Ventricular performance, pressure-volume relationships, and O2 consumption during hypothermia

1964 ◽  
Vol 206 (1) ◽  
pp. 67-73 ◽  
Author(s):  
R. G. Monroe ◽  
R. H. Strang ◽  
C. G. LaFarge ◽  
J. Levy
Keyword(s):  
Peak Pressure ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Heart Rates ◽  
Performance Pressure ◽  
Air Chamber ◽  
Lower Temperature

Left ventricular performance in the isolated heart of a dog was observed at normal temperatures (37.7 C) and under hypothermia (32.2 C) at comparable heart rates. The peak pressure of isovolumic contractions at the same ventricular end-diastolic pressures averaged 40% higher at the lower temperature. Diastolic pressure-volume relationships were similar at both temperatures. In studies in which the ventricle ejected fluid and performed work the hypothermic ventricle was capable of performing greater work at comparable heart rates, left ventricular end-diastolic pressures, and loading. When the ventricle was allowed to perform work by compressing air into a chamber of constant volume left ventricular oxygen consumption (Vo2) increased with the peak systolic pressure as the temperature was lowered. If the peak systolic pressure was maintained constant by increasing the volume of the air chamber as the temperature was lowered no consistent relationship could be shown between left ventricular Vo2 and the integral of systolic pressure in time which invariably increased with hypothermia.

The inotropic effect of digoxin on an isolated rat heart in hypercapnia and (or) hypoxia

1990 ◽  
Vol 68 (3) ◽  
pp. 455-461
Author(s):  
M. Allam ◽  
C. Saunier ◽  
A. Sautegeau ◽  
D. Hartemann
Keyword(s):  
Rat Heart ◽  
Myocardial Contractility ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Gas Mixture ◽  
Constant Frequency

The explanation for the increased frequency of troubles with digoxin therapy in patients with chronic pulmonary diseases is debated. The reported effects of hypoxia in vivo on myocardial levels of digoxin are contradictory, and there have been few studies on the effects of hypercapnia. In the past, it has been shown in rat myocardial tissue at rest in vitro that hypoxia decreased and hypercapnia acidosis increased the digoxin uptake. We performed a new study in vitro in an isolated beating rat heart perfused at constant flow (37 °C) and stimulated at a constant frequency (6 Hz). The performances were recorded with an intraventricular balloon equipped with a tip-manometer catheter. The action of digoxin was studied by recording systolic pressure (PS) and diastolic pressure (PD), the left ventricular developed pressure (LVDP = PS − PD), the (dP/dt)max, and the ratio (dP/dt)max/PS. First, the heart was perfused for 30 min with a modified Tyrode's solution perfusate aerated with carbogen (pH = 7.40; [Formula: see text]; [Formula: see text]) (1 mmHg = 133.32 Pa). Various parameters of contractions were recorded (initial control values). Then the heart was perfused for 15 min with Tyrode's solution aerated either with a hypoxic gas mixture (pH = 7.41; [Formula: see text]; [Formula: see text]), a hypercapnic gas mixture (pH = 7.08; [Formula: see text]; [Formula: see text]), or a hypoxic–hypercapnic gas mixture (pH = 7.09; [Formula: see text]; [Formula: see text]). Control hearts were continuously perfused with Tyrode's solution aerated with carbogen. During heart perfusion with hypercapnic, hypoxic, or hypoxic–hypercapnic Tyrode's solution, a decrease in LVDP and (dP/dt)max was observed. Finally, the heart was perfused with the same Tyrode's solution plus 1.75 × 10−5 M digoxin. The increase in myocardial contractility produced by digoxin was enhanced by hypercapnia and abolished by hypoxia. The addition of hypercapnia to hypoxia in Tyrode's solution seems to enhance the depressor action of the hypoxia.Key words: isolated heart, digoxin, hypoxia, hypercapnia, myocardial contractility.

Cardiac dilatation and pump dysfunction without intrinsic myocardial systolic failure following chronic β-adrenoreceptor activation

2007 ◽  
Vol 292 (4) ◽  
pp. H1898-H1905 ◽  
Author(s):  
Oleg E. Osadchii ◽  
Gavin R. Norton ◽  
Richard McKechnie ◽  
Dawn Deftereos ◽  
Angela J. Woodiwiss
Keyword(s):  
Diastolic Pressure ◽  
Systolic Function ◽  
Isolated Heart ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Pump Failure ◽  
Volume Relation ◽  
The Impact ◽  
Fractional Shortening

There is no direct evidence to indicate that pump dysfunction in a dilated chamber reflects the impact of chamber dilatation rather than the degree of intrinsic systolic failure resulting from myocardial damage. In the present study, we explored the relative roles of intrinsic myocardial systolic dysfunction and chamber dilatation as mediators of left ventricular (LV) pump dysfunction. Administration of isoproterenol, a β-adrenoreceptor agonist, for 3 mo to rats (0.1 mg·kg−1·day−1) resulted in LV pump dysfunction as evidenced by a reduced LV endocardial fractional shortening (echocardiography) and a decrease in the slope of the LV systolic pressure-volume relation (isolated heart preparations). Although chronic β-adrenoreceptor activation induced cardiomyocyte damage (deoxynucleotidyl transferase-mediated dUTP nick-end labeling) as well as β1- and β2-adrenoreceptor inotropic downregulation (attenuated contractile responses to dobutamine and salbutamol), these changes failed to translate into alterations in intrinsic myocardial contractility. Indeed, LV midwall fractional shortening (echocardiography) and the slope of the LV systolic stress-strain relation (isolated heart preparations) were unchanged. A normal intrinsic myocardial systolic function, despite the presence of cardiomyocyte damage and β-adrenoreceptor inotropic downregulation, was ascribed to marked increases in myocardial norepinephrine release, to upregulation of α-adrenoreceptor-mediated contractile effects as determined by phenylephrine responsiveness, and to compensatory LV hypertrophy. LV pump failure was attributed to LV dilatation, as evidenced by increased LV internal dimensions (echocardiography), and a right shift and increased volume intercept of the LV diastolic pressure-volume relation. In conclusion, chronic sympathetic stimulation, despite reducing β-adrenoreceptor-mediated inotropic responses and promoting myocyte apoptosis, may nevertheless induce pump dysfunction primarily through LV dilatation, rather than intrinsic myocardial systolic failure.

Evaluation of the isolated paced rat heart

1976 ◽  
Vol 41 (3) ◽  
pp. 328-331 ◽  
Author(s):  
P. B. Taylor ◽  
F. J. Cerny
Keyword(s):  
Coronary Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Aortic Pressure ◽  
Ventricular Performance ◽  
Heart Rates ◽  
Ventricular Systolic Pressure ◽  
Rat Hearts ◽  
Wide Range ◽  
Perfused Rat Hearts

Ventricular performance and coronary flow in Langendorff perfused rat hearts were measured over a wide range of perfusion pressures and heart rates. A change in aortic pressure from 60 to 120 mmHg induced a linear increasein coronary flow, ventricular systolic pressure, and contractility. Ventricular pacing from 300 to 600 beats/min under a constant afterload had no effect on coronary flow. Systolic pressure remained stable up to 400–450 beats/min and then decreased 14% at 600 beats/min compared to the nonpaced controls. When contraction rate exceeded 450 beats/min diastolic pressure progressively increased as the heart rate was elevated. Contractility decreased rapidly between 450 and 600 beats/min under all perfusion pressures. These data indicate that this heart model is physiologically stable with heart rates less than 450 beats/min and may be useful in studying tachycardia-induced work overload.

Left ventricular performance and blood catecholamine levels in the isolated heart

1966 ◽  
Vol 211 (5) ◽  
pp. 1248-1254 ◽  
Author(s):  
R. Grier Monroe ◽  
C. G. La Farge ◽  
W. J. Gamble ◽  
R. P. Hammond ◽  
R. Gamboa
Keyword(s):  
Diastolic Pressure ◽  
Isolated Heart ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Isolated Lungs ◽  
Catecholamine Levels ◽  
Catecholamine Concentration

Left ventricular performance in the isolated heart of the dog as expressed by the peak systolic intraventricular pressure was observed during control periods when the heart was perfused with blood from a healthy anesthetized donor and after the donor was removed and the heart perfused with blood oxygenated by isolated lungs. Heart rate, coronary perfusion pressure, ventricular end-diastolic pressure, and stroke volume were maintained constant throughout. While the heart was perfused with blood from a donor, ventricular performance showed no tendency to decline, although coronary flow invariably increased. On removing the donor and perfusing the heart with blood oxygenated by isolated lungs, myocardial performance declined in proportion to the decline in the total catecholamine concentration of the perfusing blood. Restoration of catecholamine levels by infusing epinephrine and norepinephrine also restored left ventricular performance.

Left ventricular dysfunction in early E. coli endotoxemia: effects of naloxone

1990 ◽  
Vol 259 (2) ◽  
pp. H504-H511 ◽  
Author(s):  
J. L. Parker ◽  
R. S. Keller ◽  
L. L. Behm ◽  
H. R. Adams
Keyword(s):  
Diastolic Pressure ◽  
Contractile Function ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Opiate Receptor ◽  
Left Ventricular ◽  
Cardiac Complications ◽  
Endogenous Opioid ◽  
Diastolic Compliance

Although the opiate receptor antagonist naloxone (NAL) has been reported to improve in vivo systolic performance of the heart in different circulatory shock syndromes, the influence of this drug on intrinsic cardiac mechanical function during hypodynamic circulatory states is unknown. The present study was designed to determine the effects of in vivo NAL on contraction-relaxation properties of isovolumic left ventricular (LV) preparations isolated from guinea pigs 4 h after induction of gram-negative endotoxemia. Animals were given a 1 mg/kg ip injection of Escherichia coli endotoxin and immediately treated intravenously with either NAL (4 mg/kg iv bolus plus 4 mg.kg-1.h-1 infusion) or an equivalent volume of saline. Endotoxin produced significant reduction of LV contractile function in coronary-perfused hearts, a response unaffected by NAL therapy. For example, LV systolic pressure at approximately 10 mmHg end-diastolic pressure averaged 78 +/- 3 and 82 +/- 6 mmHg in hearts from saline and NAL control animals, respectively, but only 41 +/- 2 and 40 +/- 2 mmHg in endotoxin and endotoxin plus NAL groups, respectively. LV end-diastolic pressure-volume relationships in endotoxin hearts were shifted upward and to the left of controls in the direction of decreased diastolic compliance (P less than 0.05). Importantly, in vivo NAL prevented the endotoxin-induced decrease in LV compliance of the isolated heart preparations (P less than 0.05). Thus intrinsic cardiac complications of early (4 h) nonhypotensive endotoxemia included decreased diastolic compliance as well as diminished contractility of the left ventricle. Only the diastolic compliance changes were NAL responsive and therefore may involve endogenous opioid systems in their pathophysiological expression.

Influence of adenosine on left ventricular performance in conscious dogs

1990 ◽  
Vol 258 (2) ◽  
pp. H424-H430
Author(s):  
G. L. Freeman ◽  
J. T. Colston ◽  
J. Hultman
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Controlled Hypotension ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Before And After ◽  
Lv Volume

Adenosine, a potent vasodilator of both the peripheral and coronary vasculature, is increasingly used to produce controlled hypotension in the clinical and experimental setting. To define the influence of adenosine on left ventricular (LV) performance in conscious closed-chest dogs were studied six chronically instrumented autonomically blocked animals before and after the administration of 0.3, 0.6, and 1.2 microM.kg-1.min-1 infusions of adenosine. Systolic performance was quantified by the end-systolic pressure-volume (Pes-Ves) and stroke work end-diastolic volume (SW-EDV) relations. Active diastolic performance was quantified by the time constant of LV relaxation (T), whereas passive diastolic properties were assessed by comparing LV pressures at a common LV volume. Despite a decrease of mean arterial pressure of 51 mmHg, adenosine did not change the slope of the Pes-Ves relation or the end-systolic volume at a pressure of 100 mmHg. The slope of the SW-EDV relation was also unchanged, and its volume axis intercept was slightly reduced. There were no differences in T or in the diastolic pressure at a common LV volume. Thus adenosine appears to have little influence on systolic or diastolic LV performance aside from its marked affect on afterload, indicating it is a useful agent for producing controlled hypotension.

Contraction-Relaxation Coupling and Impaired Left Ventricular Performance in Coronary Surgery Patients 

1999 ◽  
Vol 90 (3) ◽  
pp. 748-757 ◽  
Author(s):  
Stefan G. De Hert ◽  
Thierry C. Gillebert ◽  
Pieter W. Ten Broecke ◽  
Els Mertens ◽  
Inez E. Rodrigus ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Linear Regression Analysis ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Coronary Surgery ◽  
Tight Coupling ◽  
Fixed Rate ◽  
Ventricular Performance ◽  
Load Dependence ◽  
Contraction And Relaxation

Background Dependence of left ventricular (LV) relaxation on cardiac systolic load is a function of myocardial contractility. The authors hypothesized that, if a tight coupling would exist between LV contraction and relaxation, the changes in relaxation rate with an increase in cardiac systolic load would be related to the changes in LV contraction. Methods Coronary surgery patients (n = 120) with preoperative ejection fraction >40% were included. High-fidelity LV pressure tracings (n = 120) and transgastric transesophageal echocardiographic data (n = 40) were obtained. Hearts were paced at a fixed rate of 90 beats/min. Effects on contraction were evaluated by analysis of changes in dP/dt(max) and stroke area. Effects on relaxation were assessed by analysis of R (slope of the relation between tau and end-systolic pressure). Correlations were calculated with linear regression analysis using Pearson's coefficient r. Results Baseline LV end-diastolic pressure was 10+/-3 mm Hg (mean +/- SD). During leg raising, systolic LV pressure increased from 93+/-9 to 107+/-11 mm Hg. The change in dP/dt(max) was variable and ranged from -181 to +254 mm Hg/s. A similar variability was observed with the changes in stroke area, which ranged from -2.0 to +5.5 cm2. Changes in dP/dt(max) and in stroke area were closely related to individual R values (r = 0.87, P<0.001; and r = 0.81, P<0.001, respectively) and to corresponding changes in LV end-diastolic pressure (r = 0.81, P< 0.001; and r = 0.74, P<0.001, respectively). Conclusions A tight coupling was observed between contraction and relaxation. Leg raising identified patients who developed a load-dependent impairment of LV performance and increased load dependence of LV relaxation.

The Effect of Gypenosides on Cardiac Function and Expression of Cytoskeletal Genes of Myocardium in Diabetic Cardiomyopathy Rats

2009 ◽  
Vol 37 (06) ◽  
pp. 1059-1068 ◽  
Author(s):  
Min Ge ◽  
Shanfeng Ma ◽  
Liang Tao ◽  
Sudong Guan
Keyword(s):  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Pure Water ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Sprague Dawley ◽  
Gene Expressions ◽  
Ventricular Systolic Pressure

The relationship between changes of cardiac function and the gene expressions of two major myocardial skeleton proteins, titin and nebulin, and the effect of gypenosides on these gene expressions in diabetic cardiomyopathy rat were explored in the present study. Forty Sprague-Dawley rats were randomly divided into three groups: control group, diabetic cardiomyopathy group and gypenosides-treated diabetic cardiomyopathy group. The diabetic cardiomyopathy was induced in rats by injecting streptozotocin (STZ, 55 mg/kg) intraperitoneally. Seven weeks after the rats suffered from diabetes, the rats were treated with gypenosides 100 mg/kg per day orally for six weeks in gypenosides-treated group. In the meanwhile, the pure water was given to diabetic cardiomyopathy and the control groups. Subsequently, the cardiac functions, including left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), ± dP/dtmax and t–dP/dmaxt, as well as the mRNA content and proteins of titin and nebulin in myocardium were determined. The results indicated that (1) the diabetic cardiomyopathy rats had decreased LVSP and ± dP/dtmax, increased LVEDP, and prolonged t–dP/dtmax than normal rats; (2) LVSP and ± dP/dtmax in diabetic cardiomyopathy rats treated with gypenosides were significantly higher and LVEDP and t–dP/dtmax were significantly lower than those without giving gypenosides; (3) the mRNA contents and proteins of titin and nebulin in diabetic cardiomyopathy rats were remarkably lower than those in the control rats and gypenosides had no effect on mRNA and protein expression levels of titin and nebulin in diabetic cardiomyopathy rats. We conclude that (1) the cardiac function as well as the mRNA expressions of titin and nebulin decreased in diabetic cardiomyopathy rats; (2) gypenosides secure cardiac muscles and their function from diabetic impairment and these beneficial effects of gypenosides are not by changing the expressions of titin and nebulin.

Effect of human urotensin-II infusion on hemodynamics and cardiac function

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Urotensin Ii ◽  
Ventricular Systolic Pressure ◽  
Wide Range ◽  
Dose Dependent Decrease

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.

Abstract 4370: Intramyocardial Administration of Erythropoietin Promotes Cell Proliferation, Induces Early Angiogenesis and Attenuates Cardiac Remodeling

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ralf Gäbel ◽  
Christian Klopsch ◽  
Dario Furlani ◽  
Wenzhong Li ◽  
Can Yerebakan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Peripheral Blood ◽  
Diastolic Pressure ◽  
Troponin T ◽  
Interstitial Fibrosis ◽  
Capillary Density ◽  
Left Ventricular ◽  
Border Zone ◽  
Ki 67 ◽  
Ventricular Performance

Erythropoietin (EPO) protects the ischemic myocardium from heart failure development after myocardial infarction (MI). However, little is known about its intracardiac cell proliferation and early angiogenesis. We hypothesize that EPO may contribute to cell proliferation, angiogenesis and eventually induce a beneficial remodeling process. Following permanent LAD ligation in rats, EPO (3000 U/kg; n=99) or saline (n=95) was delivered along the infarction border. In control animals without MI (n=55) saline was injected intramyocardially. After 6 weeks follow-up, left ventricle was catheterized and analyzed for cardiac performance. The level of eNOS mRNA was dramatically increased 9.3 fold in non-infarcted area of EPO treated rats at 24 h detected by real time PCR and confirmed by immunohistology. We found a 45 % enhancement in Ki-67+ cell numbers near the infarction at 48 h after EPO treatment (n=6, P<0.001). Hematopoietic cell lineages including c-Kit+ and CD34+ cells were augmented in the peripheral blood after 48h. Capillary density was enhanced by 17% as early as 1 week (n=6, P<0.001). Myocyte apoptosis was reduced by 41% and 37% at border zone after 1 and 6 weeks (n=6, P<0.05). Cardiac troponin T level, a highly sensitive and specific indicator of myocardial cell death, was significantly reduced in peripheral blood 2 weeks after EPO injection (n=5, P<0.05). Cardiomyocyte size and interstitial fibrosis at 6 weeks were decrease by 13% and 23% (n=6, P=0.015, P<0.001). Intramyocardial EPO delivery enhanced left ventricular performance at baseline and Dobutamine stress conditions compared with MI rats (cardiac output: 65% and 71% increase at baseline and stress; end-diastolic pressure: 51% and 53% reduction respectively, n=11–14, P<0.05). To conclude, intramyocardial EPO delivery induces early cell poliferation, angiogenesis and attenuates post MI remodeling.

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