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.

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.

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.

Cardiac staircase and NMR-determined intracellular sodium in beating rat hearts

1995 ◽  
Vol 269 (1) ◽  
pp. H332-H340
Author(s):  
C. S. Lotan ◽  
S. K. Miller ◽  
T. Simor ◽  
G. A. Elgavish
Keyword(s):  
Positive Inotropic Effect ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Progressive Increase ◽  
Inotropic Effect ◽  
Enhanced Sensitivity ◽  
Group I ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Group Ii

Isolated, perfused rat hearts (30 degrees C, n = 13) were paced from 218 +/- 4 beats/min to 433 +/- 4 beats/min while systolic and diastolic pressure were recorded and intracellular Na+ concentration ([Na+]i) was monitored by 23Na nuclear magnetic resonance (NMR) spectroscopy. [Na+]i increased progressively with increasing stimulation frequency. In seven hearts (group I) an initial, progressive increase in systolic pressure was observed followed by a decrease in pressure with further increase in frequency. From the onset, a progressive decrease in systolic pressure was observed in group II (n = 6) in response to increased frequency. In group I an [Na+]i increase of up to 134 +/- 7% of control (P < 0.001) was observed, whereas in group II the gain in [Na+]i with increasing pacing rate was attenuated, reaching a maximum of 120 +/- 3% of control (P < 0.02). The differential pressure response between group I and group II hearts may reflect an enhanced sensitivity of rat hearts to the shortening of the restitution period of the sarcoplasmic reticulum, outweighing the positive inotropic effect induced by an increased [Na+]i. Only in rat hearts whose [Na+]i-induced increase in pressure outweights the restitution deficit would a complete positive inotropic effect be anticipated.

Intrinsic effects of heart rate on left ventricular performance

1963 ◽  
Vol 205 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Jere H. Mitchell ◽  
Andrew G. Wallace ◽  
N. Sheldon Skinner
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Pressure Rise ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Wide Range

The effects of heart rate on left-ventricular performance were studied in an areflexic dog right-heart bypass preparation which allowed independent control of aortic pressure, cardiac output, and heart rate. When the heart rate was increased while stroke volume and mean aortic pressure were maintained constant the left-ventricular mean rate of pressure rise during isovolumic systole, the maximal rate of pressure rise during isovolumic systole, and the mean rate of ejection were all increased without any change in left-ventricular end-diastolic pressure. Further, it was shown that the left ventricle performed the same amount of stroke work over a wide range of heart rates without an increase in end-diastolic pressure in spite of the markedly shortened time available for performing this work. This was accomplished because of the increase in stroke power. These observations demonstrate that the performance of the left ventricle becomes intrinsically "faster" as the heart rate is increased. When the transient phenomena that occur when the heart rate is increased are considered, the fact that the same stroke work is produced over a wide range of heart rates without an increase in end-diastolic pressure indicates that the left ventricle has also become "stronger" than it would have been if the adaptive change had not occurred.

scholarly journals Differential effects of acetylcholine on coronary flow in isolated hypothermic hearts from rats and ground squirrels

1993 ◽  
Vol 185 (1) ◽  
pp. 17-24
Author(s):  
R. F. Burlington ◽  
W. K. Milsom
Keyword(s):  
Coronary Flow ◽  
Systolic Pressure ◽  
Coronary Vessels ◽  
Left Ventricular ◽  
Ground Squirrels ◽  
Similar Treatment ◽  
Ventricular Systolic Pressure ◽  
Spermophilus Lateralis ◽  
Rat Hearts ◽  
Left Ventricular Systolic Pressure

This study was designed to determine whether cholinergic receptors are operative in the coronary vessels of a hibernating species (golden mantled ground squirrel, Spermophilus lateralis) and a nonhibernating species (rat, Rattus norvegicus) under normothermic and hypothermic conditions. Coronary flow and left ventricular systolic pressure were measured in isolated perfused hearts from squirrels at 37, 20 or 7 degrees C and from rats at 37 and 20 degrees C. During cooling, rat hearts became arrhythmic and failed between 15 and 12 degrees C. Squirrel hearts remained functional at 7 degrees C. Bolus injections of acetylcholine (&gt; 1.0 microgram) caused significant coronary vasoconstriction in rat hearts at 37 and 20 degrees C. Similar treatment caused mild coronary vasodilation in squirrel hearts at both temperatures. Squirrel hearts did not respond to acetylcholine at 7 degrees C. The responses in both species were blocked by atropine. Rat coronary vessels appear to contain muscarinic constrictor receptors similar to those described in humans, sheep, cattle and pigs. The coronary vessels of squirrels, by contrast, do not. In this latter species there appears to be a preponderance of muscarinic (possibly endothelial-relaxing-factor-linked) dilator receptors. Given that acetylcholine acts only as a mild vasodilator at higher temperatures in squirrels, parasympathetic regulation of coronary flow in the squirrel heart is unlikely, especially during hibernation.

Right ventricular pressure response to +GZ acceleration stress

1982 ◽  
Vol 53 (4) ◽  
pp. 908-913 ◽  
Author(s):  
J. E. Whinnery ◽  
M. H. Laughlin
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Vena Cava ◽  
Systolic Pressure ◽  
Ventricular Pressure ◽  
Miniature Swine ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
The Right ◽  
Acceleration Stress

Measurements of right ventricular pressure in miniature swine were made at +Gz levels from +1 through +9 Gz. Polyethylene catheters were chronically placed in the cranial vena cava of five 2-yr-old female miniature swine (35–50 kg). The catheters were large enough to allow the introduction of a Millar pressure transducer into the venous system for placement in the right heart. The animals were fitted with an abdominal anti-G suit, restrained in a fiberglass couch, and exposed to the various +Gz levels on a centrifuge while fully conscious and unanesthetized. Right ventricular pressure and heart rate were measured during and for 2 min following 30-s exposures to each level of +Gz stress. The maximum right ventricular systolic pressure observed during +Gz was 200 Torr at +5 Gz with the maximum diastolic pressure being 88 Torr observed at +5 Gz. Mean heart rates were 200–210 beats/min at all levels of +Gz greater than or equal to +3 Gz when the animal remained stable. Mean maximum right ventricular pressures during +Gz stress were observed to increase through +5 Gz (85 Torr) and to decrease at higher levels of +Gz, indicating that through +5 Gz there is at least a partial compensation during acceleration stress. Decompensation in response to the stress began to occur during acceleration above +5 Gz with all animals decompensating during +9 Gz.

Fasudil prevents KATP channel-induced improvement in postischemic functional recovery

2005 ◽  
Vol 288 (6) ◽  
pp. H3011-H3015 ◽  
Author(s):  
Kenya Nishizawa ◽  
Paul E. Wolkowicz ◽  
Tadashi Yamagishi ◽  
Ling-Ling Guo ◽  
Martin M. Pike
Keyword(s):  
Diastolic Pressure ◽  
Rho Kinase ◽  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphate ◽  
Cellular Processes ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Rock Activity ◽  
Mechanical Recovery

Whereas activation of ATP-dependent potassium (KATP) channels greatly improves postischemic myocardial recovery, the final effector mechanism for KATP channel-induced cardioprotection remains elusive. RhoA is a GTPase that regulates a variety of cellular processes known to be involved with KATP channel cardioprotection. Our goal was to determine whether the activity of a key rhoA effector, rho kinase (ROCK), is required for KATP channel-induced cardioprotection. Four groups of perfused rat hearts were subjected to 36 min of zero-flow ischemia and 44 min of reperfusion with continuous measurements of mechanical function and 31P NMR high-energy phosphate data: 1) untreated, 2) pinacidil (10 μM) to activate KATP channels, 3) fasudil (15 μM) to inhibit ROCK, and 4) both fasudil and pinacidil. Pinacidil significantly improved postischemic mechanical recovery [39 ± 16 vs. 108 ± 4 mmHg left ventricular diastolic pressure (LVDP), untreated and pinacidil, respectively]. Fasudil did not affect reperfusion LVDP (41 ± 13 mmHg) but completely blocked the marked improvement in mechanical recovery that occurred with pinacidil treatment (54 ± 15 mmHg). Substantial attenuation of the postischemic energetic recovery was also observed. These data support the hypothesis that ROCK activity plays a role in KATP channel-induced cardioprotection.

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.

Abstract P144: Effects of Alamandine in Post-ischemic Function

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jonathas F Almeida ◽  
Robson A Santos
Keyword(s):  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Baseline Period ◽  
Left Ventricular ◽  
Biologically Active ◽  
Ventricular Systolic Pressure ◽  
Infarcted Area ◽  
Rat Hearts ◽  
Ischemic Period ◽  
Isolated Rat

Alamandine, a biologically active peptide of the renin-angiotensin system (RAS), was recently described and characterized. Further it has been shown to present effects similar to those elicited by Ang-(1-7). It has been described that Ang-(1-7) decreases the incidence and duration of ischemia-reperfusion arrhythmias and improved the post-ischemic function in isolated perfused rat hearts. In this study we aimed to evaluate the effects of Alamandine in isolated rat hearts subjected to myocardial infarction (MI). Wistar rats weighing between 250-300g were euthanized and their hearts were placed on Langendorff apparatus to evaluate the cardiac parameters. Hearts were submitted to 30min of stabilization, 30min of partial ischemia by occlusion of the left descending coronary artery and 30min of reperfusion. Drugs (alamandine 22pM, d-pro7-ang-(1-7) 220pM) were added to the perfusion setting from the beginning of the experiment until the end. 2,3,5-trypheniltetrazolium chloride were used to evaluate the extension of infarcted area. In control hearts (CON), there was a decrease on the left ventricular systolic pressure (LVSP) on ischemic period (54,6 ± 6,9mmHg) compared to the baseline period (84,6 ± 11,6mmHg). Alamandine (ALA) attenuated that decrease in the ischemic period (66,9 ± 7,9mmHg) vs (82,3 ± 8,9mmHg). Further, ischemia led to a decrease in the left ventricular developed pressure (dLVP), dP/dt maximum and minimum when compared to baseline values. ALA, once more, kept the ischemic parameters of dLVP and dP/dt max and min (58,9 ± 8mmHg; 1629 ± 202,2mmHg/s; 1101 ± 130mmHg/s, respectively) similar to those of baseline period (68,9 ± 8,92; 1682 ± 248,8; 1179 ± 118,6 mmHg, respectively). Ischemia/reperfusion induced an arrhythmia severity index (ASI) in control hearts (4,9 ± 1,26) higher than in hearts treated with ALA (1,10 ± 0,58). ALA also reduced infarcted area (19,64 ± 2,61%) compared with CON (33,85 ± 4,55%). All those effects were blocked by D-PRO7-Ang-(1-7). In conclusion, our data shown that Alamandine exert cardioprotective effects in post-ischemic function in isolated rat hearts by preventing LVSP, dLVP , dP/dt max and min decrease. Furthermore it reduced the infarcted area and I/R arrhythmias, apparently involving MrgD receptor participation.

Nitric oxide modulates epicardial coronary basal vasomotor tone in awake dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1250-H1254 ◽  
Author(s):  
A. Chu ◽  
D. E. Chambers ◽  
C. C. Lin ◽  
W. D. Kuehl ◽  
F. R. Cobb
Keyword(s):  
Nitric Oxide ◽  
Coronary Flow ◽  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Vasomotor Tone ◽  
Coronary Vasomotor Tone ◽  
Endogenous Nitric Oxide

This study evaluates the role of endogenous nitric oxide in the modulation of basal coronary vasomotor tone by studying the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation from L-arginine, on resting epicardial coronary diameter and coronary flow. L-NMMA (5 mg/kg) was infused in seven awake dogs chronically instrumented with coronary dimension crystals for measurement of epicardial coronary diameter, and Doppler flow probes for quantitation of phasic coronary flow (vasomotion of distal regulatory resistance coronary vessels). Epicardial coronary diameter decreased 5.5% from 3.47 +/- 0.17 to 3.28 +/- 0.15 mm (mean +/- SE). The diameter change was gradual, reaching a maximum at 13 +/- 2 min after infusion, and persistent, lasting greater than 90 min. Phasic coronary flow did not change. Mean aortic pressure significantly increased from 99 +/- 3 to 111 +/- 3 mmHg and heart rate decreased from 56 +/- 4 to 46 +/- 3 beats/min. Left ventricular end-diastolic pressure and contractility were not significantly altered. L-Arginine (66 mg/kg) but not D-arginine reversed all hemodynamic parameters. These data support an important role of nitric oxide in modulating basal epicardial coronary vasomotor tone and systemic vascular resistance.

Sign in / Sign up

Export Citation Format

Share Document