[Epidemiologic study of HAV and HBV infections in persons in various environments].
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
H Abe
Publications and source records attributed to H Abe.
Loading sequence is a major determinant of afterload-dependent relaxation in intact canine heart.
To elucidate the role of loading sequence in afterload-dependent slowed relaxation in hearts in situ, the time constants (Texp from best exponential fitting method and TL from semilogarithmic method) of isovolumetric left ventricular (LV) pressure decay were studied in nine anesthetized open-chest dogs under the pharmacological blockade of autonomic nerve activity. An afterload change was imposed by clamping the ascending or descending aorta to make the peak LV pressure early or late in systole. During afterload interventions, in contractions with the peak LV pressure in late systole Texp and TL were significantly (P less than 0.05) larger than in those with the peak LV pressure in early systole in any comparable peak LV pressure range. Moreover, both time constants were directly correlated (P less than 0.01) with the time of peak LV pressure irrespective of peak LV pressure and clamp mode of aorta. In another protocol, marked differences both in Texp and TL were also observed between each of 25 pairs of contractions with different loading sequence but with comparable peak LV pressure and LV dimension (segment length). Thus afterload-dependent slowed relaxation in hearts in situ could not be attributed to an increased total load but to the altered loading sequence associated with an increase in afterload.
Animals↗
Role of histidine-related compounds to intracellular buffering in fish skeletal muscle.
Histidine-related compounds (HRC) were analyzed in fish skeletal muscle as a means of identifying their precise role in intracellular buffering. Fish muscle was used because it contains two functionally and spatially distinct fiber types, red and white. Two fish species, rainbow trout (Salmo gairdneri) and the Pacific blue marlin (Makaira nigricans), were studied because these species demonstrate widely different activity patterns. Marlin red and white muscle buffer capacity was two times higher than trout with white muscle, buffering being two times greater than red in both species. Buffer capacity was highest in the 6.5-7.5 pH range for all tissues, which corresponded to their high anserine levels. The titrated HRC buffering was greater than the observed HRC buffering, which suggested that not all HRC were available to absorb protons. The HRC contribution to total cellular buffering varied from a high of 62% for marlin white to a low of 7% for trout red. The other principal buffers were found to be phosphate and protein with taurine contributing within red muscle in the 7.0-8.0 pH range. HRC were found to be dominant in skeletal muscle buffering by principally accounting for the buffering capacity differences found between the species and fiber types.
Animals↗
Left ventricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiography: quantitative assessment of aneurysm size in relation to clinical course.
A retrospective study was performed to elucidate the process of left ventricular aneurysm formation and its influence on left ventricular enlargement based on serial two-dimensional echocardiographic observations from 150 consecutive patients with first acute anterior myocardial infarction. Echocardiograms were available and interpretable through the entire period of observation in 68 patients. Because of early death in 13 patients, echocardiograms of 55 patients, 22 with and 33 without aneurysm, were analyzed from 1 to 28 days after infarction. Patients with aneurysms were separated into two groups with large (group 1, 11 patients) and small aneurysms (group 2, 11 patients) on the basis of ratios of aneurysm to overall left ventricular circumferential length [Lcf-LV(RAO)] and area [Area-LV(RAO)], i.e., Lcf(An/LV)-RAO and Area(An/LV)-RAO, respectively, in the right anterior oblique equivalent view at the time of aneurysm formation, with reference to Forrester's subset. Group 1 consisted of patients with Lcf(An/LV)-RAO of 0.4 or greater or Area(An/LV)RAO of 0.3 or greater while group 2 included patients with Lcf(An/LV)-RAO less than 0.4 or Area(An/LV)-RAO less than 0.3. In the test for time trend in these groups with a one-way analysis of variance, Lcf-LV in RAO equivalent and apical four-chamber views and Area-LV in apical four-chamber view effectively separated group 1 from groups 2 and 3 (without aneurysm) with significance (p less than .005, p less than .01, and p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiomegaly↗
Regional distribution of rat growth hormone releasing factor-like immunoreactivity in rat hypothalamus.
A heterologous RIA for rat GH-releasing factor (rGRF) was established using synthetic rGRF-(1-43)OH for both standard reference and radioiodination with the antiserum produced against human GRF-(1-44) NH2. The regional distribution of rGRF-like immunoreactivity (LI) in rat hypothalamus was examined according to the Palkovits microdissection method and compared with that of somatostatin (SRIF)-LI. Both rGRF- and SRIF-LI contents (mean +/- SE; nanograms per mg protein) were highest in the median eminence (rGRF, 32.28 +/- 11.42; SRIF, 109.9 +/- 19.2) and next most abundant in the arcuate nucleus (rGRF, 3.50 +/- 0.47; SRIF, 12.88 +/- 0.60). Only a small amount of rGRF-LI was found in the ventromedial (1.41 +/- 0.51) and dorsomedial (1.16 +/- 0.15) nuclei and the anterior hypothalamic area (1.29 +/- 0.42), whereas rGRF-LI was not detected in the other nuclei of the hypothalamus. A considerable amount of SRIF-LI was contained in the periventricular, ventromedial, and paraventricular nuclei and the anterior hypothalamic area, in accordance with other reports. Gel filtration chromatography revealed that hypothalamic extracts contained a major peak of rGRF-LI corresponding to rGRF-(1-43)OH and two peaks of SRIF-LI equivalent to SRIF-(1-28) and SRIF-(1-14), respectively. These findings indicate that rGRF-LI is localized in the median eminence and arcuate nucleus in the rat and that rGRF-, SRIF-(1-28)-, and SRIF-(1-14)-LI are present in a 1:2.10:6.29 ratio on a molar basis.
Animals↗
Vasoactive intestinal peptide is a physiological mediator of prolactin release in the rat.
To determine whether VIP functions as a physiological PRL-releasing factor, the effects of immunoneutralization of endogenous vasoactive intestinal peptide (VIP) on the PRL secretory response to suckling and ether stress were assessed. Using a porcine VIP-thyroglobulin conjugate as antigen, a peptide-specific antiserum was generated in a rabbit which bound porcine VIP with a Kd of 5.1 X 10(-11) M and a maximum binding capacity of 1830 ng/ml. In a RIA, this antiserum demonstrated immunoreactive VIP in tissue extracts of various regions of the brain and gastrointestinal tract. IR VIP in extracts of cerebral cortex and hypothalamus coeluted with synthetic porcine VIP on Bio-Gel P-30 column chromatography. Using chronically implanted right atrial catheters for blood sampling to avoid effects of stress and anesthesia, PRL blood levels in normal controls began to rise almost immediately after initiation of suckling from basal values of 3.0 +/- 0.9 ng/ml to reach a plateau of 158.1 +/- 33.5 ng/ml after 40 min. When the VIP antiserum was administered immediately before initiation of suckling, the onset of the PRL response was delayed by 40 min, but PRL levels then rose at a slower rate to reach the plateau level of normal animals approximately 80 min later. When VIP antiserum was administered to rats who had been suckling for at least 1 h, PRL levels fell from a mean basal elevated level of 152.7 +/- 16.0 ng/ml to a nadir of 50.4 +/- 9.1 ng/ml 80 min after injection and then gradually returned to basal levels. The effect of VIP antiserum was studied in rats in whom PRL secretion was increased by exposure to ether, a stimulus that acts on the release phase of PRL secretion. In rats in whom the depletion-transformation of PRL was induced by a prior brief period of suckling, subsequent exposure to ether caused a rise in serum PRL levels. The response was completely blocked in rats given VIP antiserum, whereas animals given nonimmune serum showed a significant increase in serum PRL to 38.6 +/- 17.3 ng/ml. We conclude from these studies that VIP mediates the acute PRL response to suckling and is required for maintenance of PRL levels in continuously suckling animals but is not the only factor causing PRL elevation. Complete abolition by the VIP antiserum of the PRL response to ether indicates that the effect of the anesthetic is mediated entirely by the release of VIP. These findings are consistent with the view that VIP is a physiological PRL-releasing factor in the rat.
Animals↗
Effect of passive immunization with antisera to vasoactive intestinal polypeptide and peptide histidine isoleucine amide on 5-hydroxy-L-tryptophan-induced prolactin release in rats.
The present study was aimed to clarify, by use of the passive immunization method, the involvement of endogenous vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine amide (PHI)-like peptides in the stimulation of PRL-like immunoreactive material release induced by 5-hydroxy-L-tryptophan (5HTP), a serotonin precursor. We used conscious, freely moving male rats of the Wistar strain (BW, 250-300 g) chronically cannulated with atrial catheters. Anti-VIP serum (AVS) and anti-PHI serum (APS), each generated in rabbits against synthetic porcine VIP and natural porcine PHI, respectively, were highly potent [maximum binding capacity (Bmax): AVS, 55.5 nmol/ml; APS, 5.53 nmol/ml] and specific. Bolus injection of 5HTP (10 mg/kg BW) through the catheter caused a significant increase in plasma PRL (nanograms per ml) in rats pretreated with normal rabbit serum (NRS) [14.3 +/- (SE) 3.8----56.3 +/- 11.2], with AVS (12.3 +/- 3.5----48.5 +/- 6.2), with APS (10.5 +/- 3.9----43.5 +/- 8.8), and with AVS plus APS (9.0 +/- 1.4----28.5 +/- 2.7). The basal PRL concentrations did not differ significantly among these groups, whereas the PRL responses to 5HTP were significantly blunted in AVS plus APS-pretreated rats (P less than 0.05 vs. NRS). To eliminate the modification by dopaminergic control of 5HTP-induced PRL release, the next experiment was performed in rats repeatedly injected with sulpiride, a dopamine receptor antagonist (5 mg/kg BW), every 30 min. The first injection of sulpiride caused a prompt and marked increase in plasma PRL, followed by decreasing but still high levels of plasma PRL upon the subsequent injections of sulpiride every 30 min. The cumulative release area of PRL after pretreatment with AVS plus APS or APS alone was significantly lower than that after NRS (P less than 0.05). The same dose of 5HTP resulted in a significant further increase in plasma PRL exceeding the levels elevated by sulpiride injections in NRS-treated rats. Prior simultaneous administration of AVS and APS resulted in a complete suppression of 5HTP-induced PRL release, whereas pretreatment with either AVS or APS showed only a minimal effect. These results suggest that endogenous VIP and PHI-like peptides are PRL-releasing factors, involved at least in the mechanism of 5HTP-induced PRL release, in which the dopaminergic control may be also involved.
5-Hydroxytryptophan↗
Idiopathic growth hormone (GH) deficiency, and GH deficiency secondary to hypothalamic germinoma: effect of single and repeated administration of human GH-releasing factor (hGRF) on plasma GH level and endogenous hGRF-like immunoreactivity level in cerebrospinal fluid.
Plasma GH responses to iv administered synthetic human GH-releasing factor-(1-44)-NH2 (hGRF) and the concentration of endogenous hGRF-like immunoreactivity (hGRF-LI) in the cerebrospinal fluid (CSF) were examined in 16 children with GH deficiency (GHD). Ten patients had idiopathic GHD, and six had GHD secondary to germinoma. An iv bolus hGRF (1 microgram/kg BW) injection test was performed the day before and the day after treatment, with a daily 1-h iv infusion of hGRF (2 micrograms/kg BW) for 3 days. Plasma GH increases (greater than 5 ng/ml) after the first iv bolus injection of hGRF occurred in 2 of the 10 idiopathic GHD children and in 4 of the 6 GHD patients with germinoma whereas the first bolus hGRF injection failed to elicit GH release in the remaining 10 patients. The mean +/- SEM peak plasma GH level after the first bolus hGRF dose in the patients with germinoma (8.2 +/- 2.2 ng/ml) was significantly higher than that in the idiopathic GHD patients (2.9 +/- 0.9 ng/ml; P less than 0.05), but significantly lower than that in normal children with short stature (18.5 +/- 2.5 ng/ml; P less than 0.05). In the 2 patients with germinoma and in 5 of the 8 idiopathic GHD children who did not respond to the first hGRF bolus dose, a significant plasma GH response to hGRF occurred during a daily iv infusion of hGRF for 3 consecutive days, whereas the remaining 3 idiopathic GHD children failed to respond to the daily hGRF infusions. The plasma GH response after the second hGRF bolus dose given after treatment with daily hGRF infusions for 3 days was not different from that after the first hGRF bolus in patients with germinoma or that in the idiopathic GHD children. hGRF-LI was not detected (less than 5.8 pg/ml) in the CSF in any of 5 patients with germinoma, whereas it was present in 5 idiopathic GHD patients (mean, 17.5 +/- 0.9 pg/ml), 3 of whom were nonresponders to daily hGRF infusions. From these results, GHD secondary to destruction of hypothalamic GRF neurons might be defined by the following findings: 1) lack of a GH response to the standard provocative tests acting through the hypothalamus; 2) significant increase in plasma GH after a single bolus and/or repetitive iv administration of hGRF; and 3) undetectable or extremely low levels of endogenous hGRF-LI in the CSF. Most of the idiopathic GHD patients responded to the repetitive hGRF infusion, suggesting insufficient secretion of hypothalamic hGRF as the primary defect. However, since hGRF-LI was detectable in the CSF in some of the idiopathic GHD patients, its pathogenesis must be multifactorial.
Adolescent↗
Presence of growth hormone-releasing factor-like immunoreactivity in human cerebrospinal fluid.
Immunoreactive human growth hormone-releasing factor (I-hGRF) in human cerebrospinal fluid (CSF) was measured by radioimmunoassay using antiserum specific to the C-terminal portion of hGRF(1-44)NH2. Dilution curves of I-hGRF in the CSF were completely parallel to that of synthetic hGRF(1-44)NH2 standard. On Sephadex G-50 column chromatography a single peak of I-hGRF in the CSF was eluted at the position of synthetic hGRF(1-44)NH2. I-hGRF was present in the CSF of all control patients without any endocrine disease (mean +/- SE, 29.3 +/- 2.0 pg/ml) whereas I-hGRF in the CSF was not detectable (less than 5.8 pg/ml) in any of the patients with hypothalamic germinoma. In all patients with idiopathic GH deficiency, I-hGRF in the CSF was measurable but its concentration (15.1 +/- 1.0 pg/ml) was significantly (p less than 0.05) lower than that in the control subjects. No difference in I-hGRF levels of the CSF was observed between patients with acromegaly and control subjects. These findings demonstrate for the first time that I-hGRF is present in human CSF. Measurement of I-hGRF in the CSF may be useful for understanding the pathophysiology of hypothalamo-pituitary diseases.
Acromegaly↗
Augmentation by propranolol of growth hormone-releasing hormone-(1-44)-NH2-induced growth hormone release in normal short and normal children.
The effect of a 90-min iv infusion of propranolol, a beta-adrenergic antagonist (0.2 mg/kg BW), on basal plasma GH levels and the GH responses to an iv bolus injection of GH-releasing hormone-(1-44)-NH2 (GHRH; 1 microgram/kg BW) was examined in 10 prepubertal children (6 short but otherwise normal and 4 normal). The iv injection of GHRH resulted in significant increases in plasma GH, comparable to those after either insulin-induced hypoglycemia or arginine infusion. Only a small and inconsistent increase in plasma GH levels occurred during the iv infusion of propranolol, whereas simultaneous administration of propranolol with GHRH caused marked enhancement of GHRH-induced GH release in all subjects. The difference between the plasma GH response to GHRH given with propranolol and the response to GHRH given with 0.9% saline was significantly greater than that between the plasma GH level after propranolol and that after 0.9% saline infusion without GHRH injections. There was no difference in plasma GH responses to GHRH, propranolol, or both in the normal short children or normal children. These findings indicate that beta-adrenergic blockade potentiates GHRH-induced GH secretion in prepubertal children.
Child↗
Structure-activity relationship for antibacterial action of phenolic and aromatic nitro compounds. An attempt at systematic identification of new antibacterial agents.
Explore the source record for details and available documents.
Anti-Bacterial Agents↗
Augmented energy consumption during early systole as a mechanism of cyclical changes in high-energy phosphates in myocardium assessed by phosphorus nuclear magnetic resonance.
To evaluate the underlying mechanism of oscillatory changes in energy-related metabolites during a cardiac cycle, intramyocardial creatine phosphate (CP), inorganic phosphate (Pi), adenosine triphosphate (ATP), adenosine diphosphate (ADP) and pH were measured in isolated rat hearts by the phosphorus nuclear magnetic resonance spectrometry method gated by the left ventricular pressure. These were perfused with modified Krebs-Henseleit solution containing pyruvate. CP decreased at both early- and end-systole whereas Pi and ADP increased in these phases. Both ATP and intracellular pH decreased significantly at end-systole. The indices of the affinity for ATP hydrolysis [Pi]/[CP] and [ADP] [Pu]/[APT] increased at early-systole, indicating that a large consumption of high-energy phosphates occurred at early-systole. Furthermore, the cyclical changes in ATP, CP and Pi were augmented in the high contractile state induced by infusion of isoproterenol. These results strongly suggest that the cyclical changes in the energy-related metabolites during a cardiac cycle are caused mainly by an augmentation of energy consumption during early-systole and an insufficient energy supply during systole, probably due to the slow intracellular transport of CP.
Adenosine Diphosphate↗
Role of mesangial proliferation in angiotensin II and antidiuretic hormone induced changes in glomerular filtration rate.
The effects of administration of angiotensin II (ANG II) and antidiuretic hormone (ADH) on the glomerular filtration rate (GFR, measured as creatinine clearance) were examined in patients with mesangial proliferation. For this study, the patients whose conditions were similar to that of healthy subjects, except for asymptomatic urinary abnormalities and glomerular histological changes, were selected. Both ANG II and ADH administration significantly decreased GFR in the patients and the healthy subjects. Compared to the healthy subjects, a significantly greater drop in GFR was observed in the patients following ANG II infusion with or without SQ14225 administration, but not following ADH infusion. We conclude that mesangial proliferation may modulate an ANG II induced drop in GFR.
Adult↗
Altered loading sequence as an underlying mechanism of afterload dependency of ventricular relaxation in hearts in situ.
Underlying mechanisms of afterload dependency of ventricular relaxation rate were studied in nine isolated canine hearts and nine open chest dogs. In isolated hearts with isobaric contraction, peak LV pressure was increased by volume loading with stroke volume unchanged, and in anesthetized open chest dogs the afterload was altered by a manual clamp of the descending aorta to various extent under the pharmacological blockade of the autonomic nerve activity. Ventricular relaxation rate was assessed by the time constant (T) of isovolumic LV pressure decay. In hearts in situ of open chest dogs, T was progressively (p less than 0.01) increased as peak LV pressure increased, whereas in isolated hearts T was decreased as afterload increased (p less than 0.05), indicating that peak LV pressure is not a major determinant of ventricular relaxation rate. Between these two heart preparations loading sequence of the heart during contraction was characteristically different; in open chest dogs, as afterload increased ejection timing was accelerated and the time of peak LV pressure (TPmax) was prolonged, whereas TPmax in isolated hearts was decreased and ejection timing was progressively delayed as an increase in afterload. Consequently, TPmax showed a high correlation with T irrespective of peak LV pressure. These results indicate that T is directly dependent on loading sequence mainly regulated by ejection timing. This finding was also confirmed in open chest dog experiments in which 20 pairs of contractions with comparable peak LV pressures and LV dimensions (end-systolic and end-diastolic lengths) but characteristically different loading conditions during contraction (early maximal loading vs late maximal loading) were obtained by the manual clamp of ascending aorta; in early maximal loading conditions (TPmax: 185 +/- 8 ms) T's (66 +/- 3 ms) were significantly (p less than 0.01) smaller than those (110 +/- 10 ms) in late maximal loading conditions (TPmax: 261 +/- 11 ms). A change in loading sequence associated with afterload interventions in hearts in situ may be due to a change in compliance in peripheral arterial system. We conclude that afterload dependency of ventricular relaxation rate observed in hearts in situ could be attributed to the accompanied changes in loading sequence of the heart probably due to a change in arterial compliance. The dependency of relaxation on loading sequence of the heart might be clinically important in evaluating the effect of cardiovascular agents on ventricular relaxation since these agents may largely affect the vascular compliance as well as muscular relaxation per se.
Animals↗
Development of quantitative analysis of plasma thromboxane B2 by gas chromatography-mass spectrometry.
In order to diagnose patients in thrombotic state, it is quite important to detect increased concentration of plasma thromboxane B2 (TXB2), a stable catabolite of TXA2. To determine plasma TXB2 levels with high sensitivity and selectivity, we employed gas chromatography-mass spectrometry (GC/MS). The trimethylsilyl (TMS) ether derivatives conventionally employed in GC/MS analysis of prostanoids are not suitable for quantitation of plasma prostanoids, because the mass spectra are deficient in ions with high intensity in the high mass range and TMS ether derivatives are sensitive to moisture. To solve these problems we employed tert-butyldimethylsilyl (t-BDMS) ether derivatives, based on the observation that t-BDMS ether derivatives afforded abundant ions at [M-57]+ and showed good hydrolytic stability. The reaction conditions of tert-butyldimethylsilylation were also examined to optimize the selected ion monitoring response. The t-BDMS ether derivatives of prostanoids were successfully analyzed with a short capillary column with a relatively large diameter, with maintaining good separation. In conjunction with the use of reversed-phase high performance liquid chromatography as purification procedure, a sensitive and reproducible stable isotope dilution assay of plasma TXB2 was developed. The values obtained by this method correlated well with those obtained by the radioimmunoassay we have developed.
6-Ketoprostaglandin F1 alpha↗
[Clinical application of BRM on cancer treatments].
Explore the source record for details and available documents.
Adjuvants, Immunologic↗
[A case of renal arteriovenous fistula with giant renal aneurysm presenting as heart failure].
Explore the source record for details and available documents.
Aneurysm↗
[Benign osteoblastoma of the atlas. Case report].
Explore the source record for details and available documents.
Bone Neoplasms↗