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K Sugi

Publications and source records attributed to K Sugi.

At least 19 recordsLinked to original sources

[An experimental study of determining the appropriate frequency of radiofrequency catheter ablation in vitro and in vivo for ventricular tachycardias].

The purpose of this study was to examine the appropriate frequency of radiofrequency catheter ablation (RFA) for ventricular tachycardia. Radiofrequency energy generated by a device in which the frequency could be changed, was delivered from an electrode catheter with an electrode tip-width of 4 mm. RFA was performed for 10 seconds with 20W (50V x 0.4A) using 7 different frequencies from 10 to 500 kHz on ventricular myocardium in vitro and in anesthetized dogs. The ablated lesion was significantly larger with RFA of 200-300 kHz in both surface area and depth (p less than 0.05). The appearance of ventricular arrhythmia during RFA increased as the frequency decreased, and one dog applied with RFA of 100 kHz had spontaneous ventricular fibrillation resulting in death. All dogs with frequency less than 100 kHz had a muscle cramp during RFA. We conclude that appropriate frequency seems to be 200-300 kHz to obtain a large ablated lesion, and a frequency higher than 300 kHz seems suitable to avoid arrhythmia. We also conclude that a frequency under 100 kHz should not be used.

Animals

[Is radiofrequency catheter ablation available for treatment of ventricular tachycardias?--Effects of sequential unipolar applications using multiple electrode catheter].

The purpose of this study was to examine the effects of radiofrequency energy delivered to the canine endocardium in sequential unipolar applications using multipolar electrode catheter for treatment of ventricular tachycardias. Radiofrequency energy generated by the newly designed device (500 kHz) was delivered to the ventricular myocardium by a quadripolar electrode catheter. The device could indicate output and voltage and could calculate myocardial impedance. In order to determine the power of the ablation in vivo, sequential unipolar application was performed with various output in vitro. A continuous endocardial ablation was achieved with output beyond 15 W and with duration of 5 sec per one pole. According to our measurement, the myocardial impedance in vivo was about three times as large as that in vitro. Therefore, minimal output of 45 W in vivo was applied in the same manner in vitro, which resulted in continuous belt-shaped endocardial ablated lesion. Ventricular stimuli after sequential unipolar applications did not induce ventricular tachycardia in any of the dogs. We conclude that radiofrequency sequential unipolar application using the newly designed device produces a large ablated area and may be suitable for ablation of the foci of ventricular tachycardias.

Animals

Cardiac dysfunction after acute endotoxin administration in conscious sheep.

We evaluated cardiac function in an unanesthetized ovine model of hyperdynamic endotoxemia. The animals were instrumented for crystallographic dimension analysis of the left ventricle (LV) and measurement of LV, aortic, atrial, central venous, and pulmonary arterial pressures, and cardiac output. Seven sheep received 1.5 micrograms/kg of Escherichia coli endotoxin [lipopolysaccharide (LPS) LPS-P group] and were compared to a sham group. The sham group demonstrated no significant change in any of the variables. In the LPS-P group, the cardiac index increased (5.7 +/- 0.4 to 7.9 +/- 0.6 l.min-1.m-2) between 8 and 12 h after LPS. Concomitantly, the maximum elastance of LV end-systolic pressure-volume relations significantly decreased (2.88 +/- 0.27 mmHg/ml) compared with baseline (3.89 +/- 0.50 mmHg/ml). Other indexes of the LV contractility (maximum pressure development and ejection fraction) were also reduced. There was a simultaneous increase in the LV end-systolic and diastolic volumes. These findings confirm the hypothesis that there is a myocardial depression during LPS in the ovine model.

Animals

Thromboxane synthase inhibition and cardiopulmonary function during endotoxemia in sheep.

We studied the cardiopulmonary response to endotoxin (lipopolysaccharide, LPS) in sheep with and without the administration of a thromboxane synthase inhibitor, OKY-046. The animals were instrumented for crystalographic dimension analysis of the left ventricle (LV) and for measurement of LV, aortic, left atrial, and pulmonary arterial pressures and cardiac index, as well as lung lymph flow. They received 1.0 micrograms/kg of Escherichia coli LPS with (n = 8) and without (n = 8) OKY-046 (10 mg/kg bolus, then 10 micrograms.kg-1.min-1). OKY-046 prevented the increase of pulmonary arterial pressure and the decrease of cardiac index that occurred during the early phase of endotoxemia. Between 8 and 12 h after LPS, cardiac index increased from 6.8 +/- 0.7 to 8.9 +/- 0.51.min-1.m-2. Concomitantly, the end-systolic pressure-diameter relationship (ESPDR, sensitive myocardial contractility index) significantly decreased from 14.7 +/- 0.6 to 7.7 +/- 0.7. Other indexes of the LV contractility (+dP/dtmax) were also reduced. OKY-046 prevented the decreases of ESPDR and +dP/dtmax. OKY-046 also attenuated the increased lung lymph flow changes seen with LPS.

6-Ketoprostaglandin F1 alpha

[An experimental study on the alteration of myocardial tissue by radiofrequency catheter ablation: differences according to the frequency and the device].

To evaluate the alteration of myocardial tissue by radiofrequency (RF) catheter ablation according to differences of the frequency and the device, we applied RF catheter ablation to canine right ventricular myocardium in vitro. The devices delivering RF energy were LL-49(0. 49MHz, fixed voltage mode), RA-50 (13.56MHz, fixed watt mode) and HAT200 (0.52MHz, fixed watt mode with the capability of temperature adjustment). After RF catheter ablation were performed with a unipolar electrode catheter at various output under the same condition of contact, the ablated lesions by each device were compared. Histologically, we recognized coagulation layer with the necrosis of endocardium and the dissociation of myocardium in each experiment. The degree and the size of ablation layer was significantly larger in lower frequency delivery (p less than 0.05) and was significantly smaller by using the device with temperature adjustment as compared with the others (p less than 0.05). It was suggested that the alteration of myocardial tissue ablated with RF energy differ according to the frequency and the mode of output adjustment of the device.

Animals

Effects of allopurinol on smoke inhalation in the ovine model.

We hypothesized that the pulmonary damage induced by smoke inhalation is the result of ischemic reperfusion injury. We determined the effect of allopurinol (xanthine oxidase inhibitor) on the pulmonary microvascular fluid flux in an ovine model after inhalation of cotton smoke (n = 13) and compared these data with those from untreated similarly smoke-injured (n = 7), as well as sham- (air, n = 9) smoked, animals and sheep given an equivalent dose of CO (n = 7). Smoke injury resulted in an increased lung lymph flow, lymph-to-plasma protein ratio, lung content of polymorphonuclear cells, and extravascular lung water (gravametric), in addition to histological evidence of tissue (pulmonary) edema and destruction. No significant difference was found in these variables between the sheep that were injured with smoke whether or not they were pretreated with allopurinol. The sham-smoked and CO-insufflated animals showed no significant changes in cardiopulmonary function or morphology. We conclude that there are few data to support a role of ischemic reperfusion injury in the pulmonary damage seen after smoke inhalation.

Allopurinol

Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury.

With the inhalation of smoke, there are both cardiopulmonary changes and elevated levels of carbon monoxide (CO). We hypothesize that these changes in cardiopulmonary function are the result of a histotoxic hypoxia associated with CO poisoning. This hypothesis was tested in chronically instrumented sheep (n = 19). Piezoelectric crystals were attached to the left ventricle for the measurement of its external minor and major diameters in addition to wall thickness. A pressure transducer was placed in the left ventricle via the apex. The caudal-mediastinal lymph node was also cannulated. After a five-day recovery period, six sheep (smoke group) were insufflated with four series of 16 breaths (700 ml/breath) of cotton smoke, and five sheep (control group) were insufflated with air using a modified bee smoker (smoke group: COHb, 90 +/- 6%; control group: COHb, 6 +/- 1%). Eight sheep (CO group) were ventilated with 2% CO in air to reach a COHb of 90% (COHb, 92 +/- 1%). In the smoke group, lung lymph flow reached 42 +/- 10 ml/hr at 24 hours after smoke insufflation (baseline, 6 +/- 1 ml/hr). The maximum elastance of the left ventricle (end-systolic pressure-volume ratio), a sensitive index of myocardial contractility, was significantly decreased from a baseline of 6.5 +/- 0.9 to 3.3 +/- 0.7 mm Hg/ml. In the control and CO group, neither lung lymph flow nor maximum elastance varied from the baseline value. We conclude that the cardiopulmonary dysfunction after smoke inhalation does not occur after a similar exposure to CO. Initial CO poisoning alone is not a causative factor of cardiopulmonary dysfunction after smoke inhalation.

Animals

[The effect of percutaneous transluminal coronary recanalization (PTCR) on late potentials detected by signal-averaged electrocardiogram in patients with previous myocardial infarction].

The purpose of this study was to assess the effect of percutaneous transluminal coronary recanalization (PTCR) on late potentials (LP) in patients with previous myocardial infarction (MI). The signal-averaged ECG was recorded by Fukuda VCM-3000 in 54 patients with anterior MI (average of 32 months after onset of MI). Fifty four patients were divided into two groups: Group A was comprised of 29 patients who underwent PTCR, and Group B was comprised of 25 patients who didn't receive PTCR. Ventricular arrhythmias detected by 24 hour Holter monitoring, and left ventriculographic findings were also evaluated. The presence of LP was defined as low amplitude signals (less than 15 microV) in the last 40 msec of the filtered QRS complex. The incidence of LP was significantly higher in Group B than in Group A (32% vs 7%, p less than 0.01). The presence of PVCs and ejection fraction (EF), LV end-diastolic volume (EDV), LV end-systolic volume (ESV) and % abnormally contracting segment (% ACS) were not significantly different in each respective groups. However, ESV and % ACS were significantly larger (p less than 0.05), and EF was significantly smaller (p less than 0.01) in patients with LP (+) than in patients with LP (-). LP was present in two patients who had undergone PTCR (TIMI grade 2) unsuccessfully, whereas it was not present in the 27 patients with successful PTCR (TIMI grade 3). It was concluded that successful recanalization of the infarct-related arteries may reduce the incidence of LP.

Aged

[The effect of the co-existence of verapamil and residual propranolol on the left ventricular contractility].

The combined effect of the residual propranolol, which was administrated up to the coronary revasculization, and verapamil, anti-supraventricular tachycardia drug, on the left ventricular contractility was evaluated with left ventricular end-systolic pressure-diameter relationship. Methods; Eighteen sheep were instrumented with ultrasonic crystals on the anterior and posterior wall, endocardium and epicardium. A pressure transducer was placed in the left ventricle. Propranolol (0.15 mg/kg) (n = 6) or verapamil (0.15 mg/kg) (n = 6) or both drugs (n = 6) were administrated intravenously, and cardiac function was evaluated. Results; In combined group, end-systolic pressure-diameter ratio (Emax) was significantly decreased (2.95 +/- 0.24 mmHg/mm) as compared to the control group (7.95 +/- 0.83), propranolol group (6.27 +/- 0.78), and verapamil group (4.54 +/- 0.77). Conclusion; Co-existence of propranolol and verapamil significantly decreased cardiac contractility. Therefore verapamil should be administrated carefully in the presence of residual propranolol, and the co-existence of both drugs must be limited.

Animals

Effect of obstructive jaundice on the fate of a nephrophilic organic anion in the rat.

Renal transtubular transport of phenolsulfophthalein (PSP), a nephrophilic organic anion that circulates bound to albumin, was studied in normal and bile-duct-ligated rats. Intravenously injected PSP disappeared from the circulation more rapidly in bile-duct-ligated jaundiced rats than in intact animals. However, urinary excretion of PSP was significantly lower in the former than in the latter. Kinetic analysis revealed that binding of PSP to plasma protein(s) was significantly lower with jaundiced rats than with intact animals. Addition of albumin to plasma samples from bile-duct-ligated rats markedly increased PSP binding. The decreased PSP binding returned to normal levels after treating the jaundiced plasma with bilirubin oxidase, an enzyme that degrades amphiphilic bilirubin to water soluble metabolites. These results suggest that bilirubin might be the major metabolite that occupied the PSP binding site(s) on albumin in jaundiced rats. When PSP was injected bound to equimolar amount of albumin, the rate of PSP disappearance from the circulation decreased and urinary excretion of the ligand increased markedly; urinary excretion of PSP was significantly larger in bile-duct-ligated rats than in intact animals. These results suggest that the renal transport capacity for amphiphilic organic anions, such as PSP, might be increased compensatively in bile-duct-ligated animals, and that the apparent decrease in renal secretory transport for PSP might result from, at least in part, random distribution of the ligand to extrarenal tissues due to decrease in the binding activity of albumin.

Animals

Degradation of plasma bilirubin by a bilirubin oxidase derivative which has a relatively long half-life in the circulation.

To enhance degradation of unconjugated bilirubin in hyperbilirubinemic subjects, we synthesized a bilirubin oxidase (EC 1.3.3.5) (BO) derivative (PEGBO) by covalently linking (2,4-bis[O-methoxy(polyethyleneglycol)]-6-chloro-s-triazine) (PEG) to the enzyme. Intravenously injected BO in rats disappeared from the circulation with a half-life of 2.5 min; the half-life of PEGBO was 190 min. Intravenously injected BO minimally and transiently decreased plasma bilirubin levels in jaundiced Gunn rats and in bile-duct-ligated jaundiced rats. In contrast, PEGBO rapidly and substantially decreased plasma bilirubin levels and the effect persisted for longer than 3 h. Renal dysfunction often occurs in patients with liver diseases. To study the role of bilirubin toxicity for the kidney, functions of transtubular transport for organic anions was measured in bile-duct-ligated jaundiced animals before and after treatment with PEGBO. Bile duct ligation decreased urinary excretion of phenolsulfophthalein (PSP), an organic anion used for renal function test. Treatment of the jaundiced animals with PEGBO increased the rate of PSP disappearance from the circulation and normalized its urinary excretion. Thus, PEGBO might be useful for the study of bilirubin toxicity in jaundiced animals.

Animals

[Dissecting aortic aneurysm of DeBakey type II diagnosed by color Doppler flow imaging and treated by a Bentall surgical procedure: a case report].

A 33-year-old man with known annuloaortic ectasia was admitted to the hospital because of chest pain. A dissecting aortic aneurysm was strongly suspected, but angiography was not performed because of his history of allergic reaction to iodine contrast material. Two-dimensional echocardiography demonstrated a markedly dilated basal aorta. The aortic wall immediately above the right sinus of Valsalva appeared to divide the aortic lumen into anterior and posterior channels. A defect in the intimal flap with a diameter of two cm was also detected six cm above the aortic ring. Color Doppler flow mapping showed blood flow passing through a probable entrance tear from the true lumen into the false lumen. Reentry could not be detected by Doppler imaging. All major aortic tributaries were presumed patent and supplied via the true lumen. The patient underwent successful emergency Bentall surgical procedure and recovered. It is emphasized that in some cases of DeBakey type I or II aortic dissection, color Doppler flow imaging is helpful for determining indications for emergency surgery.

Adult

[Analbuminemia].

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Animals

The effect of leukocyte depletion on smoke inhalation injury in sheep.

Leukocytes and the production of oxygen radicals and proteolytic enzymes have been implicated in the pathogenesis of lung injury after smoke inhalation. We investigated the mechanism responsible for this form of pulmonary damage in chronically prepared sheep previously made leukopenic with intra-arterial infusions of nitrogen mustard (mechlorethamine hydrochloride). A control air insufflated group (sham: n = 6), a cotton smoke insufflated group (smoke: n = 12), and a leukopenic cotton smoke insufflation group (smoked + depleted: n = 6) were compared. Although both smoke insufflation groups had equivalent smoke exposure, which was indexed by carboxyhemoglobin, the smoked + depleted group had significant attenuation in the increases in pulmonary artery pressure, pulmonary vascular resistance, and pulmonary lymph flow. The PaO2 to FiO2 ratio (P:F) did not fall to the same extent, nor was there a fall in PaO2. The production of oxygen radicals, which was measured as plasma-conjugated dienes, and the consumption of antiprotease, as measured by alpha 2-macroglobulin levels in lung lymph, were not changed in the smoked + depleted group, whereas it was elevated in the smoked group. We conclude that circulating leukocytes and the release of oxygen radicals and proteolytic enzymes contribute to the lung injury, pulmonary microvascular permeability increase, and pulmonary edema seen after smoke inhalation.

Animals

Effects of propafenone on sinus nodal and ventricular automaticity: in vitro and in vivo correlation.

The electrophysiologic effects of the new antiarrhythmic drug, propafenone, were evaluated in anesthetized closed-chest dogs and on isolated cardiac tissues with the microelectrode technique. Propafenone (2 to 4 mg/kg intravenously) had no effect on sinus rate or on sinus nodal recovery time, but caused a dose-dependent significant decrease in the rate of idioventricular rhythm and increased the duration of ventricular overdrive suppression in dogs (n = 8) with complete atrioventricular block. On isolated canine Purkinje fibers (n = 8) manifesting automaticity with resting membrane potential less negative than -70 mV, propafenone reduced the slope of phase 4 depolarization and reduced the rate of automatic impulse initiation in a concentration-dependent manner (10(-6) M-4.10(-5) M). At these concentrations, propafenone had no effect on rabbit sinus nodal automaticity (n = 8) or on sinoatrial conduction. However, significant depression of sinus nodal automaticity occurred with propafenone concentrations above 5.10(-6) M in the presence of cholinergic or complete autonomic blockade with atropine (10(-6) M) and propranolol (5.10(-5) M). Propafenone caused a concentration-dependent decrease in the disparity of Purkinje fiber-ventricular muscle action potential duration (APD), mainly by shortening Purkinje fiber APD. We conclude: that propafenone suppresses idioventricular rhythm in the intact dog, most likely by depressing Purkinje fiber automaticity; the depressant effect of propafenone on sinus nodal automaticity is evident only during cholinergic receptor blockade; and the antiarrhythmic properties of propafenone may include removal of APD disparity by selective shortening of Purkinje fiber and not of ventricular muscle APD.

Animals