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D W Benson - One of the best experts on this subject based on the ideXlab platform.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels
Cardiovascular Research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Objective Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na+-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. Methods All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean ± standard deviation, 58 ± 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P ∞ + P oe −t/τ where P(t) = pressure at time ( t ), P ∞ = pressure asymptote, P o = pressure at the onset of relaxation and τ = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate τ and P ∞ during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Results Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged τ while chick Ringer's solution and verapamil did not. No significant change in P ∞ was observed. Conclusions This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na+-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels.
Cardiovascular research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na(+)-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean +/- standard deviation, 58 +/- 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P infinity + Poe-1/tau where P(t) = pressure at time (t), P infinity = pressure asymptote, Po = pressure at the onset of relaxation and tau = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate tau and P infinity during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged tau while chick Ringer's solution and verapamil did not. No significant change in P chi was observed. This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na(+)-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
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Heart rate perturbation in chick embryos: a comparison of two methods.
The American journal of physiology, 1991Co-Authors: B Cuneo, S Hughes, D W BensonAbstract:This report compares the effects of two methods of heart rate (HR) perturbation on stroke volume and dorsal aortic flow in the Hamburger-Hamilton stage 24 chick embryo. The sinus venosus was paced at intrinsic HR and at 150, 125, 75, and 50% of intrinsic HR (n = 23). Alternatively, a 1-mm steel probe heated to increase and cooled to decrease HR was applied to the sinus venosus (n = 15). All studies were performed in ovo at 37-38 degrees C. Aortic flow (mm3/S) and stroke volume (mm3/beat) were calculated from aortic velocity, aortic cross-sectional area, and HR. Atrioventricular (AV) inflow velocities were measured during pacing (n = 10) or probe application (n = 11) technique. Dorsal aortic flow was maximum at intrinsic HR and decreased at both increased and decreased HR. Stroke volume decreased proportionally to HR during rate increase. At decreased HR, when AV synchrony was disrupted (pacing), stroke volume was unchanged from intrinsic values. However, when AV synchrony was maintained at decreased HR (cold probe), the Embryonic Ventricle significantly increased stroke volume.
Z.j. Naheed - One of the best experts on this subject based on the ideXlab platform.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels
Cardiovascular Research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Objective Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na+-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. Methods All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean ± standard deviation, 58 ± 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P ∞ + P oe −t/τ where P(t) = pressure at time ( t ), P ∞ = pressure asymptote, P o = pressure at the onset of relaxation and τ = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate τ and P ∞ during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Results Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged τ while chick Ringer's solution and verapamil did not. No significant change in P ∞ was observed. Conclusions This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na+-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels.
Cardiovascular research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na(+)-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean +/- standard deviation, 58 +/- 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P infinity + Poe-1/tau where P(t) = pressure at time (t), P infinity = pressure asymptote, Po = pressure at the onset of relaxation and tau = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate tau and P infinity during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged tau while chick Ringer's solution and verapamil did not. No significant change in P chi was observed. This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na(+)-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
Bradley B. Keller - One of the best experts on this subject based on the ideXlab platform.
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Aortic Arch Morphogenesis and Flow Modeling in the Chick Embryo
Annals of Biomedical Engineering, 2009Co-Authors: Yajuan Wang, Kimimasa Tobita, Bradley B. Keller, Joseph P. Tinney, Michael J. Patrick, Kerem PekkanAbstract:Morphogenesis of the “immature symmetric Embryonic aortic arches” into the “mature and asymmetric aortic arches” involves a delicate sequence of cell and tissue migration, proliferation, and remodeling within an active biomechanical environment. Both patient-derived and experimental animal model data support a significant role for biomechanical forces during arch development. The objective of the present study is to quantify changes in geometry, blood flow, and shear stress patterns (WSS) during a period of normal arch morphogenesis. Composite three-dimensional (3D) models of the chick embryo aortic arches were generated at the Hamburger–Hamilton (HH) developmental stages HH18 and HH24 using fluorescent dye injection, micro-CT, Doppler velocity recordings, and pulsatile subject-specific computational fluid dynamics (CFD). India ink and fluorescent dyes were injected into the Embryonic Ventricle or atrium to visualize right or left aortic arch morphologies and flows. 3D morphology of the developing great vessels was obtained from polymeric casting followed by micro-CT scan. Inlet aortic arch flow and cerebral-to-lower body flow split was obtained from 20 MHz pulsed Doppler velocity measurements and literature data. Statistically significant variations of the individual arch diameters along the developmental timeline are reported and correlated with WSS calculations from CFD. CFD simulations quantified pulsatile blood flow distribution from the outflow tract through the aortic arches at stages HH18 and HH24. Flow perfusion to all three arch pairs are correlated with the in vivo observations of common pharyngeal arch defect progression. The complex spatial WSS and velocity distributions in the early Embryonic aortic arches shifted between stages HH18 and HH24, consistent with increased flow velocities and altered anatomy. The highest values for WSS were noted at sites of narrowest arch diameters. Altered flow and WSS within individual arches could be simulated using altered distributions of inlet flow streams. Thus, inlet flow stream distributions, 3D aortic sac and aortic arch geometries, and local vascular biologic responses to spatial variations in WSS are all likely to be important in the regulation of arch morphogenesis.
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Regional passive ventricular stress-strain relations during development of altered loads in chick embryo.
American journal of physiology. Heart and circulatory physiology, 2002Co-Authors: Kimimasa Tobita, Elizabeth A. Schroder, Joseph P. Tinney, Jason B. Garrison, Bradley B. KellerAbstract:Mechanical load influences Embryonic ventricular growth, morphogenesis, and function. However, little is known about changes in regional passive ventricular properties during the development of altered mechanical loading conditions in the embryo. We tested the hypothesis that regional mechanical loads are a critical determinant of Embryonic ventricular passive properties. We measured biaxial passive right and left ventricular (RV and LV, respectively) stress-strain relations in chick embryos at Hamburger-Hamilton stages 21 and 27 after conotruncal banding (CTB) to increase biventricular pressure load or left atrial ligation (LAL) to reduce LV volume load and increase RV volume load. In the RV, wall strains at end-diastolic (ED) pressure normalized whereas ED stresses increased after either CTB or LAL during development. In the left Ventricle, both ED strain and stress normalized after CTB, whereas both remained reduced with significantly increased myocardial stiffness after LAL. These results suggest that the Embryonic Ventricle adapts to chronically altered mechanical loading conditions by changing specific RV and LV passive properties. Thus regional mechanical load has a critical role during cardiogenesis.
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Right and left ventricular wall deformation patterns in normal and left heart hypoplasia chick embryos
American journal of physiology. Heart and circulatory physiology, 2000Co-Authors: Kimimasa Tobita, Bradley B. KellerAbstract:The vertebrate Embryonic Ventricle transforms from a smooth-walled single tube to trabeculated right ventricular (RV) and left ventricular (LV) chambers during cardiovascular morphogenesis. We hypo...
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Diastolic Filling Characteristics in the Stage 12 to 27 Chick Embryo Ventricle
Pediatric Research, 1991Co-Authors: David M Connuck, Bradley B. Keller, Edward B ClarkAbstract:ABSTRACT: Cardiac output is affected by the diastolic filling characteristics of the Ventricle. We hypothesized that the relative contributions of passive and active filling change as the Ventricle develops from a smooth-walled tube to a trabeculated four-chamber heart. In stage 12 to 27 white Leghorn chick embryos, we simultaneously measured ventricular pressure with a servo-null micropressure system and dorsal aortic and atrioventricular velocities with a 20-MHz pulsed-Doppler velocity meter. The analog waveforms were sampled at 500 Hz and converted to digital format via an analog/digital board. We partitioned diastole into passive and active components. The passive phase began with the return of the pressure curve to baseline and extended to the onset of the a-wave. The active phase began with the upstroke of the atrial velocity curve and extended to the upstroke of the ventricular pressure curve at end-diastole. Data are presented as mean ± SEM ( n ≥ 6 at each stage) and analyzed by analysis of variance and regression analysis. At similar cycle lengths ranging from 480 to 600 ms ( p > 0.05), end-diastolic pressure increased from 0.24 ± 0.02 mm Hg at stage 12 to 0.55 ± 0.01 mm Hg at stage 27. Passive and active filling volumes were 92 (0.0038 ± 0.0005 mm^3) and 8% (0.0004 ± 0.0002 mm^3), respectively, at stage 12 and changed to 24 (0.23 ± 0.08 mm^3) and 76% (0.62 ± 0.08 mm^3), respectively, at stage 27. The ratio of passive to active filling volume decreased from 7.89 to 0.35. Thus, active ventricular filling became dominant as the trabeculae formed in the Embryonic Ventricle. These observations define the diastolic filling characteristics of the Embryonic heart during primary cardiac morphogenesis.
S.f. Hughes - One of the best experts on this subject based on the ideXlab platform.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels
Cardiovascular Research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Objective Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na+-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. Methods All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean ± standard deviation, 58 ± 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P ∞ + P oe −t/τ where P(t) = pressure at time ( t ), P ∞ = pressure asymptote, P o = pressure at the onset of relaxation and τ = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate τ and P ∞ during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Results Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged τ while chick Ringer's solution and verapamil did not. No significant change in P ∞ was observed. Conclusions This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na+-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels.
Cardiovascular research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na(+)-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean +/- standard deviation, 58 +/- 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P infinity + Poe-1/tau where P(t) = pressure at time (t), P infinity = pressure asymptote, Po = pressure at the onset of relaxation and tau = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate tau and P infinity during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged tau while chick Ringer's solution and verapamil did not. No significant change in P chi was observed. This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na(+)-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
A. Lahoti - One of the best experts on this subject based on the ideXlab platform.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels
Cardiovascular Research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Objective Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na+-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. Methods All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean ± standard deviation, 58 ± 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P ∞ + P oe −t/τ where P(t) = pressure at time ( t ), P ∞ = pressure asymptote, P o = pressure at the onset of relaxation and τ = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate τ and P ∞ during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Results Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged τ while chick Ringer's solution and verapamil did not. No significant change in P ∞ was observed. Conclusions This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na+-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.
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Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels.
Cardiovascular research, 1996Co-Authors: Z.j. Naheed, A. Lahoti, S.f. Hughes, D W BensonAbstract:Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the Embryonic Ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na(+)-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the Embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean +/- standard deviation, 58 +/- 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P infinity + Poe-1/tau where P(t) = pressure at time (t), P infinity = pressure asymptote, Po = pressure at the onset of relaxation and tau = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate tau and P infinity during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged tau while chick Ringer's solution and verapamil did not. No significant change in P chi was observed. This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na(+)-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.