Search PubMed⌕ Search

Biomedical subjects

H Yaku

Publications and source records attributed to H Yaku.

At least 73 records · Page 4Linked to original sources

Energetics of the fibrillating ventricle.

We have proposed a new mechanical index, equivalent pressure-volume area (ePVA), as a measure of the total mechanical energy of a fibrillating ventricle. ePVA is an analogue of the pressure-volume area (PVA) of a contracting ventricle and the specific area surrounded by the horizontal pressure-volume line at the pressure of ventricular fibrillation (VF) and the end-systolic and end-diastolic pressure-volume relations in the beating state in the pressure-volume diagram. In the isolated, cross-circulated heart preparation, we obtained myocardial oxygen consumption (VO2) during VF and ePVA at various left ventricular volumes in the control, epinephrine, propranolol and hypothermia runs. ePVA was highly linearly correlated with VO2 in all runs (r = 0.95, 0.98, 0.96 and 0.90, respectively). We also determined equivalent heart rate (eHR) as an estimate of the contraction frequency of individual myocytes in a fibrillating ventricle from mechanically unloaded VO2 in beating and fibrillating states. Using both ePVA and eHR, VO2 during VF was estimated and correlated with directly measured VO2. Estimated VO2 almost agreed with measured VO2 in all runs. We conclude that ePVA is a primary determinant of VO2 during VF, and that VO2 of a fibrillating ventricle can be reasonably accounted for by the combination of ePVA and eHR. This paper is a review of our previous studies on the energetics of a fibrillating ventricle.

Animals↗

Ventricular fibrillation does not depress postfibrillatory contractility in blood-perfused dog hearts.

We studied whether ventricular fibrillation depresses ventricular contractility in a blood-perfused heart. In 12 excised, cross-circulated dog hearts, we measured left ventricular pressure and myocardial oxygen consumption at a middle left ventricular volume as control and induced ventricular fibrillation electrically. Six hearts were subjected to 20 minutes of ventricular fibrillation (group A), and the other six hearts were subjected to 40 minutes of ventricular fibrillation (group B). Then we defibrillated the heart with direct current shock and measured left ventricular pressure, left ventricular volume, and myocardial oxygen consumption immediately, 10 minutes, 20 minutes, and 30 minutes after the defibrillation. Coronary perfusion pressure was maintained normal (around 100 mm Hg) by the arterial pressure of the support dog throughout each experiment. Ventricular contractility was quantified by the maximum value for the instantaneous pressure/volume ratio (Emax). Pooled data of both groups A and B showed that Emax immediately after defibrillation increased to 116% +/- 28% (p less than 0.05) of control level and Emax 10 minutes after defibrillation decreased to 84% +/- 17% (p less than 0.05) of control level. Then Emax recovered to the control level: 95% +/- 18% (p greater than 0.05) of control level at 20 minutes and 100% +/- 20% (p greater than 0.05) of control level at 30 minutes after defibrillation. Emax of group A was not different from that of group B at comparable measurement times after defibrillation. Changes in myocardial oxygen consumption per beat were in proportion to the changes in Emax. We conclude that ventricular fibrillation per se for 20 to 40 minutes does not depress postfibrillatory contractility when coronary blood perfusion is maintained normal in the dog left ventricle.

Animals↗

Mechanical enhancement and myocardial oxygen saving by synchronized dynamic left ventricular compression.

Dynamic cardiomyoplasty with synchronously paced skeletal muscle grafts has recently been developed to augment the performance of impaired myocardium. This method has been reported effective to improve patients' general status and some hemodynamic parameters. It is unknown, however, how a systolic dynamic cardiac compression, as in dynamic cardiomyoplasty, affects left ventricular energetics. The purpose of this study was to characterize the effects of dynamic cardiac compression on the ventricle in terms of the pressure-volume relationship and myocardial oxygen consumption. In an isolated cross-circulated dog heart model, a dynamic cardiac compression device was set to directly compress the ventricle during systole. End-systolic pressure, contractility index (Emax), pressure-volume area, external mechanical work, coronary blood flow, and myocardial oxygen consumption were determined before and during dynamic cardiac compression. Dynamic cardiac compression significantly increased Emax. When end-diastolic and stroke volumes were fixed, end-systolic pressure, pressure-volume area, and external mechanical work significantly increased during dynamic cardiac compression while coronary blood flow and myocardial oxygen consumption remained unchanged. When end-systolic pressure was matched with the pre-dynamic cardiac compression control level by decreasing end-diastolic volume at a constant stroke volume so that external mechanical work under dynamic cardiac compression returned to the control level, both pressure-volume area and myocardial oxygen consumption significantly decreased. In contrast to a marked increase in myocardial oxygen consumption for a given increase in external mechanical work by either volume loading or dobutamine, dynamic cardiac compression did not increase myocardial oxygen consumption for the same increase in external mechanical work. Thus dynamic cardiac compression augments left ventricular pump function without increasing myocardial oxygen demand or compromising coronary blood flow.

Animals↗

[Combined therapy with prostaglandin E1 ointment and lumbar sympathetic ganglion block on intractable skin ulcers accompanied by Bürger's disease].

For the 2 patients with intractable skin ulcers and pain accompanied by thromboangiitis obliterans (Bürger's disease), we applied combined therapy with lumbar sympathetic block, continuous epidural block and prostaglandin E1 ointment. Prostaglandin E1 (PGE1) was prepared as a topical ointment by mixing with Plastibase (polyethylene resin, 5%, liquid paraffin, 95%) at a concentration of 10 micrograms.g-1. The ointment was kept in a refrigerator until use. Following debridement and washing of the surface of ulcers as required, the ointment was applied evenly onto the surrounding and over the surface of each ulcer 2 times daily after sterilization. With this therapy the ulcers were cured completely in 10 days after the start of treatment. No side effect was observed both locally and systemically. Although the combined therapy we used with prostaglandin E1 ointment was a noninvasive method, a remarkable shortening of the period of treatment was achieved.

Aged↗

Systolic pressure-volume area (PVA) as the energy of contraction in Starling's law of the heart.

We have theoretically proposed "systolic pressure-volume area" (PVA) as a measure of total mechanical energy generated by ventricular contraction. We then experimentally showed that PVA closely correlates with left ventricular oxygen consumption (Vo2) regardless of ventricular loading conditions in a stable contractile state. Although Starling's law of the heart has been generally considered to describe the relation between ventricular preload as the input and the "energy of contraction" as the output, the energy of cardiac contraction has been variously identified with cardiac output, external work, contractile element work, tension-time index, etc., by different investigators. However, none of these variables has been unanimously accepted as the total mechanical energy of contraction because they do not consistently correlate with Vo2 which represents the total energy utilization for contraction. Considering the nature of PVA which has been revealed over the last decade, we now confidently propose that PVA is the most likely expression of the total mechanical energy of contraction that has been pursued for many years as the energy of contraction in Starling's law of the heart.

Blood Pressure↗

Hyperthyroid dog left ventricle has the same oxygen consumption versus pressure-volume area (PVA) relation as euthyroid dog.

We studied the effects of hyperthyroidism on the relation between O2 consumption (Vo2) and the pressure-volume area (PVA) of the left ventricle (LV) in dogs. PVA is a measure of the total mechanical energy generated per beat of LV. Dogs were treated by daily intramuscular injection of 0.3 or 1.0 mg/kg L-thyroxine over 2-5 weeks. Hyperthyroid dogs had a 40 times higher serum T4, a 40% higher sinus heart rate, and a 35% higher LV Emax (an index of ventricular contractility) than euthyroid dogs. Hyperthyroid dog hearts had linear Vo2-PVA relations like euthyroid dog hearts. The regression line was Vo2 = A x PVA + B, where A was 2.30 (dimensionless) and B was 0.53 J/beat per 100 g LV. B was significantly increased with dobutamine and decreased with propranolol, whereas A was not significantly changed by them. These A and B values were comparable to euthyroid data. Hyperthyroidism did not significantly affect myosin Ca-ATPase activity and V3-type myosin predominance, but increased the speed of the force transient response to length perturbation by 20%-70%, suggesting similar increases in crossbridge cycling rate. We conclude that in spite of accelerated crossbridge cycling rate the Vo2-PVA relation was not altered by hyperthyroidism in dogs.

Animals↗

Effects of trimetaphan on the cardiovascular response to tracheal intubation.

In three groups of 10 patients, we have studied the effect on the cardiovascular responses to laryngoscopy and intubation of bolus doses of saline or trimetaphan 0.05 mg kg-1 or 0.1 mg kg-1 given 1.75 min before the start of laryngoscopy. Anaesthesia was induced with thiopentone 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were less in trimetaphan-treated patients compared with those of the control group (P less than 0.05). There was no significant difference in heart rate following tracheal intubation between the three groups. These data suggest that trimetaphan may be used as a supplement during induction, to attenuate the hypertensive response associated with laryngoscopy and tracheal intubation.

Anesthesia, General↗

Effects of adenosine triphosphate on the cardiovascular response to tracheal intubation.

Laryngoscopy and tracheal intubation often cause hypertension and tachycardia, which may be exaggerated during rapid-sequence induction of anaesthesia. The efficacy of adenosine triphosphate (ATP) in attenuating this response was studied in patients receiving ATP 0.05 mg kg-1 or 0.1 mg kg-1 simultaneously with the start of laryngoscopy. These data were compared with those for a control group receiving saline. Each group consisted of 10 patients undergoing elective surgery. Anaesthesia was induced with thiopentone 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1 i.v. During anaesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increase after tracheal intubation were reduced in ATP-treated patients compared with those of the control group (P less than 0.05). The data suggest that a bolus injection of ATP is a simple, practical and effective method for attenuating the hypertensive response to laryngoscopy and tracheal intubation.

Adenosine Triphosphate↗

Effects of pindolol on the cardiovascular response to tracheal intubation.

Laryngoscopy and tracheal intubation often cause hypertension, tachycardia and arrhythmias, which may be exaggerated during rapid-sequence induction of anaesthesia. We have studied the efficacy of pindolol in attenuating the cardiovascular responses to laryngoscopy and intubation in patients receiving pindolol 2 micrograms kg-1 or 4 micrograms kg-1 3 min before induction of anaesthesia in a double-blind design. The data were compared with those in a control group receiving saline. Each group consisted of 10 patients undergoing elective surgery. Anaesthesia was induced with thiopentone 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. Patients receiving saline showed a significant increase in mean arterial pressure and heart rate associated with tracheal intubation. These increases after tracheal intubation were reduced in pindolol 4 micrograms kg-1 treated patients compared with those in the control group (P less than 0.05). Pindolol 2 micrograms kg-1 attenuated tachycardia in response to intubation but did not affect hypertension. These data suggest that a bolus injection of pindolol 4 micrograms kg-1 is a simple, practical and effective method for attenuating cardiovascular responses to laryngoscopy and tracheal intubation.

Adult↗

Effects of exogenous intravenous glucose on plasma glucose and lipid homeostasis in anesthetized children.

Whether or not intravenous glucose administration during pediatric anesthesia is necessary remains a controversial issue. The current study was designed to investigate the effect of glucose infusion on concentrations of plasma glucose, nonesterified fatty acids (NEFA), triglycerides, ketone bodies, and insulin and to determine whether the use of solutions containing less than 5% glucose would maintain physiologic plasma glucose concentrations during tympanoplasty lasting about 6 h. Forty-five children aged between 1.5 and 9 yr were divided randomly into three groups of 15 patients each to receive the following intravenous solutions: LR groups, lactated Ringer's solution (LR) alone; D2LR group, 2% glucose in LR; and D5LR group, 5% glucose in LR. All fluids were infused at a rate of 6 ml.kg-1.h-1 until 1 h after anesthesia. In the LR group, the plasma glucose concentrations remained unchanged perioperatively compared with basal values, whereas in the D2LR group they showed a gradual increase during surgery but remained normoglycemic. On the other hand, in the D5LR group, the plasma glucose concentrations increased markedly both during and after the operation. Furthermore, 3 of 15 patients showed hyperglycemia of more than 300 mg.dl-1 during anesthesia. There was no evidence of lipid mobilization or impaired secretion of insulin, since plasma NEFA, triglycerides, ketone bodies, and insulin remained within normal concentration ranges throughout the sample period in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗

Multicompartment model for mechanics and energetics of fibrillating ventricle.

We propose a new mechanical model of a fibrillating ventricle to interrelate ventricular mechanics and energetics during fibrillation. The model consists of multiple asynchronously contracting compartments with identical time-varying elastances but with different contraction phase lags. Pressures in all compartments are common, and volumes of all compartments change, keeping their sum constant in the model. We evaluated the mechanical behavior of each compartment by simulating this model on a personal computer. Results showed that each compartment contracts quasi-isobarically. We calculated the pressure-volume area (PVAc) of each compartment as a measure of the total mechanical energy generated by a contraction of the compartment. We found that the sum of PVAcs of all compartments agreed with the area (equivalent PVA; ePVA) surrounded by the end-systolic and end-diastolic pressure-volume relations and the isobaric line at the mean pressure of the fibrillating ventricle. We conclude that ePVA represents the total mechanical energy of the fibrillating ventricle model. The multicompartment model is useful for insight into the interrelation between ventricular mechanics and energetics during ventricular fibrillation.

Animals↗

Sensitivities of cardiac O2 consumption and contractility to catecholamines in dogs.

We studied the effects of plasma catecholamines from the adrenal gland on systolic pressure-volume area (PVA)-independent O2 consumption (VO2) and contractility index (Emax) in the left ventricle of excised cross-circulated dog hearts. PVA is a measure of the total mechanical energy of contraction. Under baseline conditions, the PVA-independent VO2 correlated with plasma catecholamine level in the hearts (r = 0.84). Plasma epinephrine and norepinephrine levels increased gradually from 0.3 and 0.4 ng/ml to 10.3 and 2.7 ng/ml on average during adrenal sympathetic nerve stimulation of support dogs. Simultaneously, Emax and PVA-independent VO2 increased by 240 +/- 127 (SD) and 75 +/- 24%. Although their increases were monotonic in a given heart, their sensitivities to catecholamines were considerably variable among hearts. However, these two sensitivities were correlated (r = 0.96) with each other in the hearts, and the interheart variation of the sensitivity of the PVA-independent VO2 to Emax (i.e., oxygen cost of Emax) was smaller. We conclude that the oxygen cost of Emax is less variable among hearts despite large interheart variations of Emax and VO2 responses to plasma catecholamines.

Animals↗

Equivalent pressure-volume area accounts for oxygen consumption of fibrillating heart.

We attempted to find cardiac mechanical parameters to account for myocardial O2 consumption (VO2) during ventricular fibrillation (VF). We fully utilized the concept of pressure-volume (P-V) area (PVA), which is equivalent to the total mechanical energy generated by a ventricular contraction. We also utilized a multicompartment model consisting of multiple asynchronously contracting compartments, which we previously proposed to simulate the mechanics of a fibrillating ventricle. The model analysis had already validated the application of PVA to VF in terms of "equivalent PVA" (ePVA). ePVA is the area surrounded by the end-systolic and end-diastolic P-V relations in beating state and the isobaric P-V line at the VF pressure. ePVA is supposed to represent the total mechanical energy generated by single contractions of each compartment (or myocyte) in a fibrillating ventricle. We determined ePVA and correlated it with measured VO2 per minute (mVO2) at various ventricular volumes in electrically induced fibrillating left ventricles of the excised cross-circulated canine heart preparation. Correlation coefficient (r) of the mVO2-ePVA relation during VF was high (r = 0.95, P less than 0.01). Comparing mVO2 during VF with that in beating state at an unloaded ventricular volume, we calculated equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual compartments (myocytes). With the use of both ePVA and eHR, mVO2 during VF at various ventricular volumes was estimated. The relation between estimated mVO2 and directly measured mVO2 was highly linear (r = 0.88, P less than 0.01), and the regression line almost agreed with the identity line (regression coefficient = 1.05). We conclude that the new ePVA and eHR concepts can reasonably account for VO2 during VF.

Animals↗

Stability of myocardial O2 consumption-pressure-volume area relation in red cell-perfused rabbit heart.

We evaluated the mechanical and energetic stability of the isolated rabbit heart perfused with a suspension of bovine red cells in Krebs-Henseleit buffer in terms of the pressure-volume area (PVA) concept. PVA, the area surrounded by the end-systolic and end-diastolic pressure-volume (P-V) relations and the systolic P-V trajectory of the P-V diagram, represents the total mechanical energy generated by each cardiac contraction. Myocardial O2 consumption (VO2) per beat has been reported to be highly linearly correlated with PVA. We used the slope and VO2-axis intercept of the VO2-PVA relation as energetic parameters and the maximum P-V ratio (Emax) as a contractility index of the left ventricle (LV) and compared them every 30 min for 120 min. Emax, the slope, and VO2 intercept of the VO2-PVA relation did not change significantly over 120 min compared with their control values [7.3 +/- 2.9 mmHg.ml-1.100 g LV, (1.67 +/- 0.40) x 10(-5) ml O2.mmHg-1.ml-1, and (3.26 +/- 1.01) x 10(-2) ml O2.beat-1.100 g LV-1, respectively]. However, the goodness of the linear fit of the VO2-PVA relation decreased after 90 min (r = 0.94 control, 0.62 at 90 min, and 0.64 at 120 min). Therefore, we conclude that the isolated bovine red cell-perfused rabbit heart preparation is stable for mechanical and energetic studies for at least 60 min.

Animals↗

Denopamine (beta 1-selective adrenergic receptor agonist) and isoproterenol (non-selective beta-adrenergic receptor agonist) equally increase heart rate and myocardial oxygen consumption in dog heart.

The effects of denopamine (a beta 1-selective adrenergic receptor agonist) and isoproterenol (a non-selective beta-adrenergic receptor agonist) on heart rate, left ventricular contractility, and left ventricular oxygen consumption (VO2) at the same left ventricular volume were compared in excised cross-circulated dog hearts. Denopamine and isoproterenol increased heart rate and VO2 to a comparable extent at a comparably increased contractility. Moreover, the oxygen cost of contractility which quantifies VO2 for excitation-contraction coupling was the same between the two agents. These findings contradict the previously reported smaller increases in heart rate and VO2 by denopamine than by isoproterenol in open-chest dog hearts, which have been mainly attributed to the beta 1-selectivity of denopamine. Our results suggest that in isolated and denervated hearts, the degree of beta 1-selectivity of a beta-agonistic agent does not directly determine the relative potencies of its inotropic and chronotropic effects and the oxygen cost of contractility.

Adrenergic beta-Agonists↗

Calcium kinetics and energetics in myocardium. Simulation study.

We carried out a simulation study to obtain insight into the relation between calcium (Ca2+) transients and energy for handling Ca2+ in excitation-contraction (EC) coupling. The simulation incorporated basic Ca2+ kinetics among total released Ca2+ from sarcoplasmic reticulum (SR), myoplasmic free Ca2+ ion concentration, and troponin (Tn)-Ca complex concentration ([TnCa]). The total Ca2+ released from the SR was arbitrarily set as an impulse and three rate constants were used for Ca2+ binding to Tn, Ca2+ dissociation from Tn, and Ca2+ uptake by SR. The results showed that the peak Ca2+ transient varies widely as a reciprocal of the Ca2+ sensitivity of the contractile machinery, despite constant total released Ca2+ and hence, a constant energy for Ca2+ handling. This result suggests a disproportate relationship between the magnitude of Ca2+ transients and the energy for Ca2+ handling when the Ca2+ sensitivity of contractile machinery changes.

Calcium↗