Effect of stellate ganglion stimulation on coronary hemodynamics and cardiac surface electrocardiogram in open-chest anesthetized dogs (An experimental study)

The effect of electrical stimulation of unilateral right and left stellate ganglia (SG) on coronary hemodynamics and the cardiac surface electrocardiogram (ECG) was studied in openchest anesthetized dogs. The results were as follows: 1) Both right and left SG stimulation resulted in significant increase of mean coronary blood flow, stroke diastolic coronary blood flow, left ventricular segmental contraction, heart rate and aortic blood pressure, with decrease of stroke systolic coronary blood flow, and coronary vascular resistance, Except for heart rate and blood pressure, these changes caused by left SG stimulation were significantly greater in the left circumflex coronary artery (LCX) area than in the left anterior descending coronary artery (LAD) area. However, right SG stimulation disclosed no significant difference between the two coronary areas. Left SG stimulation increased the positivity of the T wave of the cardiac surface ECG of the LCX area and the negativity of the LAD area, while right SG stimulation increased the positivity of the T wave in both areas. The QT interval of the cardiac surface ECG was unchanged or slightly shortened, but the QT ratio by Bazzet's formula was increased in both areas by SG stimulation. The data obtained suggest that the functional distribution of right SG and left SG innervation to the ventricles is different, that the LAD area is predominantly innervated by right SG, and the LCX area is innervated equally by right and left SG. 2) Intravenous (I.V.) administration of phentolamine (0.1mg/kg/min.) resulted in no significant change in hemodynamics or ECG patterns produced by SG stimulation, as compared. with untreated animals. However, administration of propranolol (0.5mg/kg I.V.) inhibited the effect of SG stimulation on coronary hemodynamics and cardiac surface ECG. This suggests that the effect of electrical SG stimulation may be caused by catecholamine release at sympathetic nerve endings, hence, beta receptor stimulation at coronary artery areas

Effect of propranolol on regional myocardial function in anesthetized open-chest dogs with myocardial ischemia

Effects of propranolol on ischemic segmental function were studied in anesthetized open-chest dogs. Two segment-length gauges were used for measuring the regional myocardial function: one was sutured on to the left ventricular surface perfused by the anterior descending coronary artery (ischemic zone) and the other was on to that perfused by the circumflex coronary artery (normal zone). A bolus of propranolol (0.5 mg/kg) was injected into the right femoral vein. Five min later, the left anterior descending coronary artery (LAD) was completely occluded for one mine and thereafter released. Then a second coronary occlusion for 20 min was performed; an interval of 20 min was allowed between two occlusions. Propranolol, in the ischemic segment, apparently decreased the extent of paradoxical lengthening in the late systole following one min LAD occlusion, and facilitated improvement of segmental function after release of the occlusion. Moreover, the extent of abnormal stretching induced by 20 min occlusion during early systole, was also reduced by propranolol pretreatment. In contrast, compensatory increase in shortening by the normal segment was disturbed by propranolol. These results suggest that propranolol might exert a favourable influence on the segmental myocardial function during either transient or maintained myocardial ischemia.</p

A patient with repeated syncopal attacks after using isosorbide dinitrate

The case of a patient with repeated attacks of collapse induced by sublingual isosorbide dinitrate is reported. The patient was an 81 year-old female who was admitted to Yura Hospital because of attacks of precordial pain. Several minutes after the sublingual administration of isosorbide dinitrate (10 mg) for an anginal attack, she developed a sensation of general weakness, and thereafter because unconscious. Arterial blood pressure fell and became unmeasurable. Electrocardiograms recorded during the syncopal attack showed sinus tachycardia and significant elevation of ST-segment in right precordial leads. In response to a drip infusion of noradrenaline, arterial blood pressure returned to normal with recovery of consciousness. Two similar syncopal attacks induced by sublingual isosorbide dinitrate occurred in the next three days. These attacks were not due to augmentation of the vagal reflex. Decrease of venous return probably was the primary etiological factor.</p

Surgical Resection of Hepatic Cystic Echinococcosis Impaired by Preoperative Diagnosis

Cystic echinococcosis (CE) is a rare afferent infectious disease in Japan. This paper reports a case of a hepatic cyst being diagnosed after surgical resection. A 40-year-old Syrian male was admitted for evaluation of a hepatic cyst. Serum antibodies of echinococcosis were negative. Enhanced computed tomography of the abdomen revealed a large cystic lesion, 9 cm in diameter, in the left lateral sector of the liver, which had many honeycomb-like septa and calcified lesions. Magnetic resonance imaging of this lesion revealed high intensity in the T2 weighted image. We preoperatively diagnosed this lesion as cystadenocarcinoma or CE and performed a left hepatectomy. Pathological examination revealed the presence of protoscolices in the fluid of the cysts and led to a diagnosis of this lesion as CE. In conclusion, on seeing patients with huge hepatic cysts who come from an epidemic area, we should consider hepatic CE

Correlation of systolic time interval with abnormal myocardial contraction by coronary occlusion in anesthetized open-chest dogs.

The correlation between the systolic time interval and abnormal contraction in ischemic myocardium was studied in anesthetized open-chest dogs. A strain-gauge was sutured on the surface of the left ventricular wall perfused by the left anterior descending coronary artery (LAD) for measuring segment-length. The left ventricular stroke volume decreased progressively after occlusion of LAD. The left ventricular ejection time (LVET) was progressively shortened in close correlation with the elongation of segment-length at the onset of isometric relaxation in 20 seconds after LAD occlusion when early systolic myocardial contraction and isometric contraction time (ICT) were not affected. ICT was gradually prolonged and closely related with the lengthening of the early systolic segment-length, while LVET recovered toward the control level in spite of further decrease in stroke volume. A close relationship was observed between ICT/LVET and stroke volume (gamma = 0.76, P less than 0.01). The results suggested the possibility that LVET was normalized even when the left ventricular function was impaired, and ICT/LVET ratio was the most sensitive index of LV dysfunction.</p

Effect of myocardial ischemia and nitroglycerin on systolic time intervals in the segmental myocardium

Effects of ischemia and nitroglycerin on systolic time intervals in the segmental myocardial length were studied in anesthetized open-chest dogs. Two strain-gauges were sutured on the surface of the left ventricular wall; one was in the central area perfused by the left circumflex coronary artery (LCX) and the other was in the area perfused by the left anterior descending coronary artery. LCX was partially occluded with a screw type constrictor to the degree at which reactive hyperemia after the transient total coronary occlusion almost disappeared. After the hemodynamics stabilized nitroglycerin (20 microgram/kg) was injected into the femoral vein. In the ischemic area, contraction time was shortened and precontraction time was prolonged in association with an elongation of end-systolic and early systolic segment-length, respectively. The systolic time intervals in the ischemic segment were improved as a result of the recovery in the segment-length toward the control. The results suggest the usefulness of analyzing the segmental myocardial systolic time intervals for verifying the asynchronous contraction of the ventricle and the favourable effects of nitroglycerin on segmental myocardial function in the ischemic area.</p

The Lectures on the Development of Teaching Plans and Teaching Materials Tried in the Science Education Class in Master's Course, Okayama University

岡山大学大学院教育学研究科の理科教育専攻の講義として、教材開発・授業案開発をテーマとした新しい講義を試みたのでその報告を行う。本講義は、理科教育講座に所属する大学院生、理科教育講座の大学教員、附属学校の理科関係の教諭が三者協働で進めることが特徴である。課題設定、教材開発を含めた実践準備および実践を院生チームを組み遂行させ、さらに経験や専門性の異なる人材と論議を重ねて活動を進めることを通じ、将来、協働で学校現場の課題提案・解決を行うことのできる能力を養うことを目標とした。This is a report of the new type of lectures on the development of teaching plans and teaching materials attempted in the science class in the Master's Course, Okayama University. The lectures were conducted in collaboration of the graduate students and the academic staffs in the science education course, and the science teachers of the attached school of Okayama University. The graduate students were grouped into two teams of five or six people, assigned to decide on themes, prepare and practice the development of teaching plans and teaching materials. They conducted their activities discussing problems with people of different experience and specialty, thus developing the ability to jointly propose and solve problems at schools in future

Astrocytic dysfunction induced by ABCA1 deficiency causes optic neuropathy

Astrocyte abnormalities have received great attention for their association with various diseases in the brain but not so much in the eye. Recent independent genome-wide association studies of glaucoma, optic neuropathy characterized by retinal ganglion cell (RGC) degeneration, and vision loss found that single-nucleotide polymorphisms near the ABCA1 locus were common risk factors. Here, we show that Abca1 loss in retinal astrocytes causes glaucoma-like optic neuropathy in aged mice. ABCA1 was highly expressed in retinal astrocytes in mice. Thus, we generated macroglia-specific Abca1-deficient mice (Glia-KO) and found that aged Glia-KO mice had RGC degeneration and ocular dysfunction without affected intraocular pressure, a conventional risk factor for glaucoma. Single-cell RNA sequencing revealed that Abca1 deficiency in aged Glia-KO mice caused astrocyte-triggered inflammation and increased the susceptibility of certain RGC clusters to excitotoxicity. Together, astrocytes play a pivotal role in eye diseases, and loss of ABCA1 in astrocytes causes glaucoma-like neuropathy

Vitamin D3-induced hypercalcemia increases carbon tetrachloride-induced hepatotoxicity through elevated oxidative stress in mice.

The aim of this study was to determine whether calcium potentiates acute carbon tetrachloride (CCl4) -induced toxicity. Elevated calcium levels were induced in mice by pre-treatment with cholecalciferol (vitamin D3; V.D3), a compound that has previously been shown to induce hypercalcemia in human and animal models. As seen previously, mice injected with CCl4 exhibited increased plasma levels of alanine aminotransferase, aspartate aminotransferase, and creatinine; transient body weight loss; and increased lipid peroxidation along with decreased total antioxidant power, glutathione, ATP, and NADPH. Pre-treatment of these animals with V.D3 caused further elevation of the values of these liver functional markers without altering kidney functional markers; continued weight loss; a lower lethal threshold dose of CCl4; and enhanced effects on lipid peroxidation and total antioxidant power. In contrast, exposure to V.D3 alone had no effect on plasma markers of liver or kidney damage or on total antioxidant power or lipid peroxidation. The potentiating effect of V.D3 was positively correlated with elevation of hepatic calcium levels. Furthermore, direct injection of CaCl2 also enhanced CCl4-induced hepatic injury. Since CaCl2 induced hypercalcemia transiently (within 3 h of injection), our results suggest that calcium enhances the CCl4-induced hepatotoxicity at an early stage via potentiation of oxidative stress