In order to diagnose right ventricular hypertrophy (RVH) more precisely and quantitatively, body surface isopotential mappings (MAPs) and standard 12 lead ECGs (ECGs) were recorded in pulmonary artery banded dogs and sham operated dogs before and after surgery. MAP and pathoanatomical findings (RV/LV weight ratio) were compared, and the relationships among the MAP and ECG parameters were examined. Pathoanatomical RVH (RV/LV weight ratio>0.65) developed 12 months after PAbanding. The indices derived from MAPs were analyzed statistically by one way analysis of variance. After PA banding, R max·V gradually increased on the anterior-inferior chest surface, S max·V increased on the left high back, T max·V increased on the lower chest surface and the R max ratio and RV/LV weight ratio were correlated (r=0.55, p<0.1), so R max ratio may reflect anatomical RVH quantitatively. These changes were statistically significant (p<0.05), while the usual parameters for diagnosing RVH such as QRS axis, R/S (V1), RV1, SV5, SV6, RV1+SV5 and VAT (V1) showed no significant changes after the operation. The foregoing findings suggest that MAP is superior to conventional ECG for diagnosis of RVH.
In order to diagnose right ventricular hypertrophy (RVH) more precisely and quantita-tively, isopotential body surface mappings (MAPs) and standard 12 lead electrocardiograms (ECGs) were studied in 39 patients with three different hemodynamic types of chronic right ventricular overload. Sokolow and Lyon's criteria were useful in detecting right ventricular overload. However, ECG parameters were not useful in differentiating between hemodynamic states. The increase of R max·V from precordial leads was thought to be characteristic of right ventricular pressure overload. The Increase in S max·V from right precordial leads was thought to be characteristic of right ventricular volume overload, while the increase in S max·V from left lateral chest and left back leads reflected right ventricular volume and pressure overload. T max·V showed no significant findings. The prolongation of R max·T in the right precordial area was thought to be characteristic of right ventricular volume overload, while the prolongation of R max ·T in the left high back was regarded as indicating hypertrophy in the right ventricular outflow tract due to pressure overload. The prolongation of S max·T in the right precordial area was thought reflect right ventricular pressure overload, while the prolongation of S max·T in the left high back was regarded as indicating right ventricular volume overload. The prolongation of VAT (V1), BT time and QRS interval suggested chronic right ventricular volume overload. R max·V (F4), S max·V (I3) and QRS interval were selected for analysis of variance, and discriminant analysis was made using these variables. Twenty nine out of 39 patients were classified correctly, and the accuracy of discrimination was 74.4%.
Alpha and beta-adrenergic effect on the coronary circulation of the right ventricle were studied in comparison with those of the left in anesthetized open chest dogs. Norepinephrine was administrated and the cardiac sympathetic nerve was stimulated with beta-blocker pretreatment to determine whether there was any difference in vasoconstriction between the right and left coronary arteries. When the right and left cardiac sympathetic nerves were stimulated, coronary vasoconstriction was considerably greater in the RCA than in the LAD, while coronary vasoconstriction induced by NE injection was greater in the LAD than in the RCA. These data indicated that the pre-synaptic alpha-adrenergic stimulation caused affected the RCA and LAD differently from the post-synaptic alpha-adrenergic stimulation as to the extent of coronary vasocostriction. With phentolamine pretreatment the nerve stimulation caused no difference in the rate of increase of mean coronary blood flow between the RCA and LAD, and the rate of increase of RVSP×HR was greater than that of LVSP×HR. These results indicate that cardiac sympathetic nerve stimulation affected the right ventricle more than the left mainly through beta-adrenoceptors. The response of the right ventricle to increased oxygen demand was possibly, in part, different from that of the left.
A comparison of blood flow and myocardial O2 consumption (MVO2) in the right and left ventricle was made in 24 open-chest dogs. The effects of volume loading by arterio-venous (AV) and arterio-left atrial shunts, and of ventricular hypoperfusion by rapid removal of blood were examined in the presence and absence of the pericardium. Blood flow per unit myocardium was greater in the left anterior descending coronary artery (LAD) than in the right coronary artery (RCA). Similarly, the myocardial O2 extraction ratio (EO2) was higher in the left than in the right ventricle. The MVO2 was greater in the left than in the right ventricle. Volume loading to both ventricles by AV shunt increased MVO2 of the right ventricle by augmenting EO2 in addition to increasing the coronary arterial blood flow. Decreasing aortic pressure by rapid removal of blood increased EO2 in both ventricles, though more in the right ventricle than in the left ventricle. When the pericardium was closed by suturing, the right and left end-diastolic pressure rose, but EO2 and coronary blood flow of neither ventricle changed. We conclude that the reserve capacity of myocardial O2 extraction was greater in the right ventricle than in the left ventricle.
Using an immunoperoxidase method, we analyzed T cell subpopulation, subsets and immunoglobulin-containing cells in the mucosa of small intestines obtained from 19 patients with liver cirrhosis and 8 patients without any liver disease (controls). Percentages of IgA-containing cells in the lamina propria of the small intestines from the liver cirrhosis patients tended to be higher than in the same tissue of the controls. In contrast, percentages of pan T cells and cytotoxic/suppressor T cells in the lamina propria and numbers of intraepithelial pan T and cytotoxic/suppressor T cells in the tissues from liver cirrhosis patients tended to be lower than in the controls. Furthermore, the percentage of IgA-containing cells in the lamina propria was significantly higher and the percentage of pan T and cytotoxic/suppressor T cells in the lamina propria was significantly lower in the small intestines of patients with decompensated liver cirrhosis than in the small intestines of the controls. The lower percentage of pan T and cytotoxic/suppressor T cells observed in the small intestine of patients with liver cirrhosis, especially decompensated liver cirrhosis, may be related to general impairment of cellular immunity in liver cirrhosis and to enhanced humoral immunity in the small intestine as shown by the increase in IgA-containing cells.
Catecholamine (CA) and 5-hydroxytryptamine (5-HT) concentrations in the yolk, albumen, whole embryo, brain, heart, liver and kidney of embryonic and developing White Leghorn chicks were determined by high performance liquid chromatography. The brain, kidney, heart and liver were dissected from embryos after 12, 14, 16, 18 and 20 days of incubation, and 3, 7, 11, 15, 19, 39, 59, 99 and 159 days after hatching. 5-HT was found in the fertilized and unfertilized yolk, but CA was not found in either. The 5-HT concentration in the fertilized yolk increased until hatching, while it decreased in the unfertilized yolk. CA and 5-HT were found in the whole embryo on the 6th day, and their concentration increased with development. The CA and 5-HT concentrations in the brain increased from the embryonal stage to the 15th day after hatching, and then they became stable. The CA and 5-HT concentrations fluctuated in the heart, liver and kidney. It was interesting that the 5-HT concentration in the liver and norepinephrine concentration in the kidney showed a very large peak during hatching.
To examine the changes in the body surface isopotential maps (maps) with the increase of age, recorded maps at 87 lead points of 296 normal healthy adults, and I analyzed maps comparatively among six groups. On mean maps at the time of 10 msec from the QRS initial, the position of the maximum (the greatest positive potential at a certain time point) shifted lower on the anterior chest, and that of the minimum (the greatest negative potential at a certain time point) shifted higher on the back with increasing age. At 30 msec the potential of the maximum decreased on the left anterior chest surface in males, while it increased in females with increasing age. The maximum potential of QRS on each lead (Rmax V) slightly decreased on the antero-superior chest in males, while it clearly increased from the left anterior chest to the left back in females with increasing age. The value of % VC decreased with age in both sexes. These data suggested that the potential of Rmax V was affected by heart size and lung impedance. However in females, changes in the breast might have a greater influence on the changes in Rmax V. The sex difference in Rmax V became smaller with age. The minimum potentials of QRS (Smax V) decreased on the upper anterior chest and back surface. No sex or age differences were found in the ratio of the breakthrough recognition, although the time of the breakthrough tended to increase in both sexes. On ST and T maps, there were few changes with age, but significant sex differences were observed among every age group. These were significant differences in maps between the aged and younger groups. Careful attention should be paid to age and sex differences, when analyzing maps of aged persons.
Serum levels of α-tocopherol (α-Toc), lipoperoxide (TBARS) and lipids were studied in the acute stage of stroke. Serum α-Toc was 0.74±0.32mg/dl (n=67) within 48 hours of the onset of stroke, which was significantly lower than the level of the control group (0.99±0.22mg/dl). Concurrently, serum TBARS was 6.04±2.17nmol/ml (n=57) which was markedly higher than the level of the control group (3.22±0.89nmol/ml). No correlation was seen in serum α-Toc and TBARS. However, serum total cholesterol (TC) correlated with α-Toc in stroke. Serum α-Toc of most cases of stroke dropped to the lowest level in the first 5 to 6 days and thereafter recovered gradually. The ratio of α-Toc to TC in serum reached a minimum in the early phase and then rose gradually over two weeks. Serum TBARS increased during the first week, and thereafter decreased slowly. These results imply that α-Toc may be consumed as an antioxidant against lipoperoxide which presumably increases depending on tissue damage induced by stroke.
Serum levels of α-tocopherol (α-Toc), lipoperoxide (TBARS), total cholesterol (TC) and free fatty acid (FFA) were studied before and after the administration of vitamin E (dl-α-tocopheryl acetate) for 4 weeks (400 mg/day im for the first week, thereafter 600 mg/day po) in the acute stage of stroke. Serum α-Toc was significantly lower, but TBARS was higher than that of the control in the first day of outbreak. Vitamin E administration elevated the serum α-Toc level in a few days, but did not affect the TC level. On the otherhand, the serum TBARS level remained at a plateau for 4 weeks. These results led us to conclude that vitamin E must inhibit the elevation of TBARS, which otherwise was observed in most cases of stroke in the first week. There were three stroke patients whose serum α-Toc happened to have been measured 2 or 4 months prior to attack, and two of them had low levels of α-Toc (less than 0.5 mg/dl) at that time. Soon after stroke developed, serum α-Toc was lower in the three patients. These findings suggest that a low level of serum α-Toc could be one of the risk factors of stroke.
Endoscopic examinations were performed in 59 patients under general anesthesia just before or after surgery for cerebrovascular accidents. Acute gastric mucosal lesions were observed in 32 cases (54.2%). By the second day after the cerebrovascular accident, gastric petechiae and/or erosions in the corpus of the stomach were mainly observed. Acute duodenal ulcer became obvious from the third day after the accident. These upper gastrointestinal lesions were observed frequently in cases with low consciousness levels and cases with large hematomas. Gastrointestinal bleedings was observed in 19 cases. Bleeding in 6 cases observed by the second day after the cerebrovascular accidents was relatively mild. In contrast, bleedings in 7 cases observed 3 days after the third day from the accident was serious. Three patients died, and 2 cases underwent surgery stop to the bleeding. These data suggest that it is important to perform endoscopic examination in patients with cerebrovascular accidents as soon as possible to check for acute upper gastrointestinal lesions and bleedings. Mild bleeding observed by the second day after the accident can be treated conservatively. In contrast, since the bleeding observed after the third day can potentially be severe, immediate endoscopic treatment or an emergency operation may be necessary to stop the bleeding.
Changes in gastric mucosal prostaglandin (PG) E1 in rats with acute gastric mucosal lesions caused by water immersion stress or by brain damage were studied. Rats with brain damage were prepared by injecting cyanoacrylate into the brain. PGs were extracted from gastric mucosae, and PGE1 was separated by silicic acid column chromatography and converted into PGB by alkaline treatment. PGE1 was measured by radioimmunoassay using a double antibody method with anti-PGB1 antibody. In normal rats, values of PGE1 in the gastric mucosa were 249.3+64.3 pg/mg protein (mean+standard deviation). In the rats which underwent water immersion stress, PGE1 values were significantly elevated (p<0.01) above the normal values 2, 3, and 6 hours after the treatment. In the rats with brain damage, PGE1 values did not change significantly for 3 hours after the brain damage. However, 6 hours after the treatment, PGE1 values were significantly elevated (p<0.01) above the normal values. In the rat which underwent water immersion stress, the elevation of PGE1 was inhibited by intraperitoneal administration of atropine sulfate, diazepam, hexamethonium bromide or 6-hydroxy dopamine (6-OHDA). In contrast, in the rats with brain damage, the elevation of PGE1 was significantly suppressed only by hexamethonium bromide and 6-OHDA which suppress the sympathetic nerve.
False tendons in the heart of several mammals were investigated by light and electron microscopies. False tendons were recognized macroscopically as chordal structures in the inner surface of the ventricles in the cow, pig, monkey, dog and rabbit. The outer surface of false tendons were covered with the same endothelial cell layer as the endocardium. Under the cell layer, there was thick connective tissue whose center was occupied by several bundles of Purkinje fibers. Among Purkinje fibers, thin connective tissue was present, in which small vessels and non-myelinated nerve fibers were observed. False tendons were identified in rats by light microscopy, but they were not found in mice. Purkinje fibers in false tendons varied among species. In artiodactyla, Purkinje fibers were larger and had fewer cell organella than those of other animals. Three types of intercellular junctions, desmosomes, intermediate junctions and gap junctions (nexus), were observed. Nexuses were often observed. Nerve fibers in the false tendons were all nonmyelinated. These nerve fibers only passed through the false tendons, and nerve endings were not found. Nerve cell bodies were not found either. From these results, the roles of false tendons in heart conduction were discussed.
Guanidino compounds in various chick tissues were systematically analyzed by high performance liquid chromatography, and the changes in guanidino compound levels were studied during chick embryogenesis and development. In the whole chick embryo, arginine (Arg), creatinine (CRN), guanidinoacetic acid (GAA), β-guanidinopropionic acid (GPA), homoarginine (HArg), guanidine (G) and methylguanidine (MG) were detected. Arg, CRN and GAA appeared after the sixth day of incubation, and the other compounds appeared after the eighth day of incubation. All of the compounds, except for Arg which temporarily decreased on the eighth day of incubation, increased as embryogenesis progressed. In the yolk, Arg, CRN, GAA, GPA, HArg, G and MG were detected. Most of them dramatically increased at the late stage of embryogenesis. A slight increase in Arg, CRN and G in unfertile eggs was also observed after incubation. In the albumen, Arg, CRN, GAA, G and MG were detected. Arg, CRN, GAA, G and MG increased during embryogenesis. A slight increase in Arg, CRN and G in unfertile eggs was also observed after incubation. In the chick brain, liver, kidney and heart, Arg, CRN, GAA, GPA, HArg and MG were detected. Guanidinosuccinic acid and γ-guanidinobutyric acid, which are commonly detectable in the mammalian liver and brain, were not detectable in the chick organs. All guanidino compounds in the chick organs fluctuated greatly during development. GPA decreased as the chicks developed and was not detected in the adult organs. These observations suggest that birds have a different metabolic system of guanidino compounds from that of mammals, and that this system is activated during embryogenesis and affected by various physiological factors after hatching. It was also suggested that guanidino compounds, even at very low levels, might have some important roles in animal tissues during development.
Mice were exposed to 1, 000 ppm of 1, 1, 1-and 1, 1, 2-trichloroethane (TCE) for one hour, and the organ distribution was examined. The levels of both TCEs in the organs were in the descending order of adipose tissue, the liver and the kidneys. The levels of 1, 1, 2-TCE in adipose tissue and the kidneys were higher than those of 1, 1, 1-TCE, but the level of the former was lower than that of the latter in the liver. The biological half-life of 1, 1, 2-TCE in the organs was longer than that of 1, 1, 1-TCE.
Mice were injected intraperitoneally with 1, 1, 1-and 1, 1, 2-trichloroethane (TCE), and the amounts of their metabolites exhaled from the lungs and excreted in the urine were measured. Exhalation from the lungs ended 7 hours after the injection. The ratio of the accumulated amount of 1, 1, 1-TCE to the amount of 1, 1, 1-TCE injected was 84.7%, and the ratio for 1, 1, 2-TCE was 9.8%. The accumulated amount of total trichloro-compounds in the urine of mice to the amount of 1, 1, 1-TCE injected was 1.07%, and that for 1, 1, 2-TCE was 0.15%. The total amount exhaled from the lungs and that excreted in the urine of mice injected with 1, 1, 1-TCE was greater than that of mice injected with 1, 1, 2-TCE.
Variations in the levels of ATP and triglyceride (TG) in the liver and TG concentration and GPT activity in the plasma of mice exposed to 1, 1, 1-and 1, 1, 2-trichloroethane (TCE) were studied. The decrease in liver ATP, increase in liver TG, decrease in plasma TG and increase in plasma GPT were greater in mice exposed to 1, 1, 2-TCE than in mice exposed to 1, 1, 1-TCE. It was inferred that the biosynthesis of serum lipoprotein in the liver was inhibited, thus causing fatty liver. The increased level in plasma GPT is considered to be a sensitive and early indication of liver disturbance caused by TCE. The decrease in liver ATP, and the increase in liver TG in the mice were in the desending order of carbon tetrachloride, 1, 1, 2, 2-tetrachloroethane, 1, 1, 2-TCE, tetrachloroethylene, trichloroethylene, 1, 1, 1, 2-tetrachloroethane, and 1, 1, 1-TCE. The inhibitory effect of 1, 1, 2-TCE on the liver was stroner than that of 1, 1, 1-TCE, suggesting that the effect of 1, 1, 2-TCE is due to production of free radicals.
Although various hypotheses have been proposed about the ultrastructure of the glomerular basement membrane (GBM) of the kidney, it has not clearly revealed. At present, it is thought to be composed of a meshwork of fibrils as reported by Ota et al. We successfully observed the meshwork structure of the GBM under an electron microscope after enzymatic treatment with α-amylase and elastase. The fibrils were about 30 nm in width and were thought to be composed of type IV collagen.