Influence of nonuniformity on rate of left ventricular pressure fall in the dog

1989 ◽  
Vol 256 (1) ◽  
pp. H222-H232 ◽  
Author(s):  
W. Y. Lew ◽  
C. M. Rasmussen

We examined the influence of nonuniformity in regional ventricular function on the rate of left ventricular pressure fall in 10 anesthetized dogs. Ultrasonic segment gauges were implanted in the midwall of the anterior, lateral, and posterior left ventricle. In seven dogs, nonuniformity was produced by infusing isoproterenol (0.4 microgram/ml) into the mid-left anterior descending coronary artery at low flow (0.5 +/- 0.7 ml/min) and high flow (1.5 +/- 1.2 ml/min) rates, for total doses of 0.1 +/- 0.1 and 0.3 +/- 0.2 micrograms, respectively. This produced a dose-dependent increase in anterior segment shortening so that shortening was completed earlier and marked segment lengthening occurred during isovolumic relaxation. Lateral and posterior segments were not directly stimulated. The heart rate, left ventricular end-diastolic pressure, and peak systolic pressure remained constant. However, tau, the time constant of left ventricular pressure fall, increased from 32 +/- 8 to 37 +/- 10 ms with the low dose, and from 35 +/- 6 to 49 +/- 12 ms with the high dose of isoproterenol. Similar results occurred in two dogs when isoproterenol was infused into the proximal, mid, or distal left anterior descending and in three dogs with infusions in the left circumflex coronary artery. We conclude that nonuniformity of regional left ventricular function is an important and independent factor regulating the rate of pressure fall in the intact ejecting left ventricle.

1991 ◽  
Vol 261 (3) ◽  
pp. H805-H813 ◽  
Author(s):  
T. C. Gillebert ◽  
W. Y. Lew

We examined the influence of the systolic left ventricular pressure (LVP) waveform on the rate of isovolumetric LVP fall, as assessed by the time constant tau. Seven open-chest dogs were instrumented with a micromanometer in the left ventricle, with segment length gauges in the anterior and posterior midwall of the left ventricle, and with a balloon-tipped catheter in the proximal aorta. The intra-aortic balloon was inflated before the onset of ejection (early) or during midejection (late) to produce timed and graded increases in peak LVP of 2-20 mmHg. The rate of LVP fall slowed significantly more with late than with early increases in LVP (tau increased 1.5 +/- 0.5 vs. 0.5 +/- 0.3%/mmHg increase in peak LVP, respectively, P less than 0.001). For a similar increase in peak LVP, there was a progressively greater increase in tau when the timing of balloon inflation was progressively delayed from early to late ejection (in 10-ms increments). The differential effect of early vs. late pressure increases on tau was not related to regional differences in segment length behavior nor to an increase in regional nonuniformity between anterior and posterior sites. We conclude that under the experimental conditions of an intact, ejecting left ventricle, the systolic pressure profile is an important determinant of the rate of pressure fall. The rate of LVP fall slows in direct proportion to the magnitude of increase in systolic pressure. The sensitivity to systolic load increases progressively throughout the ejection period, so that the rate of LVP fall slows significantly more with late than with early pressure increases.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 75 (3) ◽  
pp. 1201-1207 ◽  
Author(s):  
J. H. Van Blankenstein ◽  
C. J. Slager ◽  
J. C. Schuurbiers ◽  
S. Strikwerda ◽  
P. D. Verdouw

By its nature, vaporization of atherosclerotic plaques by laser irradiation or spark erosion may produce a substantial amount of gas. To evaluate the effect of gas embolism possibly caused by vaporization techniques, air bubbles with diameters of 75, 150, or 300 microns, each in a volume of 2 microliters/kg, were selectively injected subproximal in the left anterior descending coronary artery of seven anesthetized pigs (28 +/- 3 kg). Systemic hemodynamics such as heart rate, left ventricular pressure and its peak positive first derivative, and mean arterial pressure did not change after air injection, whereas there was a minor change in peak negative first derivative of left ventricular pressure. After injection of air bubbles there was a maximal relative reduction of systolic segment shortening (SS) in the myocardium supplied by the left anterior descending coronary artery of 27, 45, and 58% for 75-, 150-, and 300-microns bubbles, respectively, and a relative increase of postsystolic SS (PSS) of 148, 200, and 257% for 75-, 150-, and 300-microns bubbles, respectively. Recovery of SS and PSS started after 2 min and was completed after 10 min. A difference in SS and PSS changes between different bubble size injections could be demonstrated. From this study it is clear that depression of regional myocardial function after injection of air bubbles could pass unnoticed on the basis of global hemodynamic measurements.


Author(s):  
Ahmad Moghaddaszade-Kermani ◽  
Peter Oshkai ◽  
Afzal Suleman

Mitral-Septal contact has been proven to be the cause of obstruction in the left ventricle with hypertrophic cardiomyopathy (HC). This paper presents a study on the fluid mechanics of obstruction using two-way loosely coupled fluid-structure interaction (FSI) methodology. A parametric model for the geometry of the diseased left ventricular cavity, myocardium and mitral valve has been developed, using the dimensions extracted from magnetic resonance images. The three-element Windkessel model [1] was modified for HC and solved to introduce pressure boundary condition to the aortic aperture in the systolic phase. The FSI algorithm starts at the beginning of systolic phase by applying the left ventricular pressure to the internal surface of the myocardium to contract the muscle. The displacements of the myocardium and mitral leaflets were calculated using the nonlinear finite element hyperelastic model [2] and subsequently transferred to the fluid domain. The fluid mesh was moved accordingly and the Navier-Stokes equations were solved in the laminar regime with the new mesh using the finite volume method. In the next time step, the left ventricular pressure was increased to contract the muscle further and the same procedure was repeated for the fluid solution. The results show that blood flow jet applies a drag force to the mitral leaflets which in turn causes the leaflet to deform toward the septum thus creating a narrow passage and possible obstruction.


Author(s):  
Jessica Shih ◽  
Hyun Jin Kim ◽  
Charles A. Taylor

The number of patients with coronary artery disease continues to rise, with approximately 469,000 coronary bypass procedures in 2005 alone [1]. A priori knowledge of the flow features within the coronary vascular system could prove useful in predicting flow changes due to coronary bypass surgery. Image-based modeling and 3-D computational simulations could be used to compute flow and pressure in a patient-specific manner. However, modeling coronary flow requires knowledge of the intramyocardial pressure that compresses coronary vessels, resulting in decreased flow in systole and increased flow in diastole. Left ventricular pressure can provide an estimate to intramyocardial pressure, but the aortic pressure and left ventricular pressure must be coupled in systole when the aortic valve is open. Previously, we have developed a method to couple a lumped-parameter heart model to the inlet of a 3-D model to compute aortic and ventricular pressure [2]. In this study, we use the lumped-parameter heart model and computational fluid dynamics to calculate flow dynamics in a patient model with coronary artery bypass grafts.


1998 ◽  
Vol 76 (12) ◽  
pp. 1103-1109 ◽  
Author(s):  
Takeshi Iwai ◽  
Hiroyuki Nakamura ◽  
Hisanori Takanashi ◽  
Kenji Yogo ◽  
Ken-Ichi Ozaki ◽  
...  

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.


1987 ◽  
Vol 51 (11) ◽  
pp. 1273-1282 ◽  
Author(s):  
KAZUHIRO KATAYAMA ◽  
TOSHIAKI KUMADA ◽  
MASUNORI MATSUZAKI ◽  
MASAHRU OZAKI ◽  
MASAFUMI YANO ◽  
...  

1990 ◽  
Vol 11 (suppl I) ◽  
pp. 124-132 ◽  
Author(s):  
T. C. Gillebert ◽  
D. L. Brutsaert

Sign in / Sign up

Export Citation Format

Share Document