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Biomedical subjects

K Sagawa

Publications and source records attributed to K Sagawa.

At least 163 records · Page 9Linked to original sources
PubMed1985

Accuracy of volume measurement by conductance catheter in isolated, ejecting canine hearts.

We evaluated the accuracy of the recently reported technique of estimating intraventricular volume by measurement of intracavitary electrical conductance in six isolated, ejecting, canine left ventricles. Left ventricular volumes were measured directly by a previously validated servosystem that employed an electroconductive balloon placed in the left ventricular cavity. The volume measured continuously by the balloon method (Vbal) was compared with that estimated by the conductance method (Vcath). For this test, the hearts were made to eject and fill physiologically by the use of a previously described computer-simulated arterial loading system. Complex ejection and filling patterns were created by stimulating the atrium mechanically, which resulted in irregular arrhythmatic contractions spanning a wide range of volumes. We found that there was a highly linear relationship (r2 = .982 +/- .014) between Vbal and Vcath: Vcath = 0.82 (+/- .05) Vbal + 26.7 (+/- 11.8) ml. Despite the wide variation in the offset term of this relationship among the different hearts, the offset within a given heart was predicted within 3.5 ml by a previously detailed "dilution" method that is applicable to the heart in situ within a closed thorax. Thus, since the offset term is obtainable in situ, the conductance method provides a signal that is proportional to the actual volume. To determine whether right ventricular volume influenced the accuracy of left ventricular measurement, we compared the relationship between Vcath and Vbal obtained with right ventricular volumes of 0 and 30 ml. Increasing the right ventricular volume shifted the relationship upward by less than 3 ml in the working range.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of heart rate on the canine end-systolic pressure-volume relationship.

Although the rate dependence of isolated muscle contractility is well known, the ventricular end-systolic pressure-volume relationship (ESPVR) has been reported to be insensitive to heart rate. To resolve this contradiction, we used an isolated, ejecting canine heart preparation perfused at a constant coronary arterial pressure. Heart rate was changed from 60 to 200 beats/min in steps of 20 beats/min. At least 10 pressure-volume loops under different filling pressures were obtained at each heart rate in each of six hearts. Over a heart rate range from 60 to 120 beats/min, the slope of the ESPVR (Ees) increased significantly from 3.5 +/- 0.4 (SE) to 5.3 +/- 0.6 mm Hg/ml. In the range between 120 and 180 beats/min there was little change in Ees (5.3 +/- 0.6 to 5.4 +/- 0.6 mm Hg/ml), but at 200 beats/min Ees increased slightly to 5.7 +/- 0.5 mm Hg/ml. The volume axis intercept (V0) of the ESPVR changed little over the range of heart rate from 60 to 160 beats/min (10.2 +/- 2 ml to 9.4 +/- 1.3 ml) but increased to 15.2 +/- 1.2 ml at a rate of 200 beats/min. The change in ESPVR with increase in heart rate from 60 to 120 beats/min (i.e., increase in Ees without change in V0) is the same as those seen with a positive inotropic intervention with calcium or cathecholamines, whereas the V0 changes over the range from 160 to 200 beats/min is similar to those seen with regional ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Postextrasystolic potentiation of the isolated canine left ventricle. Relationship to mechanical restitution.

We established, for the isolated, isovolumically beating canine left ventricle, a comprehensive description of postextrasystolic contractile strength (dP/dtmax) as a function of extrasystolic and postextrasystolic stimulus intervals. In contrast to previous studies of postextrasystolic beats in in situ hearts, these isolated ventricles contracted isovolumically so that dP/dtmax was not affected by fluctuations in preload and afterload and was therefore considered to be a reliable index of intrinsic contractility. With the interval preceding extrasystoles constant, postextrasystolic contractile strength increased monoexponentially to a plateau as the interval preceding postextrasystoles lengthened, with a mean time constant (+/- SD) of 182 +/- 44 msec (n = 53). The onset of this increase in postextrasystolic contractile strength coincided with repolarization of the extrasystolic action potential. With the interval preceding postextrasystoles held constant and long (1200 msec), postextrasystolic contractile strength decreased according to a monoexponential function as the interval preceding extrasystoles lengthened [mean time constant (+/- SD) of 176 +/- 18 msec (n = 10)]. These phenomena could be quantitatively summarized by a single equation description of postextrasystolic contractile strength which involved monoexponential functions with one time constant. The mathematical form of this description led us to a simple interpretation of these phenomena in terms of currently proposed excitation-contraction coupling models of the heart.

Animals↗
PubMed1985

Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle.

In a previous analysis of ventricular arterial interaction (Sunagawa et al., 1983), we represented the left ventricle as an elastic chamber which periodically increases its volume elastance to a value equal to the slope of the linear end-systolic pressure-volume relationship. Similarly, the arterial load property was represented by an effective elastance which is the slope of the arterial end-systolic pressure-stroke volume relationship. Since the maximal transfer of potential energy from one elastic chamber to another occurs when they have equal elastance, we hypothesized that the left ventricle would do maximal external work if the ventricular elastance and the effective arterial elastance were equal. We tested this hypothesis in 10 isolated canine left ventricles, ejecting into a simulated arterial impedance, by extensively altering arterial resistance and finding the optimal resistance that maximized left ventricular stroke work under various combinations of end-diastolic volume, contractility, heart rate, and arterial compliance. Each of these parameters was set at one of three levels while others were at control. The optimal resistance varied only slightly with arterial compliance, whereas it varied widely with contractility and heart rate. We thus determined that the ratio of the optimal effective arterial elastance to the given ventricular elastance remained nearly unity. This result supports the hypothesis that the left ventricle does maximal external work to the arterial load when the ventricular and arterial elastances are equalized.

Animals↗
PubMed1985

Mechanoelectrical feedback: independent role of preload and contractility in modulation of canine ventricular excitability.

Mechanoelectrical feedback, defined as changes in mechanical state that precede and alter transmembrane potential, may have potential importance in understanding the role of altered load and contractility in the initiation and modulation of ventricular arrhythmias. To assess the independent effects of preload and contractility on myocardial excitability and action potential duration, we determined the stimulus strength-interval relationship and recorded monophasic action potentials in isolated canine left ventricles contracting isovolumically. The strength-interval relationship was characterized by three parameters: threshold excitability, relative refractory period, and absolute refractory period. The effects of a threefold increase in left ventricular volume or twofold increase in contractility on these parameters were independently assessed. An increase in preload did not change threshold excitability in 11 ventricles but significantly shortened the absolute refractory period from 205 +/- 15 to 191 +/- 14 ms (P less than 0.001) (mean +/- SD). Similarly, the relative refractory period decreased from 220 +/- 18 to 208 +/- 19 ms (P less than 0.002). Comparable results were observed when contractility was increased as a result of dobutamine infusion in 10 ventricles. That is, threshold excitability was unchanged but the absolute refractory period decreased from 206 +/- 14 to 181 +/- 9 ms (P less than 0.003), and the relative refractory period decreased from 225 +/- 17 to 205 +/- 18 ms (P less than 0.003). Similar results were obtained when contractility was increased with CaCl2, indicating that contractility associated changes were independent of beta-adrenergic receptor stimulation. An increase in preload or contractility was associated with shortening of the action potential. A threefold increase in preload and twofold increase in contractility were associated with a decrease in action potential duration of 22 and 24 ms, respectively. There was a significant linear correlation between action potential duration and excitability (absolute refractory period). The similar effects of increased preload and contractility on threshold excitability and refractoriness can be explained by the action these perturbations have on the time course of repolarization. Therefore, excitability of the ventricle is sensitive to and is modulated by alteration of load or inotropic state. The similar effects of either increased preload or contractility on excitability may be mediated by a common cellular mechanism which results in a rise in intracellular free Ca2+ and secondary abbreviation of the action potential.

Action Potentials↗
PubMed1985

"Pan-myeloid" reagent: the monoclonal antibody MCS-2 in the routine immunodiagnostic service of leukemia phenotyping.

This retrospective analysis describes the reactivity of several monoclonal antibodies (MoAbs) which detect myelomonocytic antigens of the cells of 182 leukemias. These leukemias were assigned to definite subtypes of lymphocytic and myelo(mono)-cytic leukemias on the basis of standard leukemia phenotyping using morphological, cytochemical, isoenzymatic and mainly immunological criteria. The MoAb MCS-2 was negative in all cases of lymphocytic leukemia, whereas two of the three other commonly used "myeloid MoAbs" MCS-1, OKM-1 and 1/12/13 showed positivity in B-chronic lymphocytic leukemia (B-CLL), B-lymphoma (MCS-1), T-acute lymphoblastic leukemia (T-ALL) and Sézary syndrome (OKM-1). MCS-2 was positive in all samples of acute myelomonoblastic leukemia (AMMoL), chronic myelocytic leukemia (CML) and CML-myeloid blast crisis, which was not the case for MCS-1, OKM-1, or 1/12/13. In 14 cases (11 acute myeloblastic leukemia (AML), 3 CML-myeloid blast crisis) where MCS-2 was positive and one or all of the three other MoAbs were negative, the cells were mainly Ia-positive and peroxidase-negative. MCS-2 is a diagnostically important MoAb in the routine leukemia phenotyping of myelomonocytic leukemias. After having tested a large number of normal and malignant specimens, we would like to term MCS-2 a "pan-myeloid MoAb" reacting with the myelomonocytic cell lineage from the earliest myeloblast to granulocytes and monocytes.

Antibodies, Monoclonal↗
PubMed1984

Ventricular interaction with the loading system.

The purpose of this investigation was to develop a theoretical framework to predict stroke volume (and therefore cardiac output) when the ventricle is coupled with the arterial impedance. The ultimate objective is to arrive at an analytical description of cardiac output in the closed hydraulic loop of the entire circulatory system on the basis of the properties of the major system components. We developed the framework of analysis of ventriculo-arterial coupling by characterizing both the ventricle and arterial system in terms of the end-systolic pressure vs. stroke volume (Pes-SV) relationships. This approach, motivated by the load-insensitivity of ventricular end-systolic pressure-volume relationship (ESPVR), yielded stroke volume as the intersection between the ventricular Pes-SV relationship and arterial Pes-SV relationship. The theoretical outcome was validated by comparing the stroke volume predicted as a result of interaction between a given ventricular ESPVR and a set of arterial impedances against those SVs actually measured by imposing the same arterial impedance on the isolated canine ventricles. Furthermore, because of the mathematical simplicity of this approach, it enabled us to describe cardiac output in the closed circulatory loop with a small set of analytical equations. We conclude that the proposed framework is useful in analyzing the ventriculo-arterial coupling and various mechanisms which affect cardiac output in the closed circulatory loop.

Arteries↗
PubMed1984

Mechanical restitution of isolated perfused canine left ventricles.

We measured cardiac mechanical restitution curves, which describe the time course of recovery of ventricular contractile strength following a steady-state beat. In the first series of experiments, we studied left ventricles that beat isovolumically throughout the experiment, allowing use of dP/dtmax as a reliable index of contractile strength independent of the influence of changing ventricular pre- and afterload. The commencement of mechanical restitution was found to be associated with the onset of electrical diastole; thereafter, contractile strength rose monoexponentially to a plateau that was maintained for test pulse intervals as long as 15 s. The time constant of restitution (typically 245 ms) was independent of priming frequency and ventricular volume. These findings were interpreted in terms of a model of intracellular calcium fluxes within the myocardial cells. In a second series of experiments, we measured mechanical restitution curves from isolated ventricles that ejected against a simulated arterial impedance system. Under this condition, we did not observe the monoexponential time course of mechanical restitution as was measured under isovolumic conditions. The differences between the mechanical restitution curves measured under isovolumic and ejecting conditions were attributed to the influences of changing hemodynamic conditions on dP/dtmax that caused it to be an unreliable index of contractile strength.

Animals↗
PubMed1984

Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia.

To determine the effects of different anesthesias on the performance of the arterial baro-reflex, the open-loop characteristic of the carotid sinus reflex was analyzed in 24 rabbits under anesthesia with pentobarbital (30 mg/kg), urethan (800 mg/kg), alpha-chloralose (80 mg/kg), or a mixture of alpha-chloralose (40 mg/kg) and urethan (0.4 g/kg). For each rabbit and anesthesia, mean systemic arterial pressure and heart rate were measured as carotid sinus pressure was changed in 10-mmHg steps between 40 and 150 mmHg. This set of measurements was repeated four times at 1-h intervals. A logistic function curve was fitted to the carotid sinus pressure-arterial pressure relationship. The parameters of this curve were then analyzed to delineate the specific effects of the anesthesias on the relationship. The main finding was that the response range and the slope parameters under alpha-chloralose anesthesia were significantly smaller than those obtained under the other anesthesias. Propylene glycol, used as the solvent for chloralose, did not affect the reflex control of arterial pressure or heart rate. The reflex under chloralose-urethan anesthesia showed characteristics similar to those under urethan anesthesia. We conclude that although alpha-chloralose has traditionally been used in the dog to obtain strong reflex responses, it weakens the reflex control of arterial pressure in the rabbit.

Anesthesia, General↗
PubMed1984

Effect of thiamylal on the response to carotid occlusion and mild hemorrhage in rabbits.

The effects of anesthesia (thiamylal, 30 mg/kg) on steady-state mean arterial pressure responses to bilateral carotid occlusion (BCO) and rapid 8% hemorrhage were studied in 11 rabbits chronically instrumented with an arterial pressure catheter and balloon occluders on the common carotid arteries. The BCO was repeated in the conscious and anesthetized states both before and after transecting the aortic nerves (AN). With the AN intact, the BCO response was an increase in mean systemic arterial pressure of 23.6 +/- 2.1 (SE) mmHg in the conscious state and 24.7 +/- 1.2 in the anesthetized state. With the AN cut (AN) BCO response was 46.2 +/- 1.7 mmHg in conscious state and 45.7 +/- 2.6 in anesthetized state. There was no significant difference in BCO response between conscious and anesthetized states, whether the AN was present or absent. The hemorrhage experiment was repeated on separate days under various conditions, including carotid sinus reflex elimination (CS). With AN intact the posthemorrhage fall in mean arterial pressure (delta MAPh) was 3.2 +/- 0.6 mmHg in the conscious state. Under anesthesia, delta MAPh was 3.4 +/- 0.6 mmHg in the AN intact condition, 7.3 +/- 0.9 in AN, and 34.5 +/- 6.8 in (AN + CS). There was no significant difference in delta MAP between the conscious and anesthetized states under the intact AN condition. We conclude that, in the rabbit, thiamylal anesthesia has little effect on the BCO response and the restoration of arterial pressure after a mild hemorrhage.

Anesthesia, General↗
PubMed1984

Short-term memory in the in situ canine myocardium.

We studied the effect of intracycle (short-term) mechanical history on canine myocardial performance. Intracycle muscle force and/or length history was varied, and the resultant changes in end-systolic force-length relationship were analyzed. Antecedent isotonic shortening impaired, whereas isometric force development enhanced end-systolic myocardial performance. A history of shortening concurrent with force development produced an intermediate effect. We conclude that decreasing force or length impairs whereas increasing length or force enhances performance in the same cycle. Different combinations of antecedent force and length changes affect end-systolic performance by algebraic summation (superposition) of their disparate effects. Time measurements established that 1) total systolic time varied little with altered history, 2) isotonic shortening took longer than isometric contraction in reaching a point P in the force-length plane, and 3) less time was therefore available for contraction after P with antecedent isotonic shortening than with antecedent isometric force development. This history-dependent time differential accounts for the corresponding differential in performance.

Animals↗