In Vivo Evaluation of a Physiologic Control System for Rotary Blood Pumps Based on the Left Ventricular Pressure-Volume Loop

ASAIO Journal ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Joshua Cysyk ◽  
Choon-Sik Jhun ◽  
Ray Newswanger ◽  
Walter Pae ◽  
Jenelle Izer ◽  
...  
Keyword(s):  
Control System ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
In Vivo Evaluation ◽  
Blood Pumps ◽  
Rotary Blood Pumps

In vivo safety and accuracy of a clinically applicable telemetered left ventricular pressure module: intermediate-term results

2004 ◽  
Vol 10 (4) ◽  
pp. S67 ◽  
Author(s):  
Patrick I. McConnell ◽  
Daise de Cunha ◽  
Tanya Shipkowitz ◽  
Justin Van Hee ◽  
Phillip H. Long ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure

Hypotensive mechanism of [Leu13]motilin in dogs in vivo and in vitro

1998 ◽  
Vol 76 (12) ◽  
pp. 1103-1109 ◽  
Author(s):  
Takeshi Iwai ◽  
Hiroyuki Nakamura ◽  
Hisanori Takanashi ◽  
Kenji Yogo ◽  
Ken-Ichi Ozaki ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Gastric Antrum ◽  
Ventricular Pressure ◽  
High Dose ◽  
Aortic Blood Flow ◽  
Arterial Blood

The effects of [Leu13]motilin were examined in vivo after its intravenous administration into anesthetized dogs and in vitro with isolated preparations of canine mesenteric artery. [Leu13]Motilin (0.1-10 nmol·kg-1, i.v.) induced both strong and clustered phasic contractions in the gastric antrum and duodenum. At doses of over 1 nmol·kg-1, [Leu13]motilin also produced transient decreases in arterial blood pressure, left ventricular pressure, maximum rate of rise of left ventricular pressure, and total peripheral resistance, and an increase in aortic blood flow and heart rate. A selective motilin antagonist, GM-109 (Phe-cyclo[Lys-Tyr(3-tBu)-betaAla]betatrifluoroacetate), completely abolished the gastric antrum and duodenal motor responses induced by [Leu13]motilin. In contrast, hypotension induced by [Leu13]motilin (1 nmol·kg-1) was unchanged in the presence of GM-109. In isolated mesenteric artery preparations precontracted with U-46619 (10-7 M), [Leu13]motilin (10-8-10-5 M) induced an endothelium-dependent relaxation, and this was inhibited by a pretreatment with Nomega-nitro-L-arginine, a competitive inhibitor of NO synthase (10-4 M). A high dose (10-4 M) of GM-109 slightly decreased [Leu13]motilin-induced relaxation, and shifted the concentration-response curve of [Leu13]motilin to the right. However, the pA2 value (4.09) of GM-109 for [Leu13]motilin in the present study was conspicuously lower than that previously demonstrated in the rabbit duodenum (7.37). These results suggest that [Leu13]motilin induces hypotension via the endothelial NO-dependent relaxation mechanism and not through the receptor type that causes upper gastrointestinal contractions.Key words: motilin, gastrointestinal motility, hypotension, hemodynamics, anesthetized dog, mesenteric artery, endothelium, nitric oxide.

In vivo murine left ventricular pressure-volume relations by miniaturized conductance micromanometry

1998 ◽  
Vol 274 (4) ◽  
pp. H1416-H1422 ◽  
Author(s):  
Dimitrios Georgakopoulos ◽  
Wayne A. Mitzner ◽  
Chen-Huan Chen ◽  
Barry J. Byrne ◽  
Huntly D. Millar ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Genetically Engineered ◽  
Ventricular Pressure ◽  
Stroke Work ◽  
Time Varying ◽  
End Diastolic Volume ◽  
Novel Approach ◽  
Preload Reduction

The mouse is the species of choice for creating genetically engineered models of human disease. To study detailed systolic and diastolic left ventricular (LV) chamber mechanics in mice in vivo, we developed a miniaturized conductance-manometer system. α-Chloralose-urethan-anesthetized animals were instrumented with a two-electrode pressure-volume catheter advanced via the LV apex to the aortic root. Custom electronics provided time-varying conductances related to cavity volume. Baseline hemodynamics were similar to values in conscious animals: 634 ± 14 beats/min, 112 ± 4 mmHg, 5.3 ± 0.8 mmHg, and 11,777 ± 732 mmHg/s for heart rate, end-systolic and end-diastolic pressures, and maximum first derivative of ventricular pressure with respect to time (dP/d t max), respectively. Catheter stroke volume during preload reduction by inferior vena caval occlusion correlated with that by ultrasound aortic flow probe ( r 2 = 0.98). This maneuver yielded end-systolic elastances of 79 ± 21 mmHg/μl, preload-recruitable stroke work of 82 ± 5.6 mmHg, and slope of dP/d t max-end-diastolic volume relation of 699 ± 100 mmHg ⋅ s−1 ⋅ μl−1, and these relations varied predictably with acute inotropic interventions. The control normalized time-varying elastance curve was similar to human data, further supporting comparable chamber mechanics between species. This novel approach should greatly help assess cardiovascular function in the blood-perfused murine heart.

Mechanical interaction between the ventricles during systole

1977 ◽  
Vol 55 (3) ◽  
pp. 373-382 ◽  
Author(s):  
B. Lowell Langille ◽  
David R. Jones
Keyword(s):  
Left Ventricle ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Mechanical Interaction ◽  
Rigor Mortis ◽  
Ventricular Performance ◽  
Ventricular Afterload

The immediate effect of abrupt alteration in the function of either ventricle on pressures in both ventricles has been examined in rabbits. Increasing left ventricular afterload, by aortic occlusion, caused a marked increase in peak left ventricular pressure (an increase of 44.0 ± 5.7 mmHg, from a mean of 79.4 ± 3.4 mmHg) and simultaneously a significant increase (an increase of 3.8 ± 0.6 mmHg, from a mean of 24.2 ± 1.4 mmHg) in right ventricular pressure. On the other hand, when similar increases in left ventricular pressure were induced by sudden changes in preload no alteration in right ventricular pressure was seen. High-frequency oscillatory infusion of saline into the left ventricle produced coincident oscillations in both ventricular pressures during systole. Left ventricular pressure generation was affected by interventions with right ventricular performance which altered afterload or preload and, although interaction was minimal at normal physiological pressures, a significant interaction was observed during induced systemic hypotension. A direct transference of pressure from right to left ventricle, comparable with that seen in vivo, was also observed when the ventricles of excised hearts in rigor mortis were inflated with saline. It is concluded that mechanical interaction occurs between the ventricles during systole and, consequently, the ventricles cannot be treated as mechanically independent pumps.

cTnT1, a cardiac troponin T isoform, decreases myofilament tension and affects the left ventricular pressure waveform

2005 ◽  
Vol 288 (3) ◽  
pp. H1147-H1156 ◽  
Author(s):  
Rashid Nassar ◽  
Nadia N. Malouf ◽  
Lan Mao ◽  
Howard A. Rockman ◽  
Annette E. Oakeley ◽  
...  
Keyword(s):  
Heart Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Cardiac Troponin T ◽  
Force Development ◽  
Amino Terminal

Four isoforms of cardiac troponin T (cTnT), a protein essential for calcium-dependent myocardial force development, are expressed in the human; they differ in charge and length. Their expression is regulated developmentally and is affected by disease states. Human cTnT (hcTnT) isoform effects have been examined in reconstituted myofilaments. In this study, we evaluated the modulatory effects of overexpressing one cTnT isoform on in vitro and in vivo myocardial function. A hcTnT isoform, hcTnT1, expressed during development and in heart disease but not in the normal adult heart, was expressed in transgenic (TG) mice (1–30% of total cTnT). Maximal active tension measured in skinned myocardium decreased as a function of relative hcTnT1 expression. The pCa at half-maximal force development, Hill coefficient, and rate of redevelopment of force did not change significantly with hcTnT1 expression. In vivo maximum rates of rise and fall of left ventricular pressure decreased, and the half-time of isovolumic relaxation increased, with hcTnT1 expression. Substituting total cTnT charge for hcTnT1 expression resulted in similar conclusions. Morphometric analysis and electron microscopy revealed no differences between wild-type (non-TG) and TG myocardium. No differences in isoform expression of tropomyosin, myosin heavy chain, essential and regulatory myosin light chains (MLC), TnI, or in posttranslational modifications of mouse cTnT, cTnI, or regulatory MLC were observed. These results support the hypothesis that cTnT isoform amino-terminal differences affect myofilament function and suggest that hcTnT1 expression levels present during human development and in human heart disease can affect in vivo ventricular function.

Ketamine, but Not S  (+)-ketamine, Blocks Ischemic Preconditioning in Rabbit Hearts In Vivo 

2001 ◽  
Vol 94 (4) ◽  
pp. 630-636 ◽  
Author(s):  
Jost Müllenheim ◽  
Jan Fräßdorf ◽  
Benedikt Preckel ◽  
Volker Thämer ◽  
Wolfgang Schlack
Keyword(s):  
Cardiac Output ◽  
Coronary Artery ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Left Ventricular Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Ventricular Pressure

Background Ketamine blocks KATP channels in isolated cells and abolishes the cardioprotective effect of ischemic preconditioning in vitro. The authors investigated the effects of ketamine and S(+)-ketamine on ischemic preconditioning in the rabbit heart in vivo. Methods In 46 alpha-chloralose-anesthetized rabbits, left ventricular pressure (tip manometer), cardiac output (ultrasonic flow probe), and myocardial infarct size (triphenyltetrazolium staining) at the end of the experiment were measured. All rabbits were subjected to 30 min of occlusion of a major coronary artery and 2 h of subsequent reperfusion. The control group underwent the ischemia-reperfusion program without preconditioning. Ischemic preconditioning was elicited by 5-min coronary artery occlusion followed by 10 min of reperfusion before the 30 min period of myocardial ischemia (preconditioning group). To test whether ketamine or S(+)-ketamine blocks the preconditioning-induced cardioprotection, each (10 mg kg(-1)) was administered 5 min before the preconditioning ischemia. To test any effect of ketamine itself, ketamine was also administered without preconditioning at the corresponding time point. Results Hemodynamic baseline values were not significantly different between groups [left ventricular pressure, 107 +/- 13 mmHg (mean +/- SD); cardiac output, 183 +/- 28 ml/min]. During coronary artery occlusion, left ventricular pressure was reduced to 83 +/- 14% of baseline and cardiac output to 84 +/- 19%. After 2 h of reperfusion, functional recovery was not significantly different among groups (left ventricular pressure, 77 +/- 19%; cardiac output, 86 +/- 18%). Infarct size was reduced from 45 +/- 16% of the area at risk in controls to 24 +/- 17% in the preconditioning group (P = 0.03). The administration of ketamine had no effect on infarct size in animals without preconditioning (48 +/- 18%), but abolished the cardioprotective effects of ischemic preconditioning (45 +/- 19%, P = 0.03). S(+)-ketamine did not affect ischemic preconditioning (25 +/- 11%, P = 1.0). Conclusions Ketamine, but not S(+)-ketamine blocks the cardioprotective effect of ischemic preconditioning in vivo.

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