[Physiological significance of secretin on gastric secretion].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Shiratori.
Explore the source record for details and available documents.
We investigated the reasons for discrepancies between two-dimensional echocardiography (2DE) and left ventriculography (LVG) in detecting interventricular septal asynergy in anterior or inferior myocardial infarction. Twenty-six patients with anterior infarctions due to proximal lesions of the left anterior descending artery and 20 patients with inferior infarctions due to proximal lesions of the right coronary artery were studied by 2DE and LVG. A 2DE long-axis view, a short-axis view at the papillary muscle level, an apical four-chamber view (AP-4CV), and right and left anterior oblique left ventriculograms (RAO-LVG and LAO-LVG) were recorded. The interventricular septum (IVS) on LAO 60 degree-LVG was divided into the basal and apical portions. 2DE and LVG were independently evaluated individually by the same readers, and the interventricular septal asynergy was classified as hypokinesis, akinesis and dyskinesis. Anterior infarction About 80% of the patients with akinesis of the apical third of the IVS in a long-axis view or of the apical half of the IVS in an AP-4CV were assessed as having akinesis of the entire septum by LAO-LVG. Inferior infarction Asynergy was echocardiographically detected in the posterior IVS in a short-axis view at the papillary muscle level. LAO-LVG showed asynergy in the apical third of the posterolateral segment (segment 7) in all cases and akinesis in the apical IVS in six of 20 patients (30%). In conclusion, the extent of asynergy of the IVS in anterior infarction is overestimated by LAO-LVG compared to 2DE, and asynergy of the apex assessed by LAO-LVG in inferior infarction will correspond to that of the inferior segment by 2DE. This discrepancy is attributed to the different planes between a long-axis view and an LVG projection. We conclude both LVG and 2DE are mandatory for estimating accurately the extent of asynergy in the infarcted IVS.
In a previous report, we showed that pericardium closure is responsible for post-operative abnormal septal motion. To elucidate this hypothesis, we performed additional clinical and experimental studies. Twenty-six patients were studied during cardiac surgery. We also studied five dogs during cardiopulmonary bypass using M-mode and two-dimensional echocardiography. M-mode echograms and short-axis views of the left ventricle were obtained before and after pericardiotomy, and before and after pericardium closure. In the clinical study, the patients were divided into three groups according to pre-operative septal motion: Group 1 included six patients with atrial septal defect showing paradoxical motion, Group 2 included thirteen patients with aortic or mitral regurgitation of hyperdynamic motion, and Group 3 consisted of seven patients with ventricular septal defects or mitral stenosis showing normal systolic motion. In Group 1, septal motion became normal after closure of atrial septal defect and then, became abnormal just after pericardium closure. Again in Group 2, septal motion became normal following surgical repair, but abnormal motion appeared immediately after pericardium closure. In Group 3, normal septal motion persisted until just prior to closure of the pericardium. Abnormal septal motion in all groups persisted following chest closure. In all dogs, paradoxical septal motion resulted from pericardium closure after cardio-pulmonary bypass. We conclude that both pericardium closure and cardio-pulmonary bypass are responsible for post-operative abnormal septal motion.
Electrocardiographic features of apical hypertrophic cardiomyopathy are high QRS voltage and giant negative T waves greater than 10 mm in left precordial leads. We analyzed thirty patients with apical hypertrophic cardiomyopathy to clarify the correlation between left ventricular (LV) wall thickness and the depth of negative T waves. LV anterior wall thickness was measured by the left ventriculogram (LVG) in the RAO projection. LV posterior wall and septal thickness were measured by echocardiograms recorded from the left sternal border. THA and THM were defined as apical thickness and mid ventricular wall thickness, respectively. The results were as follows: LVG disclosed that the depth of negative T waves in apical hypertrophic cardiomyopathy was significantly related to the absolute thickness of apical segment itself rather than the difference in the distribution of thickness from the basal to apical segment of the left ventricle. This results support the clinical observation that giant negative T waves in some cases are associated with diffuse hypertrophy of the LV without a spade like configuration in LVG. Results of the echocardiographic analysis, however, revealed that the depth of negative T waves had no relation to the distribution of left ventricular hypertrophy. This is partly because of unsatisfied and difficult recordings and measurements of the true LV apical segment by echocardiography. The presence of both high QRS voltage and giant negative T waves is indispensable for the diagnosis of apical hypertrophy.
It is well known that right ventriculography has unavoidable disadvantages as a method for diagnosing tricuspid regurgitation. In this study, inferior vena caval angiography (IVC angiography) was tested as a new method for quantitatively diagnosing tricuspid regurgitation. With this method, no catheter passes through the tricuspid valve, and only a small amount (10 ml) of contrast material injected into the upper portion of the inferior vena cava visualizes the entire right atrium, and tricuspid regurgitation is manifested by turbulence or a negative jet in the right atrium. With respect to the degree, tricuspid regurgitation was graded as absent (0), mild (1+), moderate (2+) and severe (3+) using the criteria shown in Fig. 1. Mild tricuspid regurgitation was diagnosed when systolic turbulence was observed in the right atrium and did not reach the right atrial wall. Moderate tricuspid regurgitation was diagnosed when systolic turbulence reached the right atrial wall. Severe tricuspid regurgitation was diagnosed when systolic turbulence entered the inferior vena cava. Sixty-four patients with valvular heart disease and four having coronary heart disease were studied using IVC angiography and pulsed Doppler echocardiography. Using Doppler, the severity of tricuspid regurgitation was determined according to the distribution of the regurgitant signal in the right atrium. The degree of tricuspid regurgitation by IVC angiography correlated well with that by Doppler. All patients with severe (3+) regurgitation and 15 of 22 patients with moderate (2+) regurgitation required surgery, but all with no (0) regurgitation and 12 of 14 with only mild (1+) regurgitation required no surgical correction of the tricuspid valve.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Thirty-eight cases of hypertrophic cardiomyopathy associated with asymmetric septal hypertrophy (ASH) were analyzed in order to correlate the electrocardiographic findings with the distribution of hypertrophic portions identified by two-dimensional echocardiograms. The electrocardiographic features which characterize the selected cases with ASH in this study were abnormal Q waves or regression of R waves in the left precordial leads (six obstructive type and six non-obstructive type) and a pattern of left ventricular hypertrophy (LVH) (31 cases including five cases with abnormal Q waves) (Table 1). There was no significant relation between the voltage of a R wave in V1 and the degree of septal thickness. From the electrocardiographic features mentioned above, the patients were divided into two groups, i.e., 1) the patients with abnormal Q waves (12 cases) and 2) those with LVH without abnormal Q waves (26 cases). The difference in the pattern of distribution of hypertrophy was evaluated based on the presence or absence of the abnormal Q waves. The results were as follows: Although there were no differences in the degree of septal thickness in both groups, the posterior wall in the group with LVH was significantly thicker. The group with LVH showed diffuse hypertrophy in the left ventricular free wall as well as the septum. Moreover, the short-axis view of two-dimensional echocardiograms revealed that hypertrophy in the septum was diffuse in both anterior and posterior portions.(ABSTRACT TRUNCATED AT 250 WORDS)
1-Phenyl-1-hydroxy-N-pentane is a synthetic derivative of an ingredient of Curcuma longa that is used as a condiment and dye. The effects of 1-phenyl-1- hydroxy-N-pentane on release of secretin, gastrin, and pancreatic secretion of bicarbonate and protein were studied in both dogs and humans. In fasting dogs with gastric fistulas and modified Herrera's pancreatic fistulas, intraduodenal administration of 1-phenyl-1-hydroxy-N-pentane (pH 6.7) in three different doses (25, 50, and 100 mg/kg) resulted in significant increases in both plasma secretin concentration and bicarbonate output. The increases in the two variables were dose related. The bicarbonate output and plasma secretin concentration produced by the doses of 1-phenyl-1-hydroxy-N-pentane correlated well. No significant change occurred in either protein output or plasma gastrin concentration. The effect of intragastric 1-phenyl-1-hydroxy-N-pentane on release of secretin and pancreatic secretion was also studied in the digestive state. While gastric pH was maintained at 5.5 by intragastric titration with 1 N NaOH after intragastric administration of 5% liver extract solution, intragastric administration of 1-phenyl-1-hydroxy-N-pentane (100 mg/kg) resulted in significant increases in both plasma secretin concentrations and pancreatic bicarbonate output. In the same experiment, the plasma gastrin concentration did not change significantly, whereas gastric acid secretion decreased significantly after the 1-phenyl-1-hydroxy-N-pentane administration. In 6 human volunteers, both plasma secretin concentration and pancreatic bicarbonate output significantly increased when 2% 1-phenyl-1-hydroxy-N-pentane solution, 30 ml/30 min, was infused in the upper jejunum. Again, no increase in the protein output was apparent. These studies indicate that endogenous secretin is released by an agent other than acid and suggest strongly that the increased pancreatic bicarbonate secretion is attributed to the increased plasma concentration of secretin. 1-Phenyl-1-hydroxy-N-pentane may be a useful agent for release of secretin in subjects with achlorhydria, severe hyposecretory state, or total gastrectomy.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Responses of serum gastrin to both intravenous infusion of secretin (GIH secretin 3 CU/kg/hr) and intravenous bolus injection (GIH secretin 1 CU/kg) were studied in 2 Zollinger-Ellison syndrome (ZE) patients and 27 duodenal ulcer (DU) patients. In all of the DU patients, the stage of the ulcer was determined endoscopically, prior to testing, as either active or healed. We found that the responses of serum gastrin to secretin were closely related to the stage of the duodenal ulcer; serum gastrin increased in the active stage and decreased in the healed stage. In patients with active duodenal ulcer, a false positive (ZE-like) response to exogenous secretin was observed. Comparing the results of intravenous infusion and bolus administration of secretin in terms of maximal percent change of serum gastrin, there was no significant difference between the two methods, confirming the works reported by others.
The two-dimensional echocardiogram was successfully obtained during syncopal attack due to obstruction in the outflow tract of the left ventricle in a 52 years old male with hypertrophic obstructive cardiomyopathy (HOCM). The diagnosis of HOCM was confirmed by cardiac catheterization which revealed a pressure gradient of 65 mmHg in the outflow tract of the left ventricle during intravenous infusion of isoproterenol (2 micrograms/min). During the test, the patient developed convulsion as well as syncopal attack. The two-dimensional echocardiogram demonstrated a marked protrusion followed by a fixation of the whole mitral complex (SAM component) toward the hypertrophied interventricular septum throughout whole cardiac cycles. Although the mechanism of this phenomenon is not clear, it can be speculated that an abnormally sustained excitation and contraction of the papillary muscles (just like a muscle cramp) may be induced, resulting in the left ventricular outflow tract obstruction.