[A theoretical analysis of cardiac function curve. 2. Derivation of a formula representing the cardiac output curve--from Suga's theory].
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Cardiac Output↗
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The influence of isotonic exercise on cardiac hypertrophy in arterial hypertension: impact on cardiac function and on the capacity for aerobic work.
Intense physical training through isotonic exercises has controversial effects in individuals with moderate to severe hypertension. In this study, normotensive Wistar rats and rats with renovascular hypertension (Goldblatt II) were subjected to intense physical exercise involving two 50-min swimming sessions per day for a period of 12 weeks. At the end of the study, we evaluated the effect of training on arterial pressure, the capacity for aerobic work and cardiac function. Our results demonstrate that intense physical training has no effect on the arterial blood pressure of normotensive rats or of animals with moderate renovascular hypertension. Hypertensive animals with cardiac hypertrophy require a greater period of training in order to attain the same capacity for aerobic work as normotensive rats. This difference may result from an inability of the former animals to increase cardiac compliance, thereby impeding more extensive usage of the Frank-Starling mechanism to subsequently increase the systolic cardiac performance. Cardiac hypertrophy induced by exercise did not summate with that induced by arterial hypertension. Physical exercise normalized the end-diastolic left ventricular pressure in hypertensive animals without any corresponding increase in the compliance of the chamber. The first derivative of left ventricular pulse pressure (+/- dP/dt) was greater in the hypertensive trained group than in the hypertensive sedentary rats. These observations suggest that a systolic dysfunction of the left ventricle involving an elevated residual volume secondary to arterial hypertension may be corrected by physical exercise such as swimming.
Aerobiosis↗
Multi-slice dynamic imaging: complete functional cardiac MR examination within 15 seconds.
A new magnetic resonance (MR) sequence was developed to acquire real-time images in a multi-slice dynamic imaging mode to cover the complete heart in 15 seconds without the need for electrocardiogram (ECG) triggering and multiple breath holds. In 34 patients, left ventricular function was assessed with the new technique and a standard technique. The new technique proved to be feasible and accurate for functional cardiac examinations.
Adult↗
Inhibition of cyclooxygenase-2 improves cardiac function in myocardial infarction.
Induction of cyclooxygenase-2 (COX-2) in ischemic myocardium is thought to increase the production of proinflammatory prostanoids and contribute significantly to the ischemic inflammation. Left ventricular myocardial infarction (MI) was created by ligating the left coronary artery in Lewis rats. Hemodynamic measurements at 4 weeks showed better cardiac function in the group treated with a selective COX-2 inhibitor (DFU; 5 mg/kg/day) for 2 weeks after induction of MI compared to the vehicle treated group. These results suggest that induction of COX-2 contributes to myocardial dysfunction, and that selective inhibition of COX-2 could constitute an important therapeutic target for the treatment of MI.
Animals↗
Influence of transmyocardial laser revascularization (TMLR) on regional cardiac function and metabolism in an isolated hemoperfused working pig heart.
The mechanism of an indirect revascularization in ischemic myocardium by transmyocardial laser revascularization (TMLR) is not yet fully understood. An improvement of clinical symptoms caused by TMLR is reported in many clinical trials with patients in which a direct revascularization is not possible. An increase of myocardial perfusion through laser channels is doubtful, because the myocardial pressure in the wall is higher than in the cavum. Therefore we measured the local cardiac function (intramyocardial pressure, wall thickness, pressure-length curves) and acute metabolic changes (tissue lactate content, tissue pO2) in ischemic and nonischemic regions before and after TMLR in isolated hemoperfused pig hearts. An isolated heart was chosen because it enabled us to separate coronary flow from flow through ventricular channels. The ischemia was induced by coronary occlusion or microembolization (eight hearts each). It should be noted that microembolization leads to conditions which are more comparable with those found in patients selected for TMLR. In the isolated working heart, the coronary perfusion can be controlled independently from perfusion through the ventricular cavum. Under the ischemic conditions mentioned above, we observed that the intramyocardial pressure in the ischemic region decreased below the left ventricular pressure, so one premise for indirect perfusion was met. TMLR after microembolization led to a significant improvement of regional cardiac work and the tissue oxygen pressure. These acute effects demonstrate the possibility of functional and metabolic amelioration by TMLR after ischemia induced by microembolization in an isolated hemoperfused pig heart.
Analysis of Variance↗
Food restriction-induced transformations in cardiac functional and biochemical properties in rats.
The primary objective of this study was to ascertain if various degrees of marked chronic food restriction (FR) as well as the combination of FR and exercise training of moderate intensity induce changes in the functional properties of the heart that are consistent with previously reported findings indicative of downregulation of high-adenosinetriphosphatase V1 isomyosin expression. Adult female rodents were randomly assigned to one of four experimental groups: 1) free eating, 2) 50% food restricted, 3) 75% food restricted, or 4) 50% food restricted plus treadmill trained. Results show that FR induced significant depression in the functional properties (heart rate, left ventricular pressure, rate of pressure development, and double product) of the heart in all FR groups and that this depression in functional capacity corresponded to the degree of FR. These functional changes were accompanied by significant downregulation of the alpha- and upregulation of the beta-myosin heavy chain gene expressions, as studied at both the mRNA and protein levels. The exercise training induced further alterations in cardiac function; however, these alterations occurred independently of any shifts in isomyosin composition. These results suggest that although severe FR is a potent stimulus to transform both the biochemical and functional properties of the rodent heart, the underlying mechanism(s) concerning these adaptations remains unresolved.
Adenosine Triphosphatases↗
Transfection with a dominant-negative inhibitor of monocyte chemoattractant protein-1 gene improves cardiac function after 6 hours of cold preservation.
BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1), a potent chemotactic factor for monocytes, is induced during ischemia-reperfusion. As monocytes might play an important causative role in reperfusion injury, we investigated if inhibition of monocyte activation could attenuate ischemia-reperfusion injury and thereby improve cardiac preservation. To inhibit monocyte activation, we transfected a dominant-negative inhibitor of MCP-1 (7ND) gene in an animal model. METHODS AND RESULTS: We used an isolated rabbit heart preparation perfused with support-rabbit blood and transfected 7ND genes to skeletal muscle of the support rabbits (n=7) using electroporation technique; causing an elevation of serum 7ND level to 20+/-7 pg/mL at 5 days after transfection. Animals receiving empty plasmid served as controls (n=7). Five days after transfection, hearts from other rabbits were excised, stored in UW solution for 6hours, and perfused with blood from transfected support rabbits. The 7ND group showed better cardiac output (128.7+/-17.9 versus 81.6+/-19.8 mL/min; P<0.01), lower serum CK-MB levels (5.0+/-1.8 versus 11.1+/-2.9 ng/mL; P<0.01), lower serum IL-1beta levels (257.2+/-23.2 versus 311.2+/-37.4pg/mL; P<0.05), and lower serum TNF-alpha levels (19.0+/-8.4 versus 35.1+/-13.0pg/mL; P<0.05). The numbers of infiltrating cells in myocardium were significantly reduced in the 7ND group. CONCLUSIONS: Inhibition of MCP-1 with 7ND gene transfection reduced cytokine activation, attenuated myocardial damage, and improved cardiac function after 6 hours of preservation. These results show that MCP-1 plays an important role in ischemia-reperfusion injury.
Animals↗
Effects of obesity and weight loss on cardiac function and valvular performance.
OBJECTIVE: To study the consequences of long-standing obesity on myocardial function and valvular performance and to determine the effects of weight loss on these cardiovascular features. RESEARCH METHODS AND PROCEDURES: We included 41 patients with obesity referred for weight-reducing gastroplasty, 31 patients with obesity who received dietary recommendations, and 43 lean subjects. Body weight and blood pressure were measured, and cardiac function and valvular performance were estimated echocardiographically. Left ventricular ejection fraction was used to assess systolic heart function, and the ratio of transmitral early to atrial (E/A) peak flow velocity was used as an estimate of diastolic filling. All three study groups were investigated at baseline, and the two groups with obesity were re-examined at 1-year follow-up. RESULTS: Patients with obesity had higher blood pressure, greater cardiac output, lower ejection fraction, and reduced E/A ratio, compared with lean subjects (p<0.01). Surgical treatment of obesity led to significant decreases in body weight, whereas body weight remained unchanged in the group treated with dietary recommendations (p<0.001). In the weight loss group, blood pressure and cardiac output decreased and the E/A ratio increased (p<0.001). Left ventricular ejection fraction tended to increase in the weight loss group and decrease in the obese control group (p<0.01). No significant valvular disease was observed in any of the subjects with obesity at baseline or after weight loss. DISCUSSION: We conclude that weight reduction in subjects with obesity is associated with improvements in left ventricular diastolic filling and has favorable effects on left ventricular ejection fraction. Neither obesity nor weight loss seem to promote valvular heart disease.
Adult↗
Physiologically tolerable insulin reduces myocardial injury and improves cardiac functional recovery in myocardial ischemic/reperfused dogs.
This study was designed to examine whether physiologically tolerable insulin, which maintains lower blood glucose, can protect the myocardium against ischemia/reperfusion (I/R) injury in a preclinical large animal model. Adult dogs were subjected to 50 minutes of myocardial ischemia (80% reduction in coronary blood flow) followed by 4 hours of reperfusion and treated with vehicle, glucose-insulin-potassium (GIK; glucose, 250 g/L; insulin, 60 U/L; potassium, 80 mmol/L), GK, or low-dose insulin (30 U/L) 10 minutes before reperfusion. Treatment with GIK exerted significant cardioprotective effects as evidenced by improved cardiac function, improved coronary blood flow, reduced infarct size, and myocardial apoptosis. In contrast, treatment with GK increased blood glucose level and aggravated myocardial I/R injury. It is interesting that treatment with insulin alone at the dose that reduced blood glucose to a clinically tolerable level exerted significant cardioprotective effects that were comparable to that seen in the GIK-treated group. This low-dose insulin had no effect on coronary blood flow after reperfusion but markedly reduced coronary reactive hyperemia and switched myocardial substrate uptake from fat to carbohydrate. Our results suggest that lower glucose supply to the ischemic myocardium at early reperfusion may create a "metabolic postconditioning" and thus reduce myocardial ischemia/reperfusion injury after prolonged reperfusion.
Animals↗
Pentameric assembly of phospholamban facilitates inhibition of cardiac function in vivo.
Phospholamban has been proposed to coexist as pentamers and monomers in native sarcoplasmic reticulum membranes. To determine its functional unit in vivo, we reintroduced wild-type (pentameric) or monomeric mutant (C41F) phospholamban in the hearts of phospholamban knockout mice. Transgenic lines, expressing similar levels of mutant or wild-type phospholamban, were identified, and their cardiac phenotypes were characterized in parallel. Sarcoplasmic reticulum Ca2+ transport assays indicated similar decreases in SERCA2 Ca2+ affinity by mutant or wild-type phospholamban. However, the time constants of relaxation and Ca2+ transient decline in isolated cardiomyocytes were diminished to a greater extent by wild-type than mutant phospholamban, even without significant differences in the amplitudes of myocyte contraction and Ca2+ transients between the two groups. Langendorff perfusion also indicated that mutant phospholamban was not capable of depressing the enhanced relaxation parameters of the phospholamban knockout hearts to the same extent as wild-type phospholamban. Moreover, in vivo assessment of mouse hemodynamics revealed a greater depression of cardiac function in wild-type than mutant phospholamban hearts. Thus, the mutant or monomeric form of phospholamban was not as effective in slowing Ca2+ decline or relaxation in cardiomyocytes, hearts, or intact animals as wild-type or pentameric phospholamban. These findings suggest that pentameric assembly of phospholamban is necessary for optimal regulation of myocardial contractility in vivo.
Animals↗
Cardiomyocyte-specific endothelin A receptor knockout mice have normal cardiac function and an unaltered hypertrophic response to angiotensin II and isoproterenol.
Even though endothelin is recognized as an important vasoregulatory molecule, the roles of endothelin receptors in specific cell types are not yet fully understood. Mice with a null mutation in endothelin A receptor gene (ET(A)) or in the gene of its ligand (endothelin 1) die neonatally due to craniofacial and cardiac abnormalities. This early lethality has in the past hindered studies on the role of endothelin in cardiovascular physiology and pathophysiology. To overcome this obstacle, we utilized the cre/loxP technology to generate mice in which the ET(A) gene could be deleted specifically in cardiomyocytes. The cre recombinase transgene driven by the alpha-myosin heavy-chain promoter deleted the floxed ET(A) allele specifically in the hearts of these mice, resulting in a 78% reduction in cardiac ET(A) mRNA level compared to wild-type controls. Cardiomyocyte-specific ET(A) knockout animals are viable and exhibit normal growth, cardiac anatomy, and cardiac contractility, as assessed by echocardiography. In addition, these animals exhibit hypertrophic and contractile responses to 10-day infusion of angiotensin II or isoproterenol similar to those observed in control animals. These results indicate that in adult mice cardiac ET(A) receptors are not necessary for either baseline cardiac function or stress-induced response to angiotensin II or isoproterenol.
Angiotensin II↗
Left ventricular geometry and cardiac function during minimally invasive coronary artery bypass grafting.
BACKGROUND: This investigation was designed to study the changes in function and geometry of the left ventricle during two critical steps of minimally invasive direct coronary artery bypass procedures: placement of an epicardial stabilizer and occlusion of the left anterior descending coronary artery. METHODS: Between February 1997 and January 1998, 28 patients underwent bypass grafting with the left internal thoracic artery to the left anterior descending coronary artery (minimally invasive direct coronary artery bypass technique). Transesophageal echocardiography was used for determination of fractional area change and to assess left ventricular (LV) diameters in two dimensions and at the apex. RESULTS: Placement of the epicardial stabilizer resulted in a small decrease in LV end-systolic and end-diastolic dimensions; cardiac function remained unchanged. Subsequent occlusion of the left anterior descending coronary artery caused a moderate decline in cardiac index and fractional area change, an increase in LV diameters, and the development of hypokinetic segments within the LV myocardium. CONCLUSIONS: The use of an epicardial stabilizer provides a safe and effective means to stabilize the operative field during minimally invasive direct coronary artery bypass procedures. Monitoring of LV function by transesophageal echocardiography enhances the safety of such procedures and is highly recommended.
Aged↗
Relationships among Doppler-derived umbilical artery absolute velocities, cardiac function, and placental volume blood flow and resistance in fetal sheep.
We hypothesized that umbilical artery (UA) absolute blood flow velocities measured by Doppler ultrasonography reflect placental volume blood flow (Q(UA)) and placental vascular resistance (R(UA)) in a late gestation fetal sheep model. In addition, we examined the relationships between umbilical artery absolute blood flow velocities and parameters of fetal cardiac function. Twenty-six sheep fetuses were instrumented at 112-132 days of gestation. After a 5-day recovery period, experiments were performed under general anesthesia in 16 normal fetuses, in 5 fetuses after maternal administration of phenylephrine, and in 5 fetuses after placental embolization. The Q(UA) and arterial blood pressures were measured using a transit-time ultrasonic flow probe and a catheter placed into the descending aorta, respectively. UA peak systolic velocity (PSV), end-diastolic velocity (EDV), time-averaged maximum velocity (TAMXV), pulsatility index (PI), mean velocity (V(mean)), fetal cardiac output, ventricular ejection forces, and the proportion of isovolumetric relaxation time (IRT%) in the cardiac cycle were measured with the use of Doppler ultrasonography. Significant positive linear correlations were found between UA EDV, TAMXV, and V(mean) versus Q(UA), whereas UA PI had a significant negative correlation with Q(UA). Significant negative correlations were shown between UA EDV, TAMXV, and V(mean) versus R(UA). A significant positive correlation was present between UA PI and R(UA). Doppler-derived UA parameters did not correlate with fetal arterial blood pressures, cardiac output, ventricular ejection forces or IRT%. In fetal sheep, Doppler-derived UA PI and absolute velocities, except PSV, are closely related to directly measured Q(UA) and R(UA), validating the use of noninvasive Doppler velocimetry in the assessment of placental circulation.
Anesthesia↗
Cardiac function during long-term hypoxemia in fetal sheep.
To examine right ventricular function during long-term hypoxemia, we instrumented 12 fetal sheep with intravascular catheters and an electromagnetic flow probe on the pulmonary artery. In six cases, hypoxemia was induced by infusing N2 gas into the maternal trachea for 2 wk. Maternal arterial PO2 was less than 60 Torr, and fetal arterial PO2 was reduced from approximately 26 to approximately 19 Torr. Six cases served as nonhypoxic controls. We studied fetal cardiac function by increasing either preload with a volume infusion of 5% (wt/vol) dextrose or afterload by administering methoxamine (alpha-adrenergic agonist). In hypoxic animals, right ventricular output (QRV) and stroke volume (SV) were not affected on the first 2 days but fell 30% on day 3. Fetal arterial pressure (Pfa) increased 20%, hemoglobin concentration increased approximately 30%, and fetal heart rate (FHR) showed minimal changes. Within 2 wk, QRV recovered to normal values, whereas ventricular sensitivity to arterial pressure was reduced. We observed no change in plasma concentration of "cardiac enzymes" or differences in fetal growth between groups. In conclusion, during prolonged hypoxemia, right ventricular function showed a triphasic response (primary maintenance, secondary depression, and subsequent recovery), achieving a new steady state 2 wk after the start of hypoxia, characterized by decreased sensitivity to afterload, associated with polycythemia and hypertension.
Animals↗
Effect of exercise on plasma atrial natriuretic factor and cardiac function in men and women.
In order to provide an integrated view of the physiology of atrial natriuretic factor (ANF) during exercise, we studied changes of its plasma concentrations in 13 normal subjects (seven males, six females) during three graded exercise levels and two periods of recovery (5 and 30 min), concomitantly with an assessment of cardiac function and ventricular volumes by multigated radionuclide angiography. Mean ANF levels (+/- SEM) increased in all patients at the second (P less than 0.002) and third (P less than 0.002) exercise levels, and after 5-min recovery (P less than 0.01): in males from 16 +/- 7 to 30 +/- 11 pg ml-1 at the third level, in females from 27 +/- 12 to 61 +/- 33 pg ml-1. Normal values were observed after 30-min recovery. Even if mean ANF levels were all higher in females, this difference did not reach statistical significance (P = 0.06). Significant decreases of ventricular volumes, as well as increases of ejection fraction and rate pressure product, were noted during exercise and were similar in both sexes. The kinetics of plasma ANF concentrations, compared with the increase of rate pressure product, was characterized by a latency and a remanence in recovery. This remanence, also present in the changes of ventricular volumes, supports the hypothesis that other factor(s) like catecholamines might still exert their influence after the exercise stops.
Adult↗
Systolic time intervals: a review of the method in the non-invasive investigation of cardiac function in health, disease and clinical pharmacology.
Measurement of systolic time intervals is a valuable, non-invasive procedure to assess left ventricular performance, particularly when influenced by drugs. In this review, we discuss various factors affecting systolic time intervals, the therapeutic implications of the technique and its place among other non-invasive tests of cardiac function.
Adolescent↗
DNA immunizations with M2 muscarinic and beta1 adrenergic receptor coding plasmids impair cardiac function in mice.
Autoimmune mediated myocardial damage is likely to be a pathogenic mechanism for acquired dilated cardiomyopathies. Evidence confirms that autoantibodies that bind to M(2) muscarinic (M(2)AChR) and beta(1) adrenergic receptors (beta(1)AR) are present in idiopathic dilated cardiomyopathy and Chagasic patients' sera. To elucidate the role of these antibodies in cardiac functional impairment, we used a murine model immunized with plasmids encoding the M(2)AChR or beta(1)AR via gene-gun bombardment. Anti-M(2)AChR and beta(1)AR antibodies were detected over the course of 37 weeks. These antibodies were directed to the second extracellular loop (el2) of both receptors and the third intracellular loop (il3) of the M(2)AChR. Peak antibody titers from weeks 2 to 5 against M(2)AChR-el2 and beta(1)AR-el2 as well as elevated titers against M(2)AChR-il3 were detected. Anti-M(2)AChR-il3 and anti-beta(1)AR-el2 antibodies were predominant in IgG1 subclass immunoglobulins, suggesting a T-helper-2 biased lymphocyte response. Heart morphology and function was assessed by echocardiography over the course of 42 weeks. Data showed progressive decrease in left ventricular (LV) wall thickness and LV mass that was mostly evident for beta(1)AR-immunized mice albeit a small change in LV dimensions. Fractional shortening was altered and values of 41%, 37% and 48% were observed at week 42 for the M(2)AChR, beta(1)AR and control groups respectively. In support of autonomic deregulation, a twofold increase in M(2)AChR and a similar decrease in beta(1)AR density were observed in radioligand saturation assays for both experimental groups. Histological analysis revealed myofibril disarray and fibrosis, pointing towards remodeling as a consequence of the long-term presence of anti-receptor antibodies.
Amino Acid Sequence↗
Long-term improvement of cardiac function in rats after infarction by transplantation of embryonic stem cells.
OBJECTIVE: This study was designed to investigate the feasibility of and potential functional improvement with embryonic stem cell transplantation in rats 32 weeks after myocardial infarction. METHODS: Before cell transplantation, cultured embryonic stem cells were transfected with the complementary DNA of green fluorescent protein to identify engrafted cells in myocardium. Myocardial infarction was induced by ligation of the left coronary artery. Either 3 x 10(5) mouse embryonic stem cells or an equivalent volume of cell-free medium was injected into injured myocardium within 20 minutes after induction of myocardial infarction. RESULTS: Embryonic stem cell transplantation significantly increased the survival rate in rats undergoing myocardial infarction during the experimental period of 32 weeks. Hemodynamic and echocardiographic data showed that embryonic stem cell transplantation significantly improved ventricular function relative to the myocardial infarction plus medium control group. Tissue positive for green fluorescent protein was found in the injured myocardium with cell transplantation. The proportion of myocardium positively immunostained by antibodies against alpha-myosin heavy chain and cardiac troponin I was greater in the infarcted area with embryonic stem cell transplantation than in the injured myocardium with medium injection. Single green fluorescent protein-positive cells with a rod shape and clear striations were observed in cardiomyocytes isolated from infarcted hearts with embryonic stem cell transplantation. In addition, the number of blood vessels in injured myocardium was greater in the cell-transplanted myocardial infarction group than in the medium-injected myocardial infarction group. CONCLUSIONS: Engrafted embryonic stem cells differentiated into cardiomyocytes in injured myocardium, caused an angiogenetic effect, and subsequently improved cardiac function during the 32-week observation period.
Animals↗