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Biomedical subjects

K Sugi

Publications and source records attributed to K Sugi.

At least 145 records · Page 8Linked to original sources
PubMed1985

Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: studies on the site of origin and mechanism.

The electrophysiologic and arrhythmic properties of isolated infarcted right ventricle (RV) were studied in 17 dogs during the first 24 hours after complete occlusion of the right coronary artery (RCA). During the 16-to-20-hour post occlusion period, spontaneously occurring sustained monomorphic ventricular tachycardia (VT) was present in all 17 dogs. Overdrive ventricular pacing (cycle lengths 200 to 250 msec) caused significant suppression of the VT when the rate of the VT was slower than 150 bpm (range 120 to 145 bpm) (n = 9), but had negligible effect when VT rate was higher than 150 bpm (range 160 to 245 bpm (n = 8). Overdrive pacing could not terminate either the slow or the fast type of VT. Bipolar intramural electrograms have showed electrical activity in the infarcted RV zone to precede Q wave of the VT by 15.4 +/- 5.8 msec regardless of VT rate. Microelectrode studies on isolated RV endocardial infarcted tissues 24 hours after RCA occlusions have shown the presence of spontaneous repetitive activity at a rate of 87 +/- 47 bpm, which was overdrive suppressed in dogs with slow VT, and spontaneous activity at a rate of 115.2 +/- 36 bpm (p less than 0.05) which was not overdrive suppressed in dogs with fast VT. Maximum diastolic potential, action potential amplitude, and Vmax of surviving subendocardial Purkinje fibers (SEPF) in the infarct zone were slightly but significantly depressed (p less than 0.05), and they manifested enhanced phase 4 depolarization, giving rise to automatic impulse initiation. Although action potential duration of these fibers was somewhat prolonged (p less than 0.05), no conduction delay occurred. Histopathologic examinations have shown necrosis of the basal two thirds of the RV, with no left ventricular involvement. Electron microscopy revealed lipid accumulation in the surviving SEPF as the sole abnormality. We conclude (1) that occlusion of the RCA in the dog is associated with high survival rate despite extensive necrosis involving exclusively the RV and (2) that VT seen during the 20 to 24 hours after occlusion arise in the infarcted zone of the RV, by an enhanced automatic mechanism in the surviving SEPF, possibly caused by cytoplasmic lipid accumulation. This model, by virtue of its high survival rate and frequency of late VTs, should be useful in providing clues to determine factors involved in the genesis of early VT/VF and for the evaluation of new pharmacologic agents during the 20- to 24-hour VT period.

Animals↗
PubMed1985

An advanced form of familial hypertrophic cardiomyopathy showing massive myocardial fibrosis with intramural small arterial thickening. An autopsy case.

An autopsy case of an advanced form of hypertrophic cardiomyopathy (HCM) showing marked fibrosis with intramural small arterial abnormalities is presented in this report. A 52-year-old woman, who had a positive family history of HCM, was admitted because of palpitations. The chest roentgenogram showed a mildly enlarged cardiac silhouette and the electrocardiogram revealed abnormal Q waves and R wave and T wave abnormalities. The echocardiogram revealed hypokinesis with thinning of the interventricular septum and the anterior wall of the left ventricle. Percutaneous right ventricular endomyocardial biopsies demonstrated moderate interstitial fibrosis with small arterial thickening. At necropsy, the anterior and posterior walls of the left ventricle and the interventricular septum were markedly thinned and showed a massive transmural fibrosis. Moreover, the intramural small arteries, 50-300 microns in diameter, showed marked intimal and medial hypertrophy with proliferation of elastic fibers and smooth muscle cells. From these findings, it is suggested that this was originally a case of HCM which progressed to a decompensated stage because of the abnormal intramural small arteries. The significance of small arterial lesions in HCM is discussed.

Cardiomyopathy, Hypertrophic↗
PubMed1985

[Quantitative assessments of regional myocardial perfusion by digital subtraction angiography].

Regional myocardial perfusion was evaluated by computerized washout analysis of digital subtraction angiography (DSA) images. Diatrizoate meglumine (76% Urografin), 2 to 3 ml, was manually injected into the left main coronary artery. For 26 patients with ischemic heart disease (IHD), 14 patients with cardiomyopathy, and eight patients with normal coronary angiograms, DSA images of myocardial perfusions were obtained in the right anterior oblique projection. These were digitized into an image-processing computer. Time-density curves were constructed in four segments of the left ventricle perfused by the left anterior descending coronary artery (LAD) and the contrast decay half-lives (T1/2) were calculated from the decay phases of the curves, using mono-exponential least square fits. The mean T1/2 was significantly longer in patients with 75% or more LAD narrowing than in those with normal coronary arteries. By contrast, patients with 50% or less LAD narrowing had T1/2 comparable to those with normal coronary arteries. In patients with IHD, there was a significant curvilinear relationship of T1/2 with percent stenosis of the LAD. This indicates that a decrease in regional myocardial flow develops rapidly in coronary stenosis of 70-80% or more. In patients with comparable coronary stenosis, T1/2 was significantly longer in the asynergic regions than in those with normal wall motion, but T1/2 was shorter in regions perfused by collateral vessels. These findings indicate that left ventricular contraction and collateral flow could contribute to regional myocardial perfusion. In addition, patients with hypertrophic and dilated cardiomyopathy had prolonged T1/2 despite normal coronary angiograms, suggesting abnormalities in intramural coronary arteries. Thus, T1/2 derived by computerized washout analysis of DSA myocardial image proved to be a useful index for quantitative evaluation of regional myocardial perfusion.

Adult↗
PubMed1984

Factors related to the induction of ventricular fibrillation in the normal canine heart by programmed electrical stimulation.

Programmed electrical stimulation was performed in eight normal dogs using a stimulator and endocardial electrode catheters identical to those used in human studies. The right and left ventricular apex were paced at a drive cycle length of 400 ms and, in some cases, 500 ms, with a pacing sequence of single (S1S2), double (S1S2S3) and triple (S1S2S3S4) premature impulses introduced after eight paced complexes. Pacing sequences were performed using combinations of pulse width (1, 2 and 4 ms) and current strengths of 2, 5 and 10 times diastolic threshold, and in three dogs, 15 times diastolic threshold. Twenty-two episodes of ventricular fibrillation were initiated in five dogs in 170 pacing sequences using current strengths up to 10 times diastolic threshold, and six episodes of ventricular fibrillation in the two of three remaining dogs tested at 15 times diastolic threshold. Ventricular fibrillation was reproducible on seven of nine occasions. Ventricular fibrillation was never induced by S1S2 at up to 15 times diastolic threshold; it was induced by S1S2S3 in 3 (1.8%) of 170 sequences, but only at 10 times diastolic threshold. It was induced by S1S2S3S4 in 19 (11.4%) of 167 sequences using 2 to 10 times diastolic threshold, although 20 of 28 episodes only occurred with S1S2S3S4 at 10 or more times diastolic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The effect of thromboxane synthetase inhibition on cardiopulmonary function during endotoxemia in sheep.

The early pulmonary hypertension seen with endotoxin (lipopolysaccharide) has been reported as resulting from the release of thromboxane A2. We studied the cardiopulmonary response to endotoxin in sheep with and without treatment with a thromboxane synthetase inhibitor, OKY-046. The animals were implanted with instruments for crystallographic dimension analysis of the left ventricle and measurement of left ventricular, aortic, left atrial, and pulmonary arterial pressures and cardiac index. Thirteen sheep received 1.0 micrograms/kg of Escherichia coli endotoxin with (n = 6) and without (n = 7) OKY-046 (10 mg/kg bolus, then 10 micrograms/kg/min). OKY-046 prevented the increase in pulmonary arterial pressure and decrease in cardiac index usually seen during the early phase of endotoxemia. Between 8 and 12 hours after the administration of endotoxin, cardiac index increased from 6.4 +/- 0.8 to 8.4 +/- 0.8 L/min/m2. Concomitantly, the end-systolic pressure/diameter relationship (a sensitive myocardial contractility index) significantly decreased from 14.7 +/- 0.6 to 7.7 +/- 0.7 mm Hg/mm. Another index of the left ventricular contractility, the maximum rate of pressure rise was also reduced. OKY-046 prevented decreases in end-systolic pressure/diameter relationship and maximum rate of pressure rise.

Animals↗
PubMedDate not supplied

The long-term evaluation of pulmonary toxicity following isolated lung perfusion with melphalan in the rat.

The present study was conducted to evaluate the long-term pulmonary toxicity of isolated lung perfusion (ILP) with melphalan in the rat model. F344 rats were treated by ILP with 1 mg of melphalan or buffered hespan (BHE). The rats in the melphalan group were sacrificed randomly 30, 60, 90, 120, 150, and 180 days after the perfusion. Pulmonary toxicity was evaluated by pathological analysis. In the melphalan group, light and electron microscopic findings revealed perivascular and peribronchial edema, and septal thickening with cellular infiltration of the interstitial space 30 days after the perfusion, but all of these changes had disappeared by 60 days. Azan stain showed a slight increase of the connective tissue at the alveolar wall in the melphalan group, but no progressive pulmonary interstitial fibrosis was observed after 180 days. Transmission electron microscopy showed minimal proliferation of the type II pneumocytes of normal appearance in the melphalan group. In conclusion, the long-term pulmonary toxicity of ILP with melphalan is acceptable; however clinical trials of this therapy need to be conducted.

Animals↗