The influence of adenosine on left ventricular performance in conscious dogs.
Explore the source record for details and available documents.
Adenosine↗
Biomedical subjects
G L Freeman
Publications and source records attributed to G L Freeman.
Evaluation of long-term variance of left ventricular performance indexes in closed-chest dogs.
To assess the long-term variance of several parameters of left ventricular performance, we evaluated maximum rate of pressure development (dP/dtmax), ejection fraction, mean velocity of circumferential fiber shortening (VCF), the slope and volume-axis intercept of the end-systolic pressure-volume (PES-VES) relation, the stroke-work end-diastolic volume (SW-EDV) relation, and the dP/dtmax-EDV relation in six chronically instrumented dogs. Each dog was studied five times over a period of 3 wk in the conscious autonomically intact state, after autonomic blockade, and after administration of anesthesia. For each index under each set of testing conditions, a coefficient of variation was determined, defined as (SD/mean) x 100, and expressed as a percent. In conscious autonomically intact dogs, a low day-to-day variance was present in dP/dtmax (6.4%), ejection fraction (6.8%), mean VCF (6.5%), and the slope and volume intercept of the SW-EDV relation (7.2 and 6.2%), whereas higher variance was seen in the slope and intercept of the PES-VES relation (18.1 and 36.1%). The highest variance was present in parameters of the dP/dtmax-EDV relation. Thus dP/dtmax, ejection fraction, and the slope and volume intercept of the SW-EDV relation may be the most reliable indexes for long-term evaluation of left ventricular performance.
Animals↗
A simple method for measurement of left ventricular septal-lateral dimension.
In studies of myocardial performance of the intact heart, continuous measurement of the left ventricular septal-lateral diameter provides useful information. We describe a technique for placing a piezoelectric diameter gauge on the left ventricular endocardium of the intraventricular septum. This technique is simple and relatively atraumatic. It provides a way to evaluate septal-lateral dimension in either acute or chronic experiments and produces a stable signal that represents the instantaneous septal-lateral dimension of the left ventricle.
Animals↗
An unusual case of cardiac tamponade.
A 29-year-old woman with Ebstein's anomaly on anticoagulant therapy presented with chest pain. A diagnosis of pericarditis was made once a myocardial infarction and pulmonary embolus had been excluded. She was discharged but returned shortly thereafter with fever, tachypnea and tachycardia. A repeat chest film disclosed that the cardiac silhouette had enlarged greatly since prior admission. Despite the absence of pulsus paradoxus, right heart catheterization confirmed the clinical suspicion of pericardial tamponade.
Adult↗
Reduction of left ventricular mass in normal rats by captopril.
To assess the influence of captopril on left ventricular mass in 24 normal Sprague-Dawley rats, 12 were given high sodium (group 1) and 12 low sodium (group 2) diets. Half the rats given each diet were treated with 30 mg.kg-1/day captopril by gavage, the others were given placebo. Mean(SEM) arterial pressure was significantly reduced in group 2 treated rats (102.3(2.0) vs 123.4(1.5) mmHg, p less than 0.0002) but not in group 1 treated rats (113.8(2.5) vs 123.7(2.9)mmHg, NS). Blood pressure response to a 200 ng.kg-1 iv dose of angiotensin I was blocked in both group 2 (8.3(2.1) increase vs 29.7(3.6) mmHg increase for controls) and group 1 treated rats (7.8(2.8) increase vs 36.5(4.0) mmHg increase for controls). In group 2 treated rats the left ventricular to body weight ratio (X 10(-3)) was reduced compared with control (2.1(0.05) vs 2.4(0.08), p = 0.026), whereas in group 1 rats this ratio was not significantly different in the treated and control groups (2.3(0.06) vs 2.5(0.18), NS), suggesting that the reduction in left ventricular mass resulted from the influence of captopril on blood pressure. It is concluded that captopril causes a reduction in left ventricular mass in normal rats as a result of a reduction in blood pressure, independent of the effects of angiotensin I converting enzyme. This supports the concept that left ventricular mass is determined primarily by wall stress and is capable of both upward and downward regulation.
Animals↗
Effects of regional ischemia and ventricular pacing on LV dP/dtmax-end-diastolic volume relation.
We investigated the effects of coronary artery occlusion and pacing from ventricular sites on the relation of the maximum rate of rise of left ventricular pressure (dP/dtmax) to the end-diastolic volume (VED) in dogs previously instrumented to measure left ventricular pressure and to determine left ventricular volume from three ultrasonically measured dimensions. The dP/dtmax-VED relation was generated by vena caval occlusion and compared with the simultaneously produced end-systolic pressure-end-systolic volume (PES-VES) relation. The dP/dtmax-VED relation was described by a straight line during all conditions. Occlusion of the left circumflex coronary artery produced a rightward shift of the dP/dtmax-VED relation, increasing the volume intercept by 11.3 +/- 5.3 (SD) ml (P less than 0.05). Compared with atrial pacing, the dP/dtmax-VED relation was shifted to the right with the volume intercept increasing by 4.8 +/- 4.4 ml (P less than 0.05) during pacing from the right ventricular free wall, 3.7 +/- 5.0 ml (P less than 0.05) during pacing from the right ventricular apex, and 3.7 +/- 2.4 ml (P less than 0.05) during pacing from the left ventricular free wall. Similar increases were observed in the volume intercepts of the PES-VES relations during coronary occlusion or ventricular pacing. These results are consistent with the predictions of the time-varying elastance model and support its use as a conceptual framework to understand left ventricular performance during isovolumic contraction and at end systole, both in the normal ventricle and the ventricle with regional abnormalities of contraction.
Animals↗
Description of LV pressure-volume relations by time-varying elastance and source resistance.
If the left ventricle (LV) behaves as a time-varying elastance [E(t)] that is independent of load, then definition of E(t) during normal ejecting beats should permit accurate prediction of LV pressure (LVP) during a maximally afterloaded (isovolumic) beat. We tested this hypothesis in six dogs preinstrumented to measure LVP and aortic flow (Q) and to determine LV volume (V) from three dimensions. LVP and V were varied by caval occlusions. These data were used to determine E(t) and minimal volume required to generate pressure (Vo) at 10-ms intervals during systole using a simple E(t) model, P(t) = E(t) [V(t)-Vo], where P(t) is LVP at any time after the onset of contraction, and V(t) is the LV volume at t. LVP was measured during isovolumic beats generated by sudden balloon occlusion of the ascending aorta. The simple E(t) model accurately predicted isovolumic LVP during the first 70 ms of systole (r = 0.99) and also the end-systolic LVP but underestimated LVP during midsystole by 48 +/- 5 (SD) mmHg (P less than 0.05). When a pressure-dependent source resistance (K = 0.0015 s/ml) was added to the model to reduce LVP in proportion to Q, such that P(t) = E(t) [V(t)-Vo] X [1 - KQ]), LVP during the isovolumic beat was accurately predicted throughout systole (r = 0.99). However, the time to develop peak isovolumic pressure was 22 +/- 7 ms less than predicted. Similar results were obtained during inotropic stimulation with dobutamine in five animals.
Animals↗
Echocardiographic left ventricular mass and function in the hypertensive baboon.
Nonhuman primates with chronic systemic hypertension provide an ideal model for studying structural and functional alterations associated with compensatory cardiac hypertrophy. Since noninvasive techniques are useful for the longitudinal evaluation of these animals, we sought to critically asses the M-mode echocardiographic estimation of left ventricular mass in the baboon and to characterize estimates of left ventricular size and function in baboons with chronic renal hypertension. In 23 baboons (12 normotensive, 11 chronic hypertensive), M-mode echocardiography-determined left ventricular mass was 73 +/- 13 (SE) g as compared with the necropsy weight of 69 +/- 11 g (p = NS), and the correlation was excellent (r = 0.94). When 30 chronically hypertensive baboons being observed longitudinally were compared with 10 normotensive control animals studied under identical conditions, several differences were noted in measures derived from echocardiography and high fidelity pressure measurements. Left ventricular systolic pressure was considerably higher in the hypertensive baboons (113 +/- 23 vs 90 +/- 11 mm Hg; p less than 0.001), as was left ventricular mass (148 +/- 60 vs 103 +/- 38 g; p less than 0.03). However, since the ratio of posterior wall thickness to cavity dimension was larger in the hypertensive baboons (0.52 +/- 0.17 vs 0.43 +/- 0.07; p less than 0.05), this concentric hypertrophy maintained values for left ventricular meridional stress at the same level as in the control animals. Despite matched heart rate and left ventricular stress, the rates of change in left ventricular dimensions and wall thickness in systole and diastole were all approximately 25% less in the hypertrophied baboons.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Influence of heart rate on left ventricular performance in conscious dogs.
The effects of atrial pacing on the left ventricular end-systolic pressure-volume relation, a relatively load-insensitive index of left ventricular performance, were studied in 8 chronically instrumented, conscious dogs. Six of the dogs were studied while autonomically intact, and 2 were studied after autonomic blockade with 2 mg/kg i.v. propranolol and 0.2 mg/kg i.v. atropine. Left ventricular pressure was measured with a micromanometer and left ventricular volume was determined from 3 ultrasonic orthogonal dimensions. Pressure was varied by caval occlusions at control heart rate and after atrial pacing at 100, 120, 140, 160, 180, and 200 bpm. The end-systolic pressure-volume relation was linear in every case (r = 0.97 +/- 0.03, SD). In the autonomically intact dogs, Emax, the slope of the end-systolic pressure-volume relation, was directly and monotonically related to heart rate in every dog, increasing to 238 +/- 99% of control at peak pacing rate (p less than 0.05). V0, the zero pressure intercept of the relation was also directly related to heart rate in every dog and increased 8.6 +/- 5.5 ml from control to peak pacing rate (p less than 0.05). Autonomic blockade did not attenuate these effects. This rightward shift of the end-systolic pressure-volume relation results in a reduced stroke volume from any end-diastolic volume, modulating the hemodynamic benefits of enhanced contractility. T, the time constant of isovolumic pressure fall during ventricular relaxation, was determined from beats with matched end-systolic pressures. T was related to heart rate, falling by 20 +/- 10.3% over the range of rates studied in the autonomically intact dogs and by 23.1 +/- 6.2% in the autonomically blocked dogs. Thus, the ventricle relaxes more rapidly at higher heart rates. We conclude that the frequency of contraction is concluded as an important determinant of overall pump function throughout the cardiac cycle in conscious dogs.
Animals↗
Comparison of effects of dobutamine and ouabain on left ventricular contraction and relaxation in closed-chest dogs.
Because catecholamines and digitalis have different effects on the time course of myocardial intracellular calcium concentration, their effects on the time course of left ventricular contraction and relaxation may also be different. To study this question, dogs were instrumented to measure left ventricular pressure and determine left ventricular volume from three ultrasonic dimensions. After full recovery from the instrumentation, the effects of dobutamine (2-10 micrograms/kg), ouabain (0.5 mg i.v.) alone, and ouabain given after propranolol (2 mg/kg i.v.), or phentolamine (5 mg i.v.) and incremental doses of ouabain (0.25-0.75 mg i.v.) were assessed on different days. Left ventricular pressure and volume were varied by caval occlusions. Dobutamine significantly increased the slope of the left ventricular end-systolic pressure-volume relation (Emax) and the slope of the dP/dtmax-end-diastolic volume relation (dE/dtmax), while significantly decreasing the time from end-diastole to end-systole (tmax) and the time constant (T) of the isovolumic fall in left ventricular pressure. Ouabain also increased Emax and dE/dtmax but did not alter tmax or T. Dobutamine produced a greater increase in dE/dtmax than in Emax, whereas ouabain produced similar increases in both. These effects of ouabain were not altered by pretreatment with propranolol or phentolamine. We conclude that although dobutamine and ouabain are both positive inotropes that increase Emax, dobutamine speeds the rate of left ventricular contraction (tmax) and relaxation (T), whereas ouabain does not. These effects of ouabain and dobutamine on global parameters of left ventricular chamber performance mirror their influence on intracellular calcium availability. Furthermore, these observations are consistent with the predictions of the time-varying elastance model of the left ventricle and support its usefulness as a conceptual framework to understand and link events occurring during isovolumic contraction, end-systole, and isovolumic relaxation.
Animals↗
Stroke in young people--the heart of the matter.
Explore the source record for details and available documents.
Adult↗
Comparison of the cardiovascular effects of intravenous and intraaortic protamine in the conscious and anesthetized dog.
Controversy exists as to whether intraaortic (IA) administration of protamine sulfate has less adverse effects than the intravenous (IV) route. The effect of protamine on contractility is not well established. Therefore, 9 dogs underwent chronic instrumentation to monitor aortic pressure (AP), left ventricular (LV) pressure, central venous pressure, cardiac index (CI), heart rate, stroke volume index (SVI), systemic vascular resistance index, and LV volume. The end-systolic LV pressure-volume relationship was used as a load-independent measure of contractility. Each dog was administered IV and IA protamine on separate occasions after pretreatment with heparin. Studies were performed with and without anesthesia. In the awake studies, analysis of variance showed greater decreases in mean AP (p less than .03), CI (p less than .05), and SVI (p less than .02) with IA protamine infusion. In the anesthetized animals, there were no significant differences between IA and IV administration of protamine. Protamine did not decrease contractility in any group. We conclude that IA administration of protamine offers no advantage over IV administration in the dog. Protamine does not decrease contractility when given by either route.
Analysis of Variance↗
Comparison of in situ and in vitro studies of pericardial pressure-volume relation in dogs.
Whether the material properties of the pericardial membrane are the key determinants of the in situ pericardial pressure-volume relation is not known. Although both the pressure-volume relation of the intact pericardium and the stress-strain relation of isolated pericardial samples are nonlinear, it is not clear how closely these phenomena are related. To directly examine this question we compared the pressure-volume, pressure-normalized volume, and stress-strain relations of pericardia from six dogs tested both in situ and in vitro. The curves generated under the two sets of conditions were different. The transition from the compliant to the noncompliant portion of the curve was more acute under in vitro conditions. Nonlinear regression analysis using a monoexponential function of the form Y = alpha (e beta chi-1) showed beta, the proportionality constant for the slope of the curve, to be larger for each form of analysis under in vitro testing conditions as follows: 0.002 +/- 0.009 vs. 0.078 +/- 0.029, P less than 0.002 for pressure-volume; 3.52 +/- 1.75 vs. 11.03 +/- 5.31, P less than 0.005 for pressure-normalized volume; and 19.6 +/- 6.6 vs. 62.3 +/- 18.8, P less than 0.001 for stress-strain. These differences in the pressure-volume relation of the intrapericardial space in situ and the isolated pericardium in vitro suggest that pericardial attachments present in situ may buffer the loading of the membrane itself. We conclude that the pressure-volume relation of the intrapericardial space is only partly determined by the properties of the isolated pericardium alone and is also influenced by other components of the intact pericardium.
Animals↗
Determinants of intrapericardial pressure in dogs.
This study investigates factors that influence the pressure measured in the intrapericardial (IP) space. Seven dogs were studied after they were anesthetized with pentobarbital sodium. With the chest closed, intravascular volume expansion by dextran infusion from a mean left atrial (LA) transmural pressure of 8.4 +/- 1.2 (SD) to 15.5 +/- 1.6 Torr caused an increase in mean IP of from 2.6 +/- 1.2 to 3.9 +/- 1.7 Torr (P less than 0.01). This reflected a predominant increase in the influence of the cardiac fossa (CF), which accounted for 56% of the IP pressure after volume expansion. In the open-chest state an increase in mean LA transmural pressure from 9.5 +/- 2.5 to 16.4 +/- 0.6 Torr caused IP pressure to increase from 1.1 +/- 0.9 to 3.0 +/- 1.6 (P less than 0.005), representing the influence of the elastic pericardium alone. The use of positive end-expiratory pressure (PEEP) significantly increased the influence of the CF. Of note, the relation of LA to right atrial (RA) pressure was significantly different with and without the influence of the CF; the RA-to-LA ratio was higher with the chest open under each set of volume conditions with and without PEEP. In four dogs, acute transection of the pericardiodiaphragmatic ligaments led to a small (1-2 Torr) but distinct drop in IP pressure. Thus, IP pressure is affected by the intracardiac volume, the elastic pericardium, the CF, and the pericardiodiaphragmatic attachments, all of which must be considered in an analysis of diastolic properties of the heart in situ.
Animals↗
The effect of vasoactive agents on the left ventricular end-systolic pressure-volume relation in closed-chest dogs.
The left ventricular end-systolic pressure-volume relation has received intense interest as a relatively load-insensitive measure of cardiac performance. In clinical studies, pharmacologic manipulation of blood pressure has been used to determine this relation. Since previous studies have shown that acute changes in the resistance and impedance of the arterial circulation influence the left ventricular end-systolic pressure-volume relation, the use of vasoactive drugs in its determination may affect the results achieved. This study was undertaken to determine whether clinically used vasoactive drugs influence the left ventricular end-systolic pressure-volume relation. Sixteen dogs were previously instrumented with micromanometer pressure transducers and three sets of piezoelectric crystals to permit determination of left ventricular pressure and volume. The dogs were studied after autonomic blockade and sedation. End-systolic pressure-volume relations were generated by caval occlusion at control levels of blood pressure, after infusion of a vasopressor (methoxamine, n = 6; angiotensin II, n = 10), and then after infusion of nitroprusside. A composite end-systolic pressure-volume relation was also constructed with the use of control, vasopressor, and vasodilator points in each dog. Angiotensin II resulted in a leftward shift in the relation (Vo decreased from 14.32 +/- 7.3 to 8.04 +/- 10.4 ml, p less than .05) with no significant effect on slope. Methoxamine shifted the relation to the left (Vo decreased from 13.98 +/- 8.74 to -0.47 +/- 12.06 ml, p less than .05) and also reduced the slope (5.41 +/- 3.09 vs 8.28 +/- 3.94 mm Hg/ml, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin II↗
Simultaneous determination of left ventricular end-systolic pressure-volume and pressure-dimension relationships in closed-chest dogs.
The left ventricular end-systolic pressure-volume relationship is a load-insensitive measure of left ventricular performance. The relationship at end-systole between left ventricular pressure and dimension is more easily obtained, but the conflicting results of previous studies make it unclear if it has the same properties as the left ventricular end-systolic pressure-volume relationship. To address this issue, 11 dogs were instrumented to measure left ventricular pressure and three orthogonal left ventricular dimensions. Left ventricular pressure and dimensions were varied by use of caval occlusion. Left ventricular volume was calculated as an ellipsoid. The left ventricular end-systolic pressure-volume relationship and each of the three end-systolic pressure-dimension relations were described by straight lines (r = .97 +/- .02, mean +/- SD). In six animals, dobutamine produced similar significant increases (p less than .01) in the slope of the end-systolic pressure-volume relationship (244 +/- 61% of control), the end-systolic pressure-anterior-posterior dimension relationship (248 +/- 89%), the end-systolic pressure--septal-lateral dimension relationship (211 +/- 95%), and the end-systolic pressure-basal-apical dimension relationship (210 +/- 85%). The intercepts at zero pressure were relatively unchanged by dobutamine. In contrast, occlusion of the distal left anterior descending coronary artery in five animals produced a rightward shift of the left ventricular end-systolic pressure-volume relationship and the pressure--basal-apical dimension relationship, while the pressure--anterior-posterior dimension and pressure--septal-lateral dimension relationships were relatively unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Relationship between myocardial fiber direction and segment shortening in the midwall of the canine left ventricle.
Myocardial fiber orientation undergoes an orderly transition from the epicardium to the endocardium in the left ventricle, with circumferential fibers predominating in the middle one-third of the heart wall. How fibers lying at different depths in the myocardium, running in different directions, interact to produce local deformation is not known. To define the relationship between the orientation of uniaxial myocardial fibers and local wall motion, we placed three sets of ultrasonic dimension gauges in the middle one-third of the apex-to-base distance of the left ventricle of nine dogs. One pair was placed in line and two intentionally out of line with the presumed local fiber direction. The relative angle between the gauge and the local myofibers was determined by the use of postmortem radiography and histological techniques. Our results show that in the midwall of the left ventricle, myocardial segment shortening is maximal in the direction of local fibers; the shortening measured by gauges placed out of line with the local fiber axis by more than 30 degrees was significantly less than the actual in-line fiber shortening which occurred. This suggests that functional tethering between midwall fibers and endocardial or epicardial fibers does not play a major role in the pattern of midwall deformation. We also documented that an external reference line can be used to predict midwall myofiber direction. Using this line as a guide, ultrasonic dimension gauges could be placed within an average of 12 degrees (range: 0.5 to 18.5 degrees) from the local fiber axis.
Animals↗
Production of the lymphokine soluble immune response suppressor (SIRS) during chronic experimental schistosomiasis mansoni.
Chronic schistosomiasis mansoni is a helminthic infection characterized by cell-mediated anti-egg granulomatous reactions and a variety of associated immunoregulatory phenomena. Soluble immune response suppressor (SIRS) is a lymphokine produced by activated suppressor T lymphocytes in various experimental settings. This report demonstrates the presence of SIRS in the sera of mice with chronic schistosomiasis mansoni (at least 20 wk of infection), but not in the sera of mice with earlier infections. Also, cultures of isolated, intact, hepatic, egg-focused granulomas from chronically infected mice released detectable levels of SIRS. These are the immunomodulated lesions characteristic of this infection. Large, intense, unmodulated granulomas obtained from acutely infected mice did not release SIRS. There is, therefore, a strong association between the presence of SIRS in the serum, the production of SIRS by intact lesions, and the chronic, immunomodulated stage of schistosomiasis mansoni.
Animals↗