Aortico-left ventricular tunnel: two-dimensional echocardiographic and angiocardiographic features.
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Biomedical subjects
Publications and source records attributed to Y F Chen.
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This report describes a new rapid, convenient and inexpensive method of concentrating biogenic amines and their metabolites from biological samples for analysis by HPLC-EC. Recovery of standard monoamines and metabolites from artificial cerebrospinal fluid (CSF) solution following lyophilization in the presence of glutathione (1.2 mg/ml, final concentration) and EGTA (1.8 mg/ml, final concentration) was greater than 89%; the coefficient of variation was 0.6-3.7%, depending on the specific amine or metabolite concentrated. Lyophilization as a one step procedure is suitable for concentrating biogenic amines and metabolites from biological fluids such as CSF that contain low concentrations of protein and other interfering substances. When concentrating compounds from plasma, which contains large quantities of protein and other electrochemically active materials, it is necessary to add an extraction step, such as alumina extraction. By substituting 0.05 M HCl for the conventional eluent, 0.1 M HClO4, we were able to increase recoveries of catecholamines from plasma by approximately 20%. Recovery of endogenous catecholamines from plasma following the combined alumina extraction - lyophilization procedure was 81 +/- 1%.
Our previous studies demonstrated that high dietary NaCl intake causes increases in blood pressure and plasma norepinephrine (NE) levels and a decrease in NE release associated with local upregulation of alpha 2-adrenoceptor number in the anterior hypothalamic area (AHA) of NaCl-sensitive spontaneously hypertensive rats (SHR-S). Further, acute microinjection of clonidine into the AHA of SHR-S fed a high NaCl diet resulted in greater depressor and bradycardic responses than in SHR-S receiving a normal NaCl diet. The current study tested the hypothesis that the antihypertensive effect of chronic systemic administration of guanabenz (0.24 micrograms/kg/min, IV) is enhanced in SHR-S maintained on a high (8%) NaCl diet than in control rats on a normal (1% NaCl) diet. After two weeks on the diets, mean arterial pressure (MAP) and heart rate (HR) were measured and blood for NE and epinephrine (E) assay was collected from intra-arterial cannulas in conscious, unrestrained rats. The ratio of left ventricle and septum to body weight (LV + S/BW) was determined. Chronic infusion of guanabenz significantly decreased MAP (P less than .05), HR (P less than .01) and LV + S/BW (P less than .01) in 8% NaCl fed SHR-S, but not in 1% NaCl fed SHR-S (P greater than .1). Guanabenz tended to reduce plasma NE levels in 8% NaCl fed SHR-S (.1 greater than P greater than .05), but not in 1% NaCl fed rats (P greater than .1).(ABSTRACT TRUNCATED AT 250 WORDS)
Central monoaminergic neurons, particularly noradrenergic neurons, are involved in the pathogenesis of hypertension. Dietary NaCl supplementation in NaCl-sensitive spontaneously hypertensive rats (SHR-S) elevates blood pressure, increases peripheral sympathetic nervous system activity, and depresses endogenous noradrenaline stores and noradrenaline release in the anterior hypothalamus (AHA). NaCl-resistant spontaneously hypertensive rats (SHR-R) and normotensive Wistar-Kyoto (WKY) rats are resistant to the NaCl-induced alterations in blood pressure and central and peripheral noradrenergic activity, whereas uninephrectomized Sprague-Dawley rats treated with DOCA + NaCl and Dahl-S rats receiving dietary NaCl supplementation develop NaCl-induced increments in blood pressure, but not depressed AHA noradrenaline release. The AHA is a major cardiovascular regulatory region, and depressor responses elicited by pharmacological (alpha 2-adrenoceptor) stimulation of this area are exaggerated in SHR-S fed a high NaCl diet compared to SHR-S fed a basal diet and SHR-R and WKY fed a high or basal NaCl diet. alpha 2-Adrenoceptors in the AHA are increased in number in SHR-S fed a high NaCl diet, presumably reflecting upregulation in response to reduced local noradrenaline release. These findings are consistent with the hypothesis that decreased noradrenergic activity of sympathoinhibitory neurons in the AHA may mediate the exacerbation in hypertension that occurs in SHR-S during dietary NaCl supplementation.
The authors previously demonstrated that arginine vasopressin (AVP) lowers pulmonary artery pressure in rats with hypoxic pulmonary hypertension by activation of the V1 receptor. The pulmonary depressor effect of AVP in hypoxia-adapted rats is not due to its effect on cardiac output. The current study tested two alternative hypotheses: that AVP lowers pulmonary artery pressure in the hypoxia-adapted lung by (1) dilating pulmonary vasculature directly, or (2) releasing atrial natriuretic peptide (ANP) from the heart. The first hypothesis was tested by injecting AVP into the pulmonary arteries of isolated, buffer perfused lungs and monitoring pulmonary artery pressure, and by exposing preconstricted pulmonary artery rings to graded doses of AVP and monitoring the tension generated. AVP caused minimal vasodilation in perfused lungs and only a small vasodilator effect in pulmonary artery rings. The second hypothesis was tested by injecting AVP (160 ng/kg) or vehicle intravenously in conscious hypoxia-adapted (4 weeks) or air control rats and measuring ANP in arterial blood and atria, and by testing pretreatment with the V1 receptor antagonist d(CH2)5 Tyr(Me)AVP (130 micrograms/kg) on the AVP-induced increase in plasma ANP. AVP produced a 7-fold increase in plasma ANP (209 +/- 33 to 1346 +/- 233 pg/ml; p less than 0.05) in hypoxia-adapted rats and a 5-fold increase in ANP (122 +/- 22 to 573 +/- 174 pg/ml; p less than 0.05) in air controls. ANP release was abolished by pretreatment of both groups with d(CH2)5 Tyr(Me)AVP. The AVP-induced ANP release came mainly from left atrium. These data strongly suggest that the pulmonary depressor effects of AVP in hypoxia-adapted rats is due to augmented V1 receptor-induced release of ANP from left atrium.
Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.
Our previous studies demonstrated that chronic dietary NaCl supplementation is associated with significant increases in plasma atrial natriuretic factor in Wistar-Kyoto (WKY) rats but not in NaCl-sensitive spontaneously hypertensive rats (SHR-S). The current study tested the hypotheses that 1) acute volume-induced atrial natriuretic factor release is impaired in SHR-S compared with control NaCl-resistant SHR (SHR-R) and WKY rats maintained on basal (1%) NaCl diets; 2) dietary NaCl supplementation (8% NaCl for 2 weeks) alters acute volume-dependent atrial natriuretic factor release in these strains; and 3) replacement of the deficiency in circulating atrial natriuretic factor seen in NaCl-supplemented SHR-S can reverse the NaCl-sensitive component of hypertension. SHR-S and control SHR-R and WKY rats were placed on 1% or 8% NaCl diets at age 7 weeks; 2 weeks later, right atrial pressure and plasma atrial natriuretic factor were measured in conscious rats before and after acute volume expansion (7, 20, and 60 ml/kg, 5% dextrose, for 1 minute). The slopes of the right atrial pressure x plasma atrial natriuretic factor linear regression for the SHR-S fed both 1% and 8% NaCl were significantly shallower (p less than 0.01) than those of 1% NaCl-fed SHR-R or WKY rats. Dietary NaCl supplementation did not alter right atrial pressure in any strain and blunted acute volume-induced atrial natriuretic factor release in WKY rats, but not in SHR-S or SHR-R, suggesting the dietary NaCl-induced elevation in plasma atrial natriuretic factor levels in WKY rats may be related to impaired clearance, as well as enhanced release, of the peptide. The plasma levels of exogenous atrial natriuretic factor required to abolish the NaCl-induced pressor effect in SHR-S were 12-fold greater than endogenous plasma atrial natriuretic factor levels in 8% NaCl-fed WKY rats, suggesting that impairment of atrial natriuretic factor release does not play a major role in the pathogenesis of NaCl-sensitive hypertension in SHR-S.
gamma-Glutamyl transpeptidase (gamma-GT) localization in exfoliative esophageal specimens was evaluated in a population of 911 individuals aged 35 or older who lived in an area of China with a high incidence of esophageal squamous carcinoma. Of the total population, 24.4% was positive for gamma-GT. Graded histopathologic cellular classification revealed the following incidences: normal, 10.4% (43 of 413); hyperplasia, 22.0% (44 of 200); Grade I dysplasia, 42.4% (98 of 231); Grade II dysplasia, 46.0% (23 of 50); near-carcinoma, 100% (4 of 4); and squamous carcinoma, 77.0% (10 of 13). In these groups gamma-GT-positive cells were usually from normal esophageal squamous epithelium. A lower incidence of gamma-GT-positive cells was found for dysplastic cells (dysplasia grade I, 6.5% (15 of 231); grade II, 10.0% (5 of 50). The presence of gamma-GT-positive cells in normal esophageal squamous epithelium may prove useful for identification of suspect populations; the presence in dysplastic cells may serve as a diagnostic marker for patients who will soon progress to the carcinoma stage and who should receive early treatment and careful follow-up.
Our previous studies demonstrated that (a) dietary Ca2+ supplementation prevents the rise in blood pressure, activation of sympathetic outflow, and reductions in anterior hypothalamic norepinephrine (NE) content and release induced in NaCl-sensitive spontaneous hypertensive rats (SHR-S) by dietary NaCl loading; and (b) stimulation of alpha 2-adrenoceptors by microinjection of clonidine into the anterior hypothalamic area (AHA) results in an exaggerated depressor response in SHR-S fed a high NaCl diet as compared with SHR-S on a basal diet. The current study tested the hypothesis that dietary Ca2+ supplementation prevents these NaCl induced defects in AHA noradrenergic neurons. SHR-S were placed on diets containing: (a) high NaCl; (b) high Ca2+; (c) high Ca2+, high NaCl; or (d) basal NaCl, basal Ca2+ (control). Two weeks later, clonidine (0.6, 1.2, or 2.5 micrograms) was microinjected into the AHA of conscious rats. Clonidine caused dose-dependent decreases in mean arterial pressure (MAP) and heart rate (HR) that were greater in SHR-S on the high NaCl diet than on the control diet. Ca2+ supplementation prevented the exaggerated depressor response to clonidine in high NaCl-fed SHR-S, but did not reduce the response in SHR-S on the basal NaCl diet. Ca2+ supplementation had no effect on blood pressure (BP) or HR responses to clonidine in control NaCl-resistant SHR (SHR-R) or in normotensive Wistar Kyoto (WKY) rats.
CA 19-9 is a carbohydrate antigen isolated from human colon carcinoma cell line, and is reportedly a tumor marker for pancreatic carcinoma. In this study we determined serum CA 19-9 in 71 normal subjects, 103 patients with benign digestive diseases, 85 patients with periampullary cancers, and 160 patients with other digestive cancers. Serum CA 19-9 was elevated only in 2.3% of normals and benign digestive disease patients, whereas it was increased in 72.7%, 86.4%, and 89.5% of pancreatic, ampullary, and choledochal carcinoma patients, respectively. Of other digestive cancer patients, it was elevated in 23.8%. In addition, very high serum CA 19-9 (greater than 120 u/m) was more often observed in patients with pancreatic, ampullary, and biliary cancer patients than in GL cancer patients (54.1% vs 9.4%, p less than 0.001). In 18 normal subjects and 68 patients with benign and malignant diseases, it was found that CA 19-9 content in the pancreatic juice was significantly increased in pancreatic, ampullary, and choledochal cancer patients, whereas in chronic pancreatitis patients it was normal, indicating that it is a specific and valuable tumor marker in differential diagnosis of pancreatic cancer.
Two patients with Zollinger-Ellison Syndrome were diagnosed and treated in PUMC Hospital, the primary tumors were found in the stomach. On sectioning of the gastrectomized specimens, 85 tumors ranging from 0.1 to 1.0 cm in diameter were disclosed in Case 1, and a large ulcero-infiltrative carcinoma-like tumor in Case 2. Both tumors had already metastasized to regional lymph nodes and/or liver. Tumor cells in both cases exhibited gastrin, NSE, GH and hCG alpha immunoreactivity immunocytochemically, and abundant neurosecretory granules of 100-250 nm in diameter under electron microscope. The clinicopathological, immunocytochemical and ultrastructural findings of tumors from these two cases met the criteria of primary malignant gastrinoma of the stomach.
CA 19-9 is a carbohydrate antigen isolated from a human colon carcinoma cell line and reportedly related to gastrointestinal cancers and important for the diagnosis of pancreatic cancer. The present study was aimed at evaluating the diagnostic significance of CA 19-9 by determining serum and pancreatic juice CA 19-9 in 432 and 86 subjects, respectively, including pancreatic cancer patients, normal persons, and patients with a variety of benign and malignant gastrointestinal diseases. An increase of serum CA 19-9 was found in 73% of pancreatic cancer patients, 50% had levels higher than 120 mu/ml, and both of these were significantly higher than normal persons and patients with benign and other malignant diseases. CA 19-9 in the pancreatic juice of pancreatic cancer patients was significantly elevated, whereas in chronic pancreatitis patients it was entirely normal, indicating that CA 19-9 is a valuable tumor marker important for the differential diagnosis of pancreatic cancer.
From August 1985 to February 1987, 43 cases with falciparum malaria were noted in Yongkang County of Zheijiang Province, an area breed from the disease. These patients had been to the border area between Yunnan Province and Burma, approximately making up 5-7% of the returned population from the endemic area. Most of cases were found during the periods of January to March and June to August when they came home. No introduced case was reported due to prompt case diagnosis and treatment as well as immediate focal management.
Gamma-glutamyl Transpeptidase (gamma-GT) activity of abrasive balloon cytocollections from esophagus of a population aged above 35 in high risk area was studied. Gamma-GT positive rate of the 931 subjects studied was increasingly elevated with the severity of histopathologic changes as follows: normal group 10.3% (43/419), hyperplasia group 21.9% (46/210), dysplasia group 43.9% (125/285), pre-carcinoma group 100% (4/4), squamous carcinoma group 77% (10/13). All or most of the gamma-GT positive cells of each group were normal esophageal squamous epithelium (NESE). They may be initial transformed cells similar to discrete gamma-GT rich cell population without morphological changes observed during very early stages of chemical carcinogenesis. In addition, gamma-GT positive hyperplastic cells and dysplasia grade I cells were also observed in some cases, but dysplasia grade II cells with gamma-GT activity were only shown in a few cases. 1-1.5 years after the mass screening, all the gamma-GT positive cases and gamma-GT negative dysplasia cases were planned to be followed. However, only 277 cases were followed and observed. Histopathologic changes developed rapidly in fifteen cases and fourteen of them were gamma-GT positive cases 1-1.5 years before. Thus, the development of gamma-GT activity may show the trend of histopathologic progression. Gamma-GT on NESE, hyperplastic cells and dysplasia grade I cells showed two fates--progression or fade, whereas the fade rate was reversed with the severity of histopathologic changes. Thus, these changes may be the sign of doubtful population to different extents.(ABSTRACT TRUNCATED AT 250 WORDS)
A total of 111 patients underwent open heart surgery during which myocardial preservation was provided by systemic hypothermia, topical cardiac cooling and cardioplegic solution (blood cardioplegia or electrolyte cardioplegia). The purpose of this study was to determine if the use of the different types of cardioplegia correlated with the occurrence of postoperative supraventricular arrhythmias and conduction disturbances. These patients were retrospectively divided into two groups according to the difference in the infused cardioplegic solutions. The group receiving blood cardioplegia (BCP) comprised 69 patients and the group receiving electrolyte cardioplegia (ECP) had 42 patients. There were a longer ischemic time and bypass time in the BCP group as compared with those of the ECP group (68.4 +/- 36.1 minutes v.s. 50.7 +/- 37.0 minutes, p less than 0.01; 93.7 +/- 48.9 minutes v.s. 65.5 +/- 39.1 minutes, p less than 0.005). However, the result shows a significantly lower incidence of supraventricular arrhythmias and conduction disturbances in the BCP group (5.8%) as compared with the ECP group (21.4%; p = 0.013). There was no significant difference in incidence of supraventricular arrhythmias and conduction disturbances between the two groups when the ischemic time was less than 60 minutes (6.7% v.s. 17.2%, p greater than 0.05). On the other hand, there was a significant difference between the two groups when the ischemic time was a significant difference between the two groups when the ischemic time was longer than 60 minutes (5.1% v.s. 30.8%, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
There was a 45-day old small baby with 2,650 g of body weight undergoing surgical operation of patent ductus arteriosus because of congestive heart failure and severe pulmonary hypertension. A simple and rapid method as proposed by Traugott et al for obliteration the ductus with two ligaclips (Ethicon LC300) is presented.
Dietary calcium (Ca2+) supplementation lowers blood pressure in many forms of genetically mediated and experimentally induced hypertension. The present study tested the hypothesis that neuronal mechanisms underlie the blood pressure-lowering effect of dietary Ca2+ in NaCl-sensitive spontaneously hypertensive rats (SHR-S). SHR-S were fed one of the following diets: control (0.75% NaCl/0.68% Ca2+); high NaCl (8.00% NaCl/0.68% Ca2+); high Ca2+ (0.75% NaCl/2.00% Ca2+), and high NaCl/high Ca2+ (8.00% NaCl/2.00% Ca2+). SHR-S on the 8% NaCl diet for 2 weeks displayed significantly elevated blood pressure (161 +/- 4 mmHg) compared with those on the control diet (139 +/- 3 mmHg). Ca2+ supplementation prevented a rise in blood pressure in rats on the high-NaCl diet but did not alter blood pressure in rats consuming 0.75% NaCl. Plasma norepinephrine stores and turnover in the hypothalamus (anterior and posterior regions), brainstem (pons and medulla) and thoracic spinal cord were assessed using the dopamine-beta-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole. The 8% NaCl diets reduced anterior hypothalamic region norepinephrine stores and turnover. Concomitant Ca2+ supplementation restored norepinephrine turnover to normal, but did not alter norepinephrine stores in the anterior hypothalamic region. In other regions, no significant differences in norepinephrine content or turnover were observed among groups. In SHR that are resistant to high-NaCl diets (SHR-R), the diets did not alter blood pressure, and neither dietary NaCl nor Ca2+ supplementation affected norepinephrine turnover in any brain region studied. These data indicate that in SHR-S on a diet high in NaCl, Ca2+ supplementation may prevent the NaCl-induced exacerbation of hypertension by increasing norepinephrine turnover in the hypothalamus.
One thousand three hundred and two patients with carcinoma of the nasopharynx were initially treated with radiation therapy at this hospital in 1974. The overall 1-, 3-, 5-, and 10-year survival rates were 89.86%, 60.60%, 47%, and 33.03% respectively. At the end of the radiotherapeutic course the residual lesion rate was 10.52% in the nasopharynx 17.27% in cervical lymphnode. In about one-half of the cases with residual lesions, the masses disappeared without further treatment. Prognosis was not improved in the group with supplemental doses. The recurrence rates of the primary nasopharyngeal and metastatic cervical lesion were 18.43%, and 16.12% respectively within 10 years after initial treatment. The 10-year survival rate of the patients with a second course of radiotherapy was 15.04%, higher than of those not retreated (4.9%). Data of this group also reveal that the present pathological classification cannot reflect the degree of prognosis. Increase dosage or combination with chemotherapy did not improve the prognosis. Radiation encephalomyetic damage is discussed.