. Dogs were injected intravenously with saline or cyclocreatine (500 mg/kg) for 1 h before experiment. Post-bypass segmental contractility and cardiac output were significantly better in cyclocreatine hearts compared to that of controls. In a limited study, after a 3 h aortic cross-clamp time, cyclocreatine hearts achieved 91% baseline function while control hearts failed after 2 h. Results of this study suggest that cyclocreatine, without inotropic or chronotropic effect, protects the heart from global ischemic injury.

Animals↗
PubMed1991

Effects of regression of left ventricular hypertrophy following atenolol or bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats.

The effects of regression of left ventricular hypertrophy following atenolol and bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats (SHR) were studied. Atenolol (50 mg/kg/day) and bunazosin (5 mg/kg/day) were administered to SHR from 19 to 26 weeks of age, whereas tap water was given to control SHR and normotensive Wistar-Kyoto rats (WKY). Both atenolol and bunazosin significantly decreased arterial blood pressure and significantly decelerated the increase in left ventricular weight in SHR. At the end of the long-term treatment, hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The pressure-rate product and the extent of recovery of the coronary flow after reperfusion following 30 min of ischemia in the bunazosin-treated SHR were significantly higher than those in the control SHR and the atenolol-treated SHR. The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were significantly lower than those in the reperfused WKY. Both atenolol and bunazosin improved the restoration of ATP and CrP in SHR after reperfusion following 30 min of ischemia. In conclusion, antihypertensive therapy with either atenolol or bunazosin was effective in preventing cardiac hypertrophy and ischemic damage caused by different mechanisms. Factors resulting from stimulation of the cardiac alpha 1 adrenoceptor may play an important role in the development of hypertensive cardiac hypertrophy, just as factors resulting from stimulation of the beta 1-adrenoceptor do.

Adenosine Diphosphate↗
PubMed1995

Effects of Levosimendan, a cardiotonic agent targeted to troponin C, on cardiac function and on phosphorylation and Ca2+ sensitivity of cardiac myofibrils and sarcoplasmic reticulum in guinea pig heart.

A new cardiotonic agent, (R)-[[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)-phenyl] hydrazono]propanedinitrile (Levosimendan), has been developed and screened for its ability to bind to cardiac troponin C. In perfused hearts, low concentrations of 0.03 or 0.1 mumol/L Levosimendan increased +dP/dt, but did not affect the speed of relaxation and produced only a slight increase in spontaneous heart rate in the hearts perfused with 0.1 mumol/L of the drug. In these same hearts, perfusion with 0.03 mumol/L Levosimendan did not alter the 32P incorporation into troponin I or C protein, whereas a slight but significant increase was noted for phospholamban, with no detectable change in tissue cAMP levels. Administration of 0.1 or 0.3 mumol/L Levosimendan significantly increased myocardial cAMP levels as well as the phosphorylation of phospholamban, troponin I, and C protein. Levosimendan (0.03 to 10 mumol/L) reversibly increased force generated by detergent-extracted fiber bundles over a range of submaximally activating free Ca2+ concentrations with no significant effect on maximum force or on Ca2+ binding to myofilament troponin C. There was no direct effect of Levosimendan on Ca2+ uptake by vesicles of sarcoplasmic reticulum (SR). In contrast, under conditions optimal for cAMP-dependent phosphorylation, Levosimendan slightly but significantly lowered the concentration of Ca2+, yielding half-maximal uptake rates by the SR vesicles. Our results indicate that at low concentrations Levosimendan acts preferably as a Ca2+ sensitizer, whereas at higher concentrations its action as a phosphodiesterase inhibitor contributes to the positive inotropic effect.

Analysis of Variance↗