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Biomedical subjects

J W Buchanan

Publications and source records attributed to J W Buchanan.

At least 19 recordsLinked to original sources
PubMed1995

Vertebral scale system to measure canine heart size in radiographs.

A method for measuring canine heart size in radiographs was developed on the basis that there is a good correlation between heart size and body length regardless of the conformation of the thorax. The lengths of the long and short axes of the heart of 100 clinically normal dogs were determined with calipers, and the dimensions were scaled against the length of vertebrae dorsal to the heart beginning with T4. The sum of the long and short axes of the heart expressed as vertebral heart size was 9.7 +/- 0.5 vertebrae. The differences between dogs with a wide or deep thorax, males and females, and right or left lateral recumbency were not significant. The caudal vena cava was 0.75 vertebrae +/- 0.13 in comparison to the length of the vertebra over the tracheal bifurcation.

Animals↗
PubMed1994

Electrical coupling and impulse propagation in anatomically modeled ventricular tissue.

Computer simulations were used to study the role of resistive couplings on flat-wave action potential propagation through a thin sheet of ventricular tissue. Unlike simulations using continuous or periodic structures, this unique electrical model includes random size cells with random spaced longitudinal and lateral connections to simulate the physiologic structure of the tissue. The resolution of the electrical model is ten microns, thus providing a simulated view at the subcellular level. Flat-wave longitudinal propagation was evaluated with an electrical circuit of over 140,000 circuit elements, modeling a 0.25 mm by 5.0 mm sheet of tissue. An electrical circuit of over 84,000 circuit elements, modeling a 0.5 mm by 1.5 mm sheet was used to study flat-wave transverse propagation. Under normal cellular coupling conditions, at the macrostructure level, electrical conduction through the simulated sheets appeared continuous and directional differences in conduction velocity, action potential amplitude and Vmax were observed. However, at the subcellular level (10 microns) unequal action potential delays were measured at the longitudinal and lateral gap junctions and irregular wave-shapes were observed in the propagating signal. Furthermore, when the modeled tissue was homogeneously uncoupled at the gap junctions conduction velocities decreased as the action potential delay between modeled cells increased. The variability in the measured action potential was most significant in areas with fewer lateral gap junctions, i.e., lateral gap junctions between fibers were separated by a distance of 100 microns or more.

Action Potentials↗
PubMed1993

Chronic mitral valve disease in cavalier King Charles spaniels: 95 cases (1987-1991)

Systolic heart murmurs caused by chronic mitral valve disease are particularly common in Cavalier King Charles Spaniels (CKCS) in Great Britain. To determine if American-bred CKCS have a similar high prevalence of chronic valve disease, results of stethoscopic examinations on 394 CKCS were analyzed. Left apical systolic heart murmurs were found in 22% of the dogs. The prevalence ranged from 9% in dogs < 1 year old to 100% in those > or = 10 years old; prevalence was 56% in dogs > or = 4 years old. Differences were not found in prevalence between sexes and among various coat colors. Reexamination of 79 dogs after 1 year revealed an incidence of new murmurs of 21%. Comparison of ages at initial examination in 128 referral hospital cases with chronic mitral valve disease revealed a mean age of 6.25 years in 17 CKCS, in contrast to a mean age of 12 years in other breeds. Echocardiographic and necropsy findings indicated that ruptured chordae tendineae and mitral valve prolapse are major components in the chronic valve disease process in CKCS.

Age Factors↗
PubMed1991

Interstitial potential during propagation in bathed ventricular muscle.

Theoretical simulations have suggested that interstitial potential (Vis) during action potential propagation affects measurements of the transmembrane action potential in bathed ventricular muscle. To evaluate the Vis experimentally, we obtained Vis and intracellular action potential (Vic) recordings at various depths in paced guinea pig papillary muscles bathed in oxygenated Tyrode's solution. The peak-to-peak amplitude and the maximum dV/dt (dV/dtmax) of the intrinsic downward deflection of the Vis recordings were determined. The transmembrane action potential (TM) was obtained by subtracting each Vis from the corresponding Vic recording, and measurements for the phase zero depolarization and action potential foot of the Vic were compared with the measurements for the TM. At penetration depths of approximately 54 microns, the amplitude and dV/dtmax of the Vis were 13 mV and -38 V/s. When the depth was increased to 200 microns, these parameters increased to 24 mV and -59 V/s (P less than 0.005), and when the depth was further increased to 390 microns, the parameters decreased to 16 mV and -38 V/s. Because of the Vis at the various depths, the Vic underestimated dV/dtmax of phase zero of the TM by 20-31%, which would reduce estimates of Na+ current obtained from dV/dt. Also, the Vic overestimated the time constant of the 2-8 mV foot of the action potential by 48-82%, which would reduce estimates of the "effective" membrane capacitance by 33-45%. These influences of the Vis on measurements may affect results of quantitative studies of the ventricular action potential.

Action Potentials↗
PubMed1990

Pulmonic stenosis caused by single coronary artery in dogs: four cases (1965-1984).

Single right coronary artery (CA) associated with pulmonic stenosis was found in 3 English Bulldogs and a Boxer, suggesting a genetic predisposition for the associated anomalies. The left main coronary branch arose from the single right CA, encircled the pulmonic root over hypoplastic pulmonic valves at the level of the obstruction, and appeared to be the primary cause of underlying pulmonic stenosis. Patch-graft surgery to relieve pulmonic stenosis caused death in 1 dog when the unrecognized anomalous CA was served during the procedure. The anomalous left CA was detectable by use of angiocardiography in all 4 dogs and was recognized before surgery in 2 of them. In 1 dog, a right ventricle-to-pulmonary trunk-bridging conduit was implanted to improve outflow from the right side of the heart.

Angiocardiography↗
PubMed1989

Influence of rate-dependent cellular uncoupling on conduction change during simulated ischemia in guinea pig papillary muscles: effect of verapamil.

This study was performed to determine if the changes in cellular coupling induced by simulated ischemia were rate-dependent and if they contributed to the rate-dependent conduction slowing that occurs in this setting. We also sought to determine if the known ability of verapamil to prevent ischemia-induced conduction changes might be related to the preservation of cellular coupling. We studied the effects of increasing stimulation frequency from 0.5 to 2.0 Hz on the simultaneous changes in the maximum rate of rise (Vmax) of the action potential upstroke, conduction velocity, and internal longitudinal resistance (ri) determined by the voltage ratio method in superfused guinea pig papillary muscles under conditions of simulated ischemia (SI). When stimulation frequency was 0.5 Hz, 30 minutes of SI caused a 16.5% decrease in Vmax, a 16% increase in ri, and a 12.9% decrease in conduction velocity. When stimulation frequency was increased to 2.0 Hz, 30 minutes of SI caused a 30% decrease in Vmax, a 72.9% increase in ri, and a 21.4% decrease in conduction velocity. Thus, the changes were rate-dependent. Verapamil (1 X 10(-6) M) did not influence the changes in these parameters during SI at 0.5 Hz nor the decrease in Vmax during SI at 2.0 Hz, but it did prevent the rate-dependent increase in ri. Verapamil also prevented the rate-dependent decrease in conduction velocity induced by SI. Our results suggest that during simulated ischemia the rate-dependent component of the increase in Ri contributes to the rate-dependence of the conduction slowing.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1988

Use dependence of amiodarone during the sinus tachycardia of exercise in coronary artery disease.

The QRS duration at rest and during exercise was studied in 19 patients with coronary artery disease before and after oral amiodarone therapy to determine if this drug produces detectable rate-dependent conduction slowing during physiologic increases in heart rate. QRS duration did not change significantly during exercise in the absence of the drug. However, after amiodarone, QRS duration at rest increased from 99 to 114 ms (p less than 0.001), and increased further from 114 to 127 ms (p less than 0.001) during the 45 beats/min mean increase in heart rate produced by exercise. The magnitude of this effect was related to the resting QRS duration. After amiodarone therapy, the QRS increased during exercise by only 6% in 8 patients with QRS less than 110 ms, while in 12 patients with QRS greater than or equal to 110 ms, the QRS increased by 15% (p less than 0.05). Rate-dependent conduction slowing occurs during the sinus tachycardia of exercise in patients treated with amiodarone, presumbably due to use-dependent sodium channel blockade. This result is most pronounced in patients with abnormal ventricular conduction at rest.

Administration, Oral↗
PubMed1988

Automatic drawing of the left epicardial region of interest on thallium 201 scintigraphic images.

An algorithm has been written which automatically selects a left epicardial region of interest on 201Tl myocardial images. It accomplishes a radial search from the geometric center of the myocardium. On each of the 30 profiles, the local maximum of the 1st derivative is selected as the epicardial edge. The algorithm has been tested in 40 patients at stress and redistribution. In ten patients, conventional planar images were obtained in three views. In 30 patients conventional short axis tomographic images were obtained after reconstruction of 32 projections acquired over 180 degrees. The rate of success is 97% for both imaging modalities. This procedure is another step towards fully automated assessment of myocardial defects and redistribution.

Algorithms↗
PubMed1988

Non-invasive measurement of pulmonary arterial pressure: I. A haemodynamic modelling approach.

In order to monitor pulmonary arterial pressure (P) by any non-invasive imaging technique, a haemodynamic model of blood flow kinetics and wall mechanics has been developed. It is a one-dimensional model of pulsatile flow in an elastic pulmonary arterial trunk, assuming that blood is an incompressible fluid and viscous effects are negligible. The equations are P(t)-Pd = rho c2lnS(t)/Sd-1/2pw-2(t) Pd = (Sd/Ss)1/2Pp where, at any time of the ejection phase of systole, P(t), S(t) and w(t) are the pulmonary arterial pressure, cross-sectional area of the pulmonary artery and blood velocity averaged on the cross section S, respectively, PP is the pulse pressure, the difference between the peak systolic pressure and the diastolic pressure Pd; rho is blood density, c pulse wave velocity, and Ss and Sd are maximum (systolic) and minimum (diastolic) values of the cross-sectional area S. Using these equations, P(t) can be calculated if the three parameters, i.e. c, S(t) and w(t) are measured. So far, it has been impossible to measure the pulse wave velocity c non-invasively. We have investigated the calculation of c from S(t) and w(t) using the equation of continuity in the absence and presence of reflected pressure waves. The hypotheses of the haemodynamic model are discussed.

Blood Flow Velocity↗
PubMed1988

Non-invasive measurement of pulmonary arterial pressure: II. A radionuclide method.

Pulmonary artery pulse pressure (PP) and diastolic pressure (Pd) may be obtained by applying a haemodynamic model of blood flow kinetics and wall mechanics to the pulmonary artery: Pp = rho(ws/(Ss/Sd-1))2log(Ss/Sd)-1/2 rho w2s Pd = (Sd/Ss)1/2Pp where rho is blood density, ws is peak ejection velocity, and Ss and Sd are peak maximal and end diastolic cross-sectional areas of the main pulmonary artery. The different parameters of the equations were measured from radionuclide first pass and equilibrium studies. Radionuclide first pass studies were performed in 24 patients with intravenous injection of 20 mCi of 99Tcm red blood cells with a gamma camera in a 20 degrees right anterior oblique position: data were collected in list mode, i.e. a continuous sequence of spatial and temporal coordinates of each photon. Pulmonary arterial pressure was recorded simultaneously with a microtip catheter during the first pass study. Gated first pass images of the right side of the heart were reconstructed, regions of interest drawn over the right ventricle and the main pulmonary artery (MPA) and time-activity curves generated. Peak systolic (Cs) and end diastolic (Cd) counts obtained from the MPA curve were proportional to the cross sections Ss and Sd of the MPA and Ss/Sd = Cs/Cd. The diameter (D) of the pulmonary artery was calculated as the distance between the two zeros of the second derivative of a cross-sectional profile. The averaged cross-sectional area was S = pi D2/4. ECG gated blood pool studies were performed in a LAO 40 degrees position when the tracer was at equilibrium; they were processed automatically and the right ventricular end diastolic counts (EDC) converted into volume (EDV) using an aortic volume/count ratio. Right ventricular peak ejection rate (PER) was obtained from the RV time-activity curve and the instantaneous peak ejection velocity was calculated, ws = PER X EDV/S X EDC. PP and Pd were calculated in mmHg and the radionuclide method yielded pressure values that correlated reasonably with catheterisation values: PP(rad) = 0.99 PP(cath)-0.55, r = 0.84 and Pd(rad) = 0.67 Pd(cath) + 4.91, r = 0.74. We conclude that radionuclide techniques can provide a non-invasive method based on a haemodynamic model for measuring pulmonary arterial pressure.

Adult↗
PubMed1988

Accuracy of gated equilibrium radioventriculography in measuring left ventricular function in dogs.

To assess the precision of gated equilibrium radioventriculography in measuring changes in left ventricular stroke volume (LVSV), we studied five dogs each with a chronically implanted electromagnetic flowmeter on the ascending aorta. Per cent changes in left ventricular stroke counts (LVSC) were compared to those in LVSV following acute changes induced by positive end respiratory pressure. We have compared LVSCs calculated in five different ways: (1) Manual outlining of LV region of interest (LVROI), either single fixed enddiastolic (ED) ROI or ED and endsystolic (ES) ROIs with the aid of functional images (first harmonic of Fourier analysis); (2-5) automatic outlining of LV ROI (the algorithm generated 30 profiles on which the maximum of second derivative delineated the LV edges) was performed either on ED image or both ED and ES images. For these four methods a crescent-shaped ROI for background correction was manually drawn at the border of the LV ROI. The fifth method used an automatically drawn single fixed LVED ROI with interpolative background substraction (IBS) between LV and RV edges. LVSC changes, calculated with the IBS method correlated better with LVSV changes than the other four methods. Thus assessment of small LVSC changes is highly processing-dependent.

Animals↗
PubMed1988

Rate-dependent effects of hypoxia on internal longitudinal resistance in guinea pig papillary muscles.

We have studied the independent and combined effects of 30 minutes' exposure to hypoxia and an increase in stimulation frequency from 0.5 Hz to 3.0 Hz on internal longitudinal resistance (ri) and conduction in guinea pig papillary muscles through the use of the voltage ratio method with air as the external insulator. Increasing stimulation frequency from 0.5 to 3.0 Hz in the presence of O2 caused no significant change in ri. Hypoxia to a level of PO2 = 30 mm Hg caused an increase in ri that averaged 13.7% at a stimulation frequency of 0.5 Hz and 46% at 3.0 Hz. In all experiments, the increase in ri during hypoxia at 3.0 Hz was greater than the increase at 0.5 Hz, but conduction velocity did not change at either rate. These results indicate that hypoxia causes rate-dependent cellular uncoupling but, under the conditions of our experiments, does not cause significant changes in conduction.

Action Potentials↗
PubMed1987

Relationship between extracellular potassium accumulation and local TQ-segment potential during acute myocardial ischemia in the porcine.

Depolarization of resting membrane potential during acute myocardial ischemia is strongly correlated with the accumulation of extracellular potassium ([K+]e). Also, diastolic currents of injury flowing across the ischemic border that occur as a result of local differences in resting membrane potentials cause changes in the TQ-segments of unipolar, DC-coupled, extracellular electrograms. Further, the changes in [K+]e and TQ-segment potentials during acute ischemia and reperfusion follow a similar time course. For these reasons, a predictable relationship between [K+]e and TQ potentials might be expected to exist. If found, easily obtainable local TQ potential measurements could serve as an index of the resting membrane depolarization induced by [K+]e accumulation and, by extension, as an index of ischemic injury. We measured local [K+]e and TQ potentials from 30 mid-myocardial sites in central and marginal ischemic zones in 2 isolated, Langendorff-perfused porcine hearts during a single, 10-min ligation of the left anterior descending coronary artery. In general, we found a linear relationship between [K+]e and TQ potential for both ischemic zones when data was taken as a whole, but the slopes (S) and correlation coefficients (R) were markedly different between the two locations (-2.24 vs -1.28 and -0.73 vs -0.51 for central and marginal zones, respectively). Further, we found a time dependent change in both S and R that was biphasic. Both were low during the first minutes, attained their maximum values at 4 mins, and then fell during the remainder of the occlusion. We conclude, therefore, that local TQ potentials cannot be used as an index of the severity of ischemic changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1987

Enhancement of procainamide-induced rate-dependent conduction slowing by elevated myocardial extracellular potassium concentration in vivo.

Procainamide, a type 1A antiarrhythmic drug, blocks sodium channels and reduces the maximum rate of rise of the cardiac action potential (Vmax) in a rate-dependent fashion. In vitro, the magnitude of this rate-dependent reduction in Vmax is greater in tissue that is partially depolarized at rest than in tissue with a normal resting potential. Reductions in Vmax produced by drugs that block sodium channels are also directly related to the reductions in longitudinal conduction velocity of action potential propagation in papillary muscle preparations. We therefore sought to determine whether the rate-dependent conduction slowing induced by procainamide in the intact canine heart is enhanced in myocardial tissue abnormally depolarized by an elevated myocardial extracellular potassium concentration, [K+]o. QRS duration and epicardial activation times were measured as indexes of myocardial conduction. QRS duration and epicardial activation times were measured at control (4.0 mM) and at intermediate (6.5 mM) and high (9.2 mM) myocardial [K+]o in the presence or absence of a clinically relevant procainamide concentration (12.2 +/- 2.6 g/ml) at the longest obtainable interstimulus interval of 440 msec and at 330, 280, and 250 msec. Intermediate and high myocardial [K+]o alone induced rate-dependent conduction slowing as the frequency of stimulation increased (cycle length 440 msec to 330, 280, and 250 msec). In the presence of procainamide, rate-dependent conduction slowing was observed at all levels of myocardial [K+]o, and the amount of rate-dependent change in conduction time increased as the myocardial [K+]o was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Skeletal muscle ventricles in circulation. One to eleven weeks' experience.

Skeletal muscle ventricles were constructed from canine latissimus dorsi and connected to the thoracic aorta in six dogs. These ventricles were stimulated to contract synchronously during diastole. The skeletal muscle ventricles were capable of continuous stroke work when placed within the arterial circulation for several weeks. Effective synchronous diastolic counterpulsation was produced. These results demonstrate that diastolic counterpulsators can be constructed from skeletal muscle and in the future may provide a feasible therapeutic alternative for the treatment of end-stage cardiac failure.

Animals↗
PubMed1986

A method for measurement of internal longitudinal resistance in papillary muscle.

We have modified the original Weidmann method for the measurement of internal longitudinal resistance in ventricular muscle by using air rather than silicon oil to insulate guinea pig papillary muscles and by omitting the tetrodotoxin inactivation of a portion of the preparation and have examined the requirements necessary for the theoretical assumptions to be satisfied by this or similar preparations. We found a homogeneous depolarization wavefront beyond about 1 mm from the stimulating electrodes. The adequacy of the interelectrode spacing was identified by a discrete plateau in the extracellular potential recording. The extracellular resistance in this preparation was sensitive to changes in the volume of the extracellular compartment, which we manipulated by changing inflow and outflow rates, and to changes in total ionic content of the superfusate. Our results establish the essential nature of maintaining constant flow rates and total ionic content and suggest that changes in volume and ionic content of a restricted extracellular space could conceivably influence conduction in vivo.

Action Potentials↗
PubMed1985

The effects of antiarrhythmic drugs, stimulation frequency, and potassium-induced resting membrane potential changes on conduction velocity and dV/dtmax in guinea pig myocardium.

For one-dimensional propagation, a nonlinear relationship between Vmax and conduction velocity is predicted by cable theory, and, under experimental conditions, Vmax and conduction velocity may change in opposite directions. Using standard microelectrode techniques, we have measured Vmax and conduction velocity in guinea pig papillary muscles exposed to tetrodotoxin and low sodium (agents expected primarily to decrease, directly, the rapid inward current), increased extracellular potassium (an agent which decreases the rapid inward current at least partially by inactivation mediated by depolarization of the resting membrane potential), and, over a wide range of stimulation frequencies, the antiarrhythmic drugs, quinidine, lidocaine, and procainamide. In all cases, except for the region of potassium-induced "supernormal conduction" between 5.4 and 9 mM, Vmax and conduction velocity varied as predicted by one-dimensional cable theory; that is, changes in Vmax were always proportional to changes in the square of conduction velocity. We conclude that the relationship between Vmax and conduction velocity predicted by cable theory occurs experimentally in guinea pig papillary muscle subjected to commonly used antiarrhythmic drugs and other interventions expected to reduce the sodium inward current. This relationship may be useful in applying known effects of drugs on Vmax to action potential propagation.

Animals↗