Quantification of cardiac pumping mechanics in rats by using the elastance–resistance model based solely on the measured left ventricular pressure and cardiac output

A rapid and efficient circulatory support system may save a patient in cardiogenic shock. Left heart bypass with percutaneous and trans-septal placement of the aspiration cannula simplifies the circuit and eliminates the need for an oxygenator. In this pre-clinical study we assessed left heart bypass support with a centrifugal pump using new cannulae prepared for percutaneous placement (14 F arterial catheter and 16 F left atrial aspiration line) in 5 anaesthetized pigs. Animals were supported for two hours at a mean flow of 3.2 l/min (4,033 rpm), a mean haematocrit of 29% and low heparinisation (ACT double baseline). Hemodynamic measurements and blood samples were taken at baseline (A), 10 minutes (B), one hour (C) and 2 hours (D) on support. Results show maintenance of hemodynamic parameters throughout the 2 hour support period. Only systolic arterial and left ventricular pressure decreased by 12% and 20% respectively from baseline to the end of the support period with a 13% increase in cardiac output. When the pump was turned on (0–3 l/min) there was usually a decrease in heart rate, systolic pressure and left ventricular pressure, with unchanged cardiac output (non failing model). Potassium increased from 3.9 to 4.2 mmol/l (ns), and plasma hemoglobin from 6.0 to 18.2 mg/dl (p<0.05). Thrombocytes decreased from 187 to 155 109/1 (ns). In conclusion, this preclinical study demonstrated the feasibility of an efficient left heart bypass of short duration with a centrifugal pump using cannulae prepared for percutaneous placement. Left heart bypass was well tolerated hemodynamically and no significant laboratory change occurred within the two hours of support. This opens several possibilities for the short term support of patients in cardiogenic shock and eventually also for patients submitted to minimally invasive cardiac surgery.

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Cardiac output assessment using oxygen consumption estimated from the left ventricular pressure-volume area

2010 Annual International Conference of the IEEE Engineering in Medicine and Biology ◽

10.1109/iembs.2010.5626867 ◽

2010 ◽

Cited By ~ 1

Author(s):

J A Negroni ◽

E C Lascano ◽

A M Bertolotti ◽

Carmen B Gómez ◽

Carlos A Rodríguez Correa ◽

...

Keyword(s):

Cardiac Output ◽

Oxygen Consumption ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure

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In situ measurement of left ventricular pressure and cardiac output in rat heart after acute and chronic Adriamycin application

Methods in Clinical Pharmacology ◽

10.1007/978-3-663-14027-6_45 ◽

1980 ◽

pp. 329-333

Author(s):

B. Höfling ◽

H.-D. Bolte

Keyword(s):

Cardiac Output ◽

Rat Heart ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

In Situ Measurement ◽

Ventricular Pressure

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Evaluation of the sensitivity of a new fully implantable telemetry device and the importance of simultaneously measuring cardiac output and left ventricular pressure

Journal of Pharmacological and Toxicological Methods ◽

10.1016/j.vascn.2014.01.003 ◽

2014 ◽

Vol 69 (3) ◽

pp. 229-236 ◽

Cited By ~ 5

Author(s):

Jeffrey McKee ◽

Justin Daller ◽

Bernhard Baumgartner ◽

Steve Pettinger

Keyword(s):

Cardiac Output ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure

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Effect of lactic acidosis on canine hemodynamics and left ventricular function

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.258.4.h1193 ◽

1990 ◽

Vol 258 (4) ◽

pp. H1193-H1199 ◽

Cited By ~ 4

Author(s):

K. Teplinsky ◽

M. O'Toole ◽

M. Olman ◽

K. R. Walley ◽

L. D. Wood

Keyword(s):

Cardiac Output ◽

Lactic Acidosis ◽

Stroke Volume ◽

Venous Return ◽

Diastolic Pressure ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Right Atrial ◽

Lactic Acidemia

Hypoperfusion states cause lactic acidosis, and the acidemia further reduces the inadequate cardiac output. Conceivably, the adverse effect of lactic acidemia on cardiac output is due to depressed contractility demonstrated in isolated myocardium. Alternatively, factors governing venous return cause a relative hypovolemic state and/or acidemic pulmonary vasoconstriction-induced right ventricular dysfunction. We reasoned that examination of left ventricular pressure-volume relationships at end systole and end diastole would determine which of these potential mechanisms accounted for reduced cardiac output during progressive lactic acidosis in anesthetized, mechanically ventilated dogs. Left ventricular (LV) volume was estimated from two pairs of epicardial ultrasonic crystals placed in the anterior-posterior and longitudinal planes, and LV pressure was obtained rom a catheter-tipped transducer. During progressive acidemia induced by a continuous intravenous infusion of 0.5 N lactic acid, cardiac output, stroke volume, and mean systemic arterial pressure fell significantly while mean pulmonary artery pressure and right atrial pressure increased significantly. These variables did not change with time in control (no-acid infusion) dogs. Lactic acidemia caused a 40% reduction in stroke volume, which could be attributed to depressed LV contractility, characterized by a decrease in maximum dP/dt as well as a fall in slope (Emax) with no change in volume intercept (Vo) of the left ventricular pressure-volume relationship at end systole. Neither the measured left ventricular end-diastolic pressure nor the estimated left ventricular end-diastolic volume (LVEDV) decreased with acidemia, suggesting that the reduced venous return did not result from relative hypovolemia. However, acidemic pulmonary hypertension may have interfered with the expected response to myocardial depression, which is an increase in LVEDV.

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Pharmacodynamics and Pharmacokinetics of Injectable Pimobendan and Its Metabolite, O-Desmethyl-Pimobendan, in Healthy Dogs

Frontiers in Veterinary Science ◽

10.3389/fvets.2021.656902 ◽

2021 ◽

Vol 8 ◽

Author(s):

Poonavit Pichayapaiboon ◽

Lalida Tantisuwat ◽

Pakit Boonpala ◽

Nakkawee Saengklub ◽

Tussapon Boonyarattanasoonthorn ◽

...

Keyword(s):

Cardiac Output ◽

Vascular Resistance ◽

Maximum Rate ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Cardiac Contraction ◽

Ventricular Pressure ◽

Right Atrial ◽

Pulmonary Capillary ◽

Pulmonary Arterial

Objectives: This study was designed to thoroughly evaluate the effects of bolus pimobendan at a dose of 0.15 mg/kg on cardiac functions, hemodynamics, and electrocardiographic parameters together with the pharmacokinetic profile of pimobendan and its active metabolite, o-desmethyl-pimobendan (ODMP), in anesthetized dogs.Methods: Nine beagle dogs were anesthetized and instrumented to obtain left ventricular pressures, aortic pressures, cardiac outputs, right atrial pressures, pulmonary arterial pressures, pulmonary capillary wedge pressures, electrocardiograms. After baseline data were collected, dogs were given a single bolus of pimobendan, and the pharmacodynamic parameters were obtained at 10, 20, 30, 60, and 120 min. Meanwhile, the venous blood was collected at baseline and 2, 5, 10, 20, 30, 60, 120, 180, 360, and 1,440 min after administration for the determination of pharmacokinetic parameters.Results: Compared with baseline measurements, the left ventricular inotropic indices significantly increased in response to intravenous pimobendan, as inferred from the maximum rate of rise in the left ventricular pressure and the contractility index. Conversely, the left ventricular lusitropic parameters significantly decreased, as inferred from the maximum rate of fall in the left ventricular pressure and the left ventricular relaxation time constant. Significant increases were also noted in cardiac output and systolic blood pressure. Decreases were observed in the systemic vascular resistance, pulmonary vascular resistance, left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, right atrial pressure, and pulmonary arterial pressure. The heart rate increased, but the PQ interval decreased. There was no arrhythmia during the observed period (2 h). The mean maximum plasma concentration (in μg/L) for ODMP was 30.0 ± 8.8. Pimobendan exerted large volume of distribution ~9 L/kg.Conclusions: Intravenous pimobendan at the recommended dose for dogs increased cardiac contraction and cardiac output, accelerated cardiac relaxation but decreased both vascular resistances. These mechanisms support the use of injectable pimobendan in acute heart failure.

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Vasopressin contributes to the cardiovascular response to dynamic exercise

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.264.5.h1701 ◽

1993 ◽

Vol 264 (5) ◽

pp. H1701-H1707 ◽

Cited By ~ 9

Author(s):

C. L. Stebbins ◽

J. D. Symons

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Cardiovascular Response ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Dynamic Exercise ◽

Ventricular Pressure ◽

Receptor Inhibition ◽

Exercise Induced ◽

Developed Pressure

Vasopressin is a powerful vasoconstrictor that is released into the systemic circulation during exercise. We tested the hypothesis that this peptide contributes to the cardiovascular response during treadmill exercise in the pig. Seventeen miniswine were instrumented with epicardial electrocardiogram leads, left atrial and aortic catheters, and a left ventricular pressure transducer for measurement of heart rate (HR), regional blood flow, arterial blood pressure (MAP), and myocardial contractility [first derivative of left ventricular pressure (dP/dt) at 40 mmHg developed pressure] at rest and during exercise. At a work intensity of 80% of each animal's maximal HR reserve, exercise-induced increases in MAP, HR, dP/dt at 40 mmHg developed pressure, and cardiac output were measured. On a separate day, the workload performed by each animal was replicated in the presence of selective vasopressin V1-receptor inhibition using the specific V1 antagonist, [d(CH2)5Tyr(Me)]arginine vasopressin (10-14 micrograms/kg iv). During exercise, MAP was lower (96 +/- 3 vs. 104 +/- 2 mmHg) and cardiac output was higher (13.5 +/- 0.6 vs. 12.6 +/- 1.0 l/min) in the presence of V1-receptor blockade than during unblocked conditions, respectively. Furthermore, we observed an attenuation of exercise-induced decreases in blood flow to the colon. Increases in vascular resistance in the stomach, small intestine, colon, and pancreas also were diminished by V1-receptor inhibition. However, HR and myocardial contractile responses to exercise were not affected. These results suggest that vasopressin contributes to increases in MAP and to the redistribution of cardiac output during dynamic exercise in the miniswine.

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Model-based estimation of left ventricular pressure and myocardial work in aortic stenosis

PLoS ONE ◽

10.1371/journal.pone.0229609 ◽

2020 ◽

Vol 15 (3) ◽

pp. e0229609 ◽

Cited By ~ 2

Author(s):

Kimi P. Owashi ◽

Arnaud Hubert ◽

Elena Galli ◽

Erwan Donal ◽

Alfredo I. Hernández ◽

...

Keyword(s):

Aortic Stenosis ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Model Based

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Performance of diabetic rat hearts: effects of anoxia and increased work

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1980.239.5.h614 ◽

1980 ◽

Vol 239 (5) ◽

pp. H614-H620 ◽

Cited By ~ 4

Author(s):

C. G. Ingebretsen ◽

P. Moreau ◽

C. Hawelu-Johnson ◽

W. R. Ingebretsen

Keyword(s):

Cardiac Output ◽

Coronary Flow ◽

Mechanical Performance ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Diabetic Rat ◽

Ventricular Performance ◽

Pressure Development ◽

Heart Preparation

An isolated perfused working rat heart preparation was used to assess the effect of alloxan-induced diabetes on myocardial performance. Ventricular performance was assessed under different aortic afterload, isoproterenol-stimulated and anoxic conditions. Basal left ventricular pressure development and rate of rise of ventricular pressure were depressed in hearts from diabetic animals. Neither coronary flow nor cardiac output were affected by diabetes. The dose and temporal responses to an infusion of isoproterenol were unaltered in diabetic hearts. Isoproterenol increased coronary flow by 50% and elevated ventricular pressure, dP/dt, and cardiac output by two- to threefold. Anoxia depressed ventricular pressure to below 20% of control within 5 min in both diabetic and normal hearts. Reoxygenation after 10 min of anoxia produced equivalent recovery in both groups working against a 52-mmHg aortic afterload, whereas recovery after 20 or 30 min of anoxia, was depressed in diabetic hearts. Elevating aortic afterload decreased performance of diabetic hearts and decreased their ability to recover from a 10-min anoxic exposure. Many of these observed differences in mechanical performance of diabetic hearts can be overcome by high glucose or insulin in the perfusion media.

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Role of Tyrosine Kinase in Desflurane-induced Preconditioning

Anesthesiology ◽

10.1097/00000542-200403000-00014 ◽

2004 ◽

Vol 100 (3) ◽

pp. 555-561 ◽

Cited By ~ 7

Author(s):

Dirk Ebel ◽

Jost Müllenheim ◽

Hendrik Südkamp ◽

Thomas Bohlen ◽

Jan Ferrari ◽

...

Keyword(s):

Cardiac Output ◽

Coronary Artery ◽

Tyrosine Kinase ◽

Tyrosine Kinase Inhibitor ◽

Treatment Period ◽

Kinase Inhibitor ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Control Group

Background Short administration of volatile anesthetics preconditions myocardium and protects the heart against the consequences of subsequent ischemia. Activation of tyrosine kinase is implicated in ischemic preconditioning. The authors investigated whether desflurane-induced preconditioning depends on activation of tyrosine kinase. Methods Sixty-four rabbits were instrumented for measurement of left ventricular pressure, cardiac output, and myocardial infarct size (IS). All rabbits were subjected to 30 min of occlusion of a major coronary artery and 2 h of subsequent reperfusion. Rabbits underwent a treatment period consisting of either no intervention for 35 min (control group, n = 12) or 15 min of 1 minimum alveolar concentration desflurane inhalation followed by a 10-min washout period (desflurane group, n = 12). Four additional groups received the tyrosine kinase inhibitor genistein (5 mg/kg) or lavendustin A (1.3 mg/kg) at the beginning of the treatment period with (desflurane-genistein group, n = 11; desflurane-lavendustin A group, n = 12) or without desflurane inhalation (genistein group, n = 9; lavendustin A group, n = 8). Results Hemodynamic values were similar in all groups during baseline (left ventricular pressure, 87 +/- 14 mmHg (mean +/- SD]; cardiac output, 198 +/- 47 ml/min), during coronary artery occlusion (left ventricular pressure, 78 +/- 12 mmHg; cardiac output, 173 +/- 39 ml/min), and after 2 h of reperfusion (left ventricular pressure, 59 +/- 17; cardiac output, 154 +/- 43 ml/min). IS in the control group was 55 +/- 10% of the area at risk. The tyrosine inhibitors had no effect on IS (genistein group, 56 +/- 13%; lavendustin A group, 49 +/- 13%; each P = 1.0 vs. control group). Desflurane preconditioning reduced IS to 40 +/- 15% (P = 0.04 vs. control group). Tyrosine kinase inhibitor administration had no effect on IS reduction (desflurane-genistein group, 44 +/- 13%; desflurane-lavendustin A group, 44 +/- 16%; each P = 1.0 vs. desflurane group). Conclusion Desflurane-induced preconditioning does not depend on tyrosine kinase activation.

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