Biomedical subjects
Publications and source records attributed to D Jordan.
The progress about the control by the pituitary gland of TSH secretion involves the clinical use of TRH test. However some TSH deficiencies are due to an hypothalamic disorder. A better knowledge about the aminergic regulation of the TRH secretion is necessary to design a new test exploring the hypothalamic structures which control TSH secretion.
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Previous studies have shown that in heat exposed rats, a decreased plasma T4 concentration was associated with a normal biologically active TSH concentration. This study was designed to clarify this apparent discrepancy in the regulation of TSH secretion. In experimental rats (34 degrees C for 25 days) and controls (25 degrees C), plasma total T4 was 3.2 vs. 5.7 x 10(-8) mol/l. (P less than 0.01), plasma total T3: 2.4 vs. 5.7 x 10(-10)mol/l. (P less 0.01) and plasma TSH: bioassay 0.34 vs 0.29 mU/ml (ns), radioimmunoassay: 1.04 vs. 0.87 microgram RP1/ml (ns). After TRH, plasma TSH increased identically in the two groups. In heat-exposed rats, the dialysable fraction of T4 and T3 were were increased: 0.032 vs. 0.020% (P less than 0.05) and 0.102 vs. 0.086% (P less than 0.05), respectively; accordingly, free T4 concentration was normal and that of free T3 was low; total plasma proteins were slightly increased. It is concluded that in heat-exposed rats: (1) plasma thyroid hormone binding activity was decreased as shown by the association: decreased plasma total T4--elevated free T4 fraction. The normality of the free T4 concentration accounted for the normal plasma TSH. (2) the combination of normal plasma TSH, normal plasma free T4, low plasma free T3 concentrations would suggest that T4 is predominantly involved in the regulation of TSH secretion.
The duration, contour, and amplitude of atrial flutter wave (f) was studied by electrocardiogram (ECG) and vectorcardiogram (VCG) in 32 patients and was related to the size of the left atrium (LA) measured by the echocardiogram (E). The following ECG parameters were analyzed: (1) the duration of left atrial depolarization, i.e., LA wave; (2) the amplitude of LA wave; (3) the surface area of LA wave; (4) maximum amplitude (A) of f in Leads 2 and V1. There was good correlation between LA size and the duration of depolarization and surface area (p less than 0.01), but the maximum amplitude of the f wave in Leads 2 and V1 failed to predict LA size. The post-conversion sinus P wave showed abnormal LA depolarization time (P greater than 0.12 sec.) in 62 per cent of patients with enlarged left atrium (ELA) and in 43 per cent of patients with normal size LA (NLA). The VCG of the flutter wave revealed two patterns, (1) an eliptical smooth fsE loop in 63 per cent of patients with NLA, and (2) distorted fsE loop in 67 per cent of patients with ELA. Both VCG patterns were subdivided in two subgroups according to the number and location of conduction delays. The VCG of post-conversion P wave confirmed conduction delays in both groups. We conclude that both the size of the left atrium and conduction delays play a basic role in the duration and contour of left atrial wave.
Injection of serotonin (5-HT) into the third ventricle of the rat resulted in a rapid increase of serum TSH; a significant effect was observed 5 min after injection, whereas the maximal effect appeared 10 min after the injection of 1 microgram 5-HT. This stimulating effect of 5-HT was completely prevented by pretreatment with cyproheptadine, a blocker of 5-HT receptors, whereas fluphenazine, a dopamine receptor blocker, was unable to block it. Third venticle injection of 5-HT in rats bearing anterior hypothalamic lesions (which did not affect the suprachiasmatic nucleus or the medio-basal hypothalamus) also induced an increase of serum TSH similar to that observed in normal rats despite the fact that these animals show a lower basal TSH. In vitro, the addition of 5-HT to an incubation medium containing one hemi-anterior pituitary did not modify medium TSH, whereas 5-HT addition induced an increase of medium TSH in the system containing one hemi-anterior pituitary and two hypothalami. We conclude that 5-HT acts on TSH function probably through a stimulation of TRH release.
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Compound action potentials evoked by electrical stimulation in the brainstem of anaesthetized, paralyzed cats and rabbits were recorded distally in the carotid sinus nerve. The latencies of the components of the responses were indicatives of fibres with conduction velocities between 0.5 and 32 m/s. These include both myelinated and unmyelinated fibres. Using histological reconstruction of the 'responsive sites', the termination of the primary afferent fibres of the sinus nerve within the medulla was mapped. In both cat and rabbit these responsive sites were restricted to the doromedial medulla in the vicinity of the NTS 0--3 mm rostral to the obex. Although in the cat the fast conducting myelinated fibres (conduction velocities greater than 12.5 m/s) were discretely localized to the ventrolateral area of the NTS, the slower conducting myelinated and unmyelinated fibres were found more diffusely, spreading into areas dorsal and medial to the NTS. In the the rabbit the terminals of all types of fibre were mainly confined to the NTS although some C fibres appeared to be grouped in the juxta-alar region. Responses were never evoked from the medial reticular formation or nucleus ambigus in either cats or rabbits. The organization of the sinus nerve input to the medulla is discussed in the light of these results.
The mechanism of action of adiphenine on in vitro rat anterior pituitary TSH release was compared to that of the physiological stimulator TRH. The comparative study showed that adiphenine and TRH were able to increase TSH release in a dose-dependent manner, had similar time courses of action for equipotent stimulating concentrations and produced similar aspects of stimulated TSH cells. However, there were several differences between the effects of adiphenine and TRH. Adiphenine action was inhibited by 20 mM K+; was not calcium dependent; was inhibited by neither thyroid hormones nor somatostatin; was little affected by energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the TSH release pathway and could be a useful pharmacological tool for studying the mechanism of TSH release.
The volume overload type of heart often observed in endurance athletes, was simulate a diseased heart. We used a battery of noninvasive graphic techniques, i.e., echocardiogram, apexcardiogram, carotid pulse, electrocardiogram, vectorcardiogram, phonocardiogram, systolic time intervals, and treadmill stress testing in 12 professional marathon runners, mean age 33.8 +/- 11.1. Twenty nonathletes matched for age, height, sex, and weight served as a control group. Left ventricular (LV) end-diastolic dimension in marathon runners averaged 5.53 +/- 0.5 cm compared to 4.81 +/- 0.04 cm in nonathletes (p less than 0.001), LV end-diastolic volume was 172.69 +/- 43.3 ml compared to 113.57 +/- 30.41 ml in nonathletes (p less than 0.001), stroke volume was 122.27 +/- 32.8 ml compared to 78.42 +/- 20.44 ml in non-athletes (p less than 0.001), the thickness of the posterior LV wall was 1.0 +/- 0.2 cm compared to 0.7 +/- 0.1 cm in nonathletes (p less than 0.001), and LV mass was significantly increased, 212.43 +/- 55.8 g compared to 123.48 +/- 24.54 g in non-athletes (p less than 0.01). Left atrium and aortic root were also relatively larger in athletes (p less than 0.01). Right ventricular end-diastolic dimension was enlarged in marathon runners (2.02 +/- 0.65 cm). No statistically significant differences were noted in ejection fraction, percentage of internal diameter shortening (% delta D) and PEP/LVET. The carotid tracing had a bisferiens pulse in five marathon runners. The apexcardiogram showed a bifid systolic thrust in three and absence of abnormal A wave. These abnormalities were related to the overload type of heart as proven by echocardiogram. "Early repolarization syndrome" (abnormal RS-T segment elevation) and notched T waves in ECG had a counterpart a semilunar configuration in the VCG. Three athletes met ECG criteria and one met VCG criteria of LVH. The treadmill exercise ECG was negative in all 12 athletes. Biventricular enlargement and increased left ventricular mass are present in the marathon runner's heart. Myocardial contractility at rest was, however, not statistically different from nonathletes.
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Previous investigations into the dissolution kinetics of sulphathiazole Form 1 have shown the process to be first order with respect to driving force. However, below 37 degrees first order kinetics did not apply, due to the surface reaction becoming the rate controlling factor. The present study examines the kinetics of crystallization over the temperature range 25 to 50 degrees. Crystallization is a process greatly dependent upon the high-entropy surface integration step which, unlike the dissolution process, is much more sensitive to crystal growth inhibitors. In the absence of inhibitors crystallization above 34 degrees follows first order kinetics but below 34 degrees the process changes to third order. Similar temperature effects on the dissolution of sulphathiazole have been previously reported.
The demonstration and identification of monoamines and of aminergic tracts in the central nervous system has permitted a study of their role in the control of the liberation of hypothalamic releasing hormones. Knowledge of the role of these hypothalamic neurohormones in the release of pituitary hormones is at present under study. The role of monoamines in the control of pituitary hormone functions depends narrowly on pharmacological methods intervening either in the synthesis of neuroamines or in their action on a specific receptor. The authors consider successively the implication of monoamines in the control of liberation of ACTH, GH, TSH, prolactin and gonadotropic hormones. The role of aminergic mechanisms in the physiology of pituitary releasing hormones forms an integral part of homeostasis. Knowledge of these mechanisms leads to a clinical study of their role in disorders of hypothalamo-pituitary function.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.