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Biomedical subjects

M Takaki

Publications and source records attributed to M Takaki.

At least 73 records · Page 4Linked to original sources
PubMed1996

Left ventricular volumetric conductance catheter for rats.

Left ventricular (LV) volume (V) is an essential parameter for assessment of the cardiac pump function. Measurement of LVV in situ by a conductance catheter method has been widely used in dogs and humans but not yet in small experimental animals such as rats. We instituted a miniaturized six-electrode conductance catheter (3-F) for rat LVV measurement and its signal processing apparatus. We compared stroke volumes (SVs) simultaneously measured with this conductance catheter introduced into the LV through the apex and an electromagnetic flow probe placed on the ascending aorta during gradual decreases in LVV by an inferior vena caval occlusion. A high and linear correlation (r = 0.982) was obtained between these differently measured by SVs pooled from six rats. In another group of three rats, LV pressure was simultaneously measured with a 3-F catheter-tip micromanometer introduced into the LV through the apex. We obtained the slope of the end-systolic pressure-volume (P-V) relationship (Emax) by a gradual ascending aortic occlusion. After administration of propranolol, Emax obviously decreased with no change in volume intercept of the P-V relationship. The conductance volumetry proved to be useful in rats.

Animals↗
PubMed1995

Logistic time constant of isovolumic relaxation pressure-time curve in the canine left ventricle. Better alternative to exponential time constant.

BACKGROUND: The time constant of left ventricular (LV) relaxation derived from a monoexponential model has been widely used as an index of LV relaxation rate or lusitropism, although this model has several well-recognized problems. In the present study, we proposed a logistic model and derived a "logistic" time constant (TL) as a better alternative to the conventional "exponential" time constant (TE). METHODS AND RESULTS: A total of 189 beats (147 isovolumic and 42 ejecting beats) were investigated in seven canine excised cross-circulated heart preparations. We found that the logistic model fitted much more precisely all the observed LV isovolumic relaxation pressure-time [P(t)] curves than the monoexponential model (P < .05). The logistic model also fitted well both the time curve of the first derivative of the observed P(t) (dP/dt) and the dP/dt-P(t) phase-plane curve. Like TE, TL indicated that volume loading depressed LV lusitropism and that increasing heart rate and ejection fraction augmented it. TL was independent of the choice of cutoff point defining the end of isovolumic relaxation; TE was dependent on that choice. CONCLUSIONS: We conclude that the logistic model better fits LV isovolumic relaxation P(t) than the monoexponential model in the present heart preparation. We therefore propose TL as a better alternative to TE for evaluating LV lusitropism.

Animals↗
PubMed1995

Suppression of myocardial mitochondrial respiratory function in acute failing hearts made by a short-term Ca2+ free, high Ca2+ coronary perfusion.

We made acute cardiac failure in excised cross-circulated canine hearts by a new coronary perfusion protocol consisting of Ca2+ free Tyrode perfusion for the first 10 min, high Ca2+ (16 mmol/l) Tyrode perfusion for the next 5 min, and normal Tyrode perfusion for the last 5 min interrupting blood cross circulation. After 50 min from the blood recirculation, left ventricular contractility was stably depressed to 60% of control. We studied mechanoenergetics of these acute failing hearts for the next 1-3 h. Then, we prepared mitochondria from these excised failing hearts and the support dogs' normal hearts to examine their mitochondrial respiratory function by the respiratory control index (RCI) and the oxygen consumption rate in state III (State III O2). RCI and State III O2 were significantly smaller in the failing hearts than in the normal hearts. However, sham protocol consisting of normal Tyrode coronary perfusion for 20 min did not affect RCI and State III O2. These results revealed that the mitochondrial respiratory function was moderately impaired in these acute failing hearts made by the new short-term Ca2+ intervention. However, no ultrastructural injuries of mitochondria were detected in these failing hearts.

Animals↗
PubMed1995

Ca(2+)-free, high-Ca2+ coronary perfusion suppresses contractility and excitation-contraction coupling energy.

We studied the mechanoenergetic effects of a short-term Ca(2+)-free, high-Ca2+ Tyrode solution coronary perfusion in eight excised, cross-circulated canine hearts. The perfusion protocol consisted of coronary perfusion with Ca(2+)-free Tyrode solution for 10 min followed by high-Ca2+ (16 mM) Tyrode solution for 5 min. This new protocol successfully induced acute contractile failure in seven hearts, without myocardial ultrastructural changes. We studied the end-systolic pressure-volume relation (slope = Emax, a contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA) in these failing hearts. These hearts had no increase in end-diastolic pressure at a given volume, a 40% decrease in Emax and a proportional decrease in the PVA-independent VO2 for 1-4 h, but no decrease in the oxygen cost of PVA, defined as the slope of the VO2-PVA relation. The oxygen cost of Emax for Ca2+ handling, defined as the slope of the relation between PVA-independent VO2 and Emax, was unchanged in the failing hearts. We conclude that the present protocol induced left ventricular contractile failure, primarily involving the suppression of Ca2+ handling energy for excitation-contraction coupling.

Animals↗
PubMed1995

Logistic characterization of left ventricular isovolumic pressure-time curve.

Although some investigators have attempted to express the left ventricular pressure-time curve by mathematical functions such as exponential and sinusoidal functions, none of them reasonably fits the left ventricular pressure-time curve. In the present study, we hypothesized that a ventricular isovolumic pressure-time curve could be expressed as the difference between two S-shaped curves for pressure rising and falling, and proposed a new "hybrid logistic" function to express the left ventricular isovolumic pressure-time curve. We investigated how well this hybrid logistic function fits left ventricular isovolumic pressure curves experimentally observed under physiological preload and contractility in the excised cross-circulated left ventricles of 10 dogs. The new function precisely fitted the isovolumic pressure curves regardless of preload and contractility with correlation coefficients above 0.9996, much better than the previously proposed functions. The observed values characterizing the magnitude and time course of the isovolumic pressure curve such as peak +/- dP/dt also closely correlated with the corresponding theoretical values calculated by the present best-fit function. We conclude that our new hybrid logistic function reasonably characterizes the canine left ventricular isovolumic pressure-time curve within physiological ranges of preload and contractility. The present results indicate that this hybrid logistic function is useful to evaluate left ventricular contraction and relaxation comprehensively.

Animals↗
PubMed1995

Sinusoidal and exponential decays of postextrasystolic transient alternans in excised blood-perfused canine hearts.

We have recently reported that the postextrasystolic contractile potentiation decays in alternans after a compensatory pause in canine left ventricles even under normal coronary and contractile conditions. The transient alternans appears to consist primarily of a small-magnitude exponential decay and a large-magnitude sinusoidal decay. We, therefore, hypothesized that the contractility (y) of the postextrasystolic alternans beats (beat number x) could be expressed as y = a x exp[-(x-1)/b] + c x exp[-(x-1)/d] x sin[pi(x-0.5)] + yo, where a and c are the normalized magnitudes (relative to the preceding regular beat) of the two exponential terms in the first postextrasystolic beat, b and d are their time constants, and yo is the normalized magnitude of the post-alternans regular beat (approximately 1). The first exponential term represents the monotonic decay. The sine term multiplied by the second exponential term represents the alternating decay. Mathematical curve-fitting indicated: 1) the above equation very closely fitted the alternans data with a squared correlation coefficient of 0.9996 on average, 2) c was 7 times on average greater than a, indicating dominance of the sine component, 3) b and d were 2.5 and 1.0 beats on average, indicating a faster decay of the sine component, and 4) this b was comparable to the time constant of the exponential decay of the postextrasystolic potentiation after no compensatory pause. This study suggests that myocardium has a mechanism to switch the postextrasystolic potentiation between the exponential and alternans decays depending on the first postextrasystolic interval.

Animals↗
PubMed1995

Left ventricular mechanoenergetics under altered coronary perfusion in guinea pig hearts.

Coronary perfusion pressure (CPP) is well known to affect left ventricular (LV) mechanoenergetics (Gregg's phenomenon). The garden hose effect via the Frank-Starling mechanism caused by coronary distension has long been considered to be the underlying mechanism of this phenomenon. However, recent studies have revealed a close correlation between CPP and the excitation-contraction coupling in myocytes. The aim of this study was to investigate the mechanoenergetic aspects of Gregg's phenomenon by the ventricular contractility (Emax) dependency of the myocardial oxygen consumption (VO2)-total mechanical energy (PVA, systolic pressure-volume area) relationship. Experiments were performed in the excised, cross-circulated guinea pig heart preparation. The protocol consisted of LV volume loading (VOL run), changing coronary perfusion pressure at a fixed LV volume (CPP run) and intracoronary calcium (Ca) infusion also at the same LV volume (Ca run). In all seven hearts, we obtained a linear VO2-PVA relation in VOL run. The VO2-PVA relations in CPP and Ca runs, which equally enhanced Emax, were highly linear and had no significant difference in their slopes, both significantly steeper than in VOL run. These findings suggest no significant difference in the oxygen cost of Emax between CPP and Ca runs. The enhanced LV mechanoenergetics under increasing CPP is characterized by increases in the VO2 component primarily for the excitation-contraction coupling to a greater degree than expected from the mechanical (garden hose) effect.

Animals↗
PubMed1994

Effects of capsaicin on mechanoenergetics of excised cross-circulated canine left ventricle and coronary artery.

Capsaicin selectively acts on sensory nerve endings in cardiac muscles and coronary arterial smooth muscles. Capsaicin at high doses has cell-nonselective effects including both inhibition of cardiac muscle exciteability and enhancement of vascular smooth muscle tone. We studied whether and how intracoronary infusion of capsaicin affects mechanoenergetics of the excised blood-perfused canine heart and coronary vascular resistance. We found that capsaicin at low concentrations increased Emax (a contracility index) and oxygen consumption (VO2) possibly due to a specific action on capsaicin-sensitive sensory nerves in left ventricular muscles, though in a small number of hearts (3/10). This result coincides with the reported histochemical observations that the distribution of capsaicin-sensitive sensory nerves in the canine left ventricle is not dense. Capsaicin at high doses dose-dependently decreased Emax and proportionally decreased coronary flow. It also lowered the linear VO2-PVA (pressure-volume area; total mechanical energy) relationship without a change in the slope, decreasing unloaded VO2 (VO2 intercept of the VO2-PVA relation). These effects of high-dose capsaicin seem to be direct negative inotropic action on cardiac muscles associated with enhancement of coronary arterial smooth muscle tone, since these effects were not desensitized. No morphological changes of myocardial cells or mitochondria were detected. Therefore, the negative inotropic action is not due to the toxic effect of capsaicin.

Animals↗
PubMed1994

Postextrasystolic transient contractile alternans in canine hearts.

We found that postextrasystolic potentiated contractility after a spontaneous extrasystole most frequently decayed as a transient alternans over several beats in excised, cross-circulated, atrially paced canine hearts. This type of heart preparation; which we have been using consistently in mechanoenergetic studies, had normal coronary blood perfusion pressure as well as flow and mechanoenergetic performance. Spontaneous atrial and ventricular extrasystoles occurred occasionally in every heart. Arrhythmic changes in left ventricular (LV) pressure at a fixed volume reflected corresponding changes in contractility. We analyzed nearly 3,600 cases of postextrasystolic potentiation in 68 hearts; 84% decayed as transient alternans, 6% decayed exponentially, and 10% belonged to neither type. We found that a postextrasystolic compensatory pause always preceded the transient alternans after either an atrial or ventricular extrasystole at any constant atrial pacing rate (85-188 beats/min). The decay was either exponential or nonalternating when the pause did not exist after an atrial extrasystole during occasional pacing failure. Therefore, the compensatory pause after either an atrial or ventricular extrasystole seems essential for the postextrasystolic transient alternans of LV contractility in the type of canine heart preparation we have been using.

Animals↗
PubMed1994

Energetics of the negative and positive inotropism of pentobarbitone sodium in the canine left ventricle.

OBJECTIVE: Pentobarbitone (sodium) is an anaesthetic widely used in animal experiments. It is known to be a cardiovascular depressant and a coronary dilator, but its effects on myocardial energetics in relation to its negative and positive (due to Gregg's phenomenon) inotropism have not been studied. The aim of this study was therefore to determine whether and how pentobarbitone affects cardiac mechanoenergetics compared with other negative inotropic agents for which data are already available. METHODS: The effects of graded doses of intracoronary pentobarbitone on mechanoenergetics were studied in the excised cross circulated left ventricles of 12 dogs. The framework of the Emax (a contractility index)--VO2 (myocardial oxygen consumption)--PVA (systolic pressure-volume area, a measure of total mechanical energy) relationships was fully utilised. RESULTS: Pentobarbitone increased Emax at low doses in five of the 12 hearts. In two of these five hearts, a marked coronary dilatation was found. Pentobarbitone decreased Emax dose dependently at high doses in all the hearts and lowered the VO2 intercept but not the slope (oxygen cost of PVA) of the VO2-PVA relation. There was no difference in oxygen cost of Emax between pentobarbitone and CaCl2, although they have opposite inotropism. These findings suggest that pentobarbitone depresses myocardial mechanoenergetics via suppression of total calcium handling in the excitation-contraction-relaxation coupling. CONCLUSIONS: Pentobarbitone at low doses partly acts as a positive inotropic agent, but at high doses it acts as a negative inotropic agent like beta blockers and calcium antagonists on cardiac mechanoenergetics in canine blood perfused hearts.

Animals↗
PubMed1994

Estimation of total carbon dioxide contents in canine coronary arterial and venous whole blood samples.

We examined whether total carbon dioxide content (CCO2) estimation equations for human whole blood in the literature are applicable to canine coronary arterial and venous blood samples. PCO2 of the tested blood samples covered 19-52 mmHg; PO2 19-398 mmHg. Three CCO2 estimation equations developed by Kelman, Godfrey, and Douglas et al yielded CCO2 values over a range of 26.7-54.9 vol%, where plasma CCO2 values calculated by the Henderson-Hasselbalch equation ranged over 27.7-62.2 vol%. The estimated blood CCO2 values were almost identical among the three equations. They also closely correlated with plasma CCO2 values measured after hemolysis with saponin. We conclude that the human whole blood CCO2 estimation equations are applicable to canine coronary arterial and venous blood samples. These CCO2 equations may be used for canine cardiac metabolic studies.

Animals↗
PubMed1993

Adenosine inhibits efferent function of extrinsic capsaicin-sensitive sensory nerves in the enteric nervous system.

Capsaicin (1-3 microM) and electrical stimulation of mesenteric nerves in the presence of hexamethonium and guanethidine antidromically stimulate extrinsic sensory nerve fibers to produce a specific slow depolarizing response of myenteric neurons and a contractile response of muscles in the isolated guinea-pig ileum, mediated by release of substance P and acetylcholine. Adenosine (1-100 microM) inhibited the response to mesenteric nerve stimulation. Adenosine (10-100 microM) suppressed the contractile response to a threshold concentration of capsaicin (1 microM) while leaving the contractile response to a submaximal concentration of substance P (1 nM) and acetylcholine (0.1 microM) intact. Adenosine (1-10 microM) inhibited dose dependently the capsaicin 10 microM)-induced depolarization of myenteric neurons, but did not inhibit the depolarizing response to exogenous substance P. The adenosine P1 receptor antagonist, 8-phenyltheophylline (1-10 microM), antagonized the inhibitory effect of adenosine (1-10 microM) on the mechanical responses. We conclude that adenosine-induced prejunctional inhibition of the mechanical responses is mediated by adenosine P1 receptors.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Ca2+ sensitivity of contractile machinery and Ca2+ handling energy. Simulation.

Myocardial Ca2+ handling during excitation-contraction coupling has been modelled mathematically to gain a better insight into the expectation that Ca2+ sensitization of contractile machinery may save myocardial energy utilization for Ca2+ handling. The basic model of myocardial Ca2+ kinetics and mechanoenergetics involved the sarcoplasmic reticulum (SR), sarcoplasm, troponin C (Tn) and crossbridges (CB). The relations among the released Ca2+ ions from the SR, peak concentrations of sarcoplasmic free Ca2+ ([Ca2+]i) and Ca(2+)-bound troponin ([TnCa]) and peak contractile force were computed, based upon the assumptions that the released Ca2+ ions diffuse as free Ca2+ in sarcoplasm, bind kinetically with Tn with an association rate constant of k1, dissociate from TnCa with a dissociation rate constant of k2, and are sequestered into the SR with consumption of ATP. TnCa was associated with CB cycling to develop force with a set of given on and off rate constants. The association constant Ka (= k1/k2) of TnCa as an index of Ca2+ sensitivity of Tn was varied 32-fold from 0.25 to 8/microM. Results showed that Ca2+ sensitization from a lower Ka level could most sharply decrease the total Ca2+ release required to develop the same contractile force. Thus, it would reduce the total Ca2+ handling energy that the SR uses to maintain the same contractility.

Calcium↗
PubMed1993

[Difference in perceived health between blue- and white-collar workers of a manufacturing factory by a self-administered questionnaire].

In order to examine the differences in which blue- and white-collar workers perceive their own health status, a survey using self-administered questionnaire was conducted. The subjects were 1,428 male workers in a tire manufacturing factory, consisting of 1,185 blue-collar workers and 243 white-collar workers. Most of the blue-collar workers were engaged in shift work consisting of three shifts/d. The questionnaire included 32 items concerning health habits, life and job satisfaction, mental stress, and type A behavior. The following findings were obtained. Good daily health habits were related to age. Older workers had better health habits than the younger ones both in white- and blue-collar workers. The white-collar workers were more satisfied with their life and jobs, and also showed type A behaviors at a higher rate. As for fatigue and dissatisfaction association with shift work, the workers' complaints increased in the order of day shift, evening shift and midnight shift. The older workers had fewer complaints than the younger ones. These results suggested that health management and education will be more effective if the working conditions and the background of each worker are taken into consideration.

Adult↗
PubMed1993

Nipradilol depresses cardiac contractility and O2 consumption without decreasing coronary resistance in dogs.

Nipradilol (3,4-dihydro-8-(2-hydroxy-3-isopropylamino) propoxy-3-nitroxy-2H-1-benzopyran) is a newly synthesized chemical agent designed to possess beta-adrenoceptor blocking and vasodilating actions. Nipradilol decreased left ventricular contractility index (Emax, slope of the ventricular end-systolic pressure-volume relation), systolic pressure-volume area (PVA, a measure of ventricular total mechanical energy) and oxygen consumption in cross-circulated excised dog hearts. However, nipradilol did not decrease total coronary resistance. These results indicate that nipradilol, like propranolol, depresses myocardial mechanoenergetics and that the vasodilating action of nipradilol could not be detected in the present study.

Adrenergic beta-Antagonists↗
PubMed1993

Left ventricular ORS widening decreases Emax without lowering VO2-PVA relation in dog hearts.

We observed a few rare spontaneous cases of a suddenly widened QRS wave of left ventricular ECG associated with a simultaneous decrease in left ventricular (LV) contractility (Emax, end-systolic pressure-volume ratio) in excised cross-circulated dog heart experiments. The decreased Emax was not associated with a descent of the relation between cardiac oxygen consumption (VO2) and LV systolic pressure-volume area (PVA, a measure of total ventricular mechanical energy). This result is intriguing because ventricular VO2-PVA relation generally changes its elevation in proportion to Emax under various inotropic interventions. We suspected the unusual observation to reflect no change in myocardial contractility despite ventricular asynchrony augmented by an intraventricular conduction defect.

Animals↗