scholarly journals CHANGES IN CIRCULATING LEUKOCYTES INDUCED BY THE ADMINISTRATION OF PITUITARY ADRENOCORTICOTROPHIC HORMONE (ACTH) IN MAN

Blood ◽  
1948 ◽  
Vol 3 (7) ◽  
pp. 755-768 ◽  
Author(s):  
A. GORMAN HILLS ◽  
PETER H. FORSHAM ◽  
CLEMENT A. FINCH

Abstract 1. Pituitary adrenocorticotrophic hormone (ACTH), when administered in a single intramuscular dose of 25 mg. to human subjects with unimpaired adrenal function, results in a characteristic alteration of the leukocytic pattern. This consists of an increase of circulating neutrophils and a decrease of circulating lymphocytes and eosinophils. 2. The decrease in circulating lymphocytes and eosinophils is contingent upon the stimulation of a functionally competent adrenal cortex, and does not occur in its absence. The neutrophilic response is present but somewhat diminished in adrenal insufficiency. 3. The entire pattern of leukocytic alterations found in normal subjects after administration of ACTH can be induced in patients with Addison’s disease by 17-hydroxycorticosterone (20 mg.) but not with desoxycorticosterone glucoside (30 mg.). 4. Prolonged adrenal stimulation by ACTH, given over a four day period in a dose of 10 mg. every six hours, results in a sustained and striking elevation of neutrophils and depression of eosinophils; the lymphocytes, after an initial depression lasting not more than twenty-four hours, may increase above their initial levels in spite of the continued increased secretion of adrenal hormones. 5. The relation of the adrenal cortex to the characteristic nonspecific leukocyte pattern, observed as a response of the organism to any type of insult, is discussed.

1998 ◽  
Vol 84 (4) ◽  
pp. 1144-1150 ◽  
Author(s):  
Vernon W. H. Lin ◽  
Caleb Hsieh ◽  
Ian N. Hsiao ◽  
James Canfield

The purpose of this study was to assess the effectiveness of functional magnetic stimulation (FMS) for producing expiratory function in normal human subjects. Twelve able-bodied normal subjects were recruited for this study. FMS of the expiratory muscles was performed by using a magnetic stimulator and placing the magnetic coil along the lower thoracic spine. Results showed that peak expired pressure, volume, and flow rate generated by FMS at the end of normal inspiration (102.5 ± 13.62 cmH2O, 1.6 ± 0.16 liters, and 4.8 ± 0.35 l/s, respectively) were comparable to their voluntary maximal levels ( P > 0.1). The optimal coil placement was between T7 and T11, and the optimal stimulation parameters were a frequency of 25 Hz and 70–80% of maximal intensity. We conclude that 1) FMS of the lower thoracic nerves in normal subjects resulted in a significant expiratory function comparable to their voluntary maximum; 2) FMS was noninvasive and was well tolerated by all subjects; and 3) FMS may be useful to produce cough in patients in critical care or perioperative settings, or in patients with neurological disorders.


1970 ◽  
Vol 48 (1) ◽  
pp. 73-81 ◽  
Author(s):  
F. J. EBLING ◽  
ERIKA EBLING ◽  
J. SKINNER ◽  
AUDREY WHITE

SUMMARY Administration of 1 i.u./24h of adrenocorticotrophic hormone (Cortrophin ZN, ACTH) to hypophysectomized—castrated rats significantly increased sebum production to the level of that in castrated rats with intact pituitaries. The incidence of mitoses in the sebaceous glands was also significantly increased. Neither the preputial glands nor the seminal vesicles showed any response. No significant increase in sebum production in hypophysectomized—castrated rats could be detected 24 days after giving implants releasing 0·2 or 0·6 mg testosterone/24 h, although sebaceous mitoses were significantly increased in both instances. Concomitant administration of both ACTH and testosterone raised sebum production to the same extent as ACTH alone, and raised the incidence of sebaceous mitoses to a level equal to that produced by ACTH plus testosterone. It is concluded that the sebaceous glands respond—either directly or indirectly as the result of stimulation of the adrenal cortex—to ACTH and that this response is less dependent on the presence of the pituitary than is the action of testosterone. ACTH does not itself facilitate the response of the sebaceous glands to testosterone.


1986 ◽  
Vol 112 (2) ◽  
pp. 157-165 ◽  
Author(s):  
J. Schopohl ◽  
A. Hauer ◽  
T. Kaliebe ◽  
G. K. Stalla ◽  
K. von Werder ◽  
...  

Abstract. ACTH secretion was studied in response to repetitive and continuous administration of human corticotropin releasing factor (CRF) in 14 healthy volunteers and 2 patients with secondary adrenal insufficiency. ACTH increases during repetitive CRF administration were within the same range in normal subjects independent of the intervals (60– 180 min) between the CRF pulses (100 μg iv). When CRF was infused continuously (100 μg/h for 3 h) after an initial CRF bolus injection (100 μg iv), ACTH and cortisol remained elevated during the infusion at a nearly constant level (ACTH: 60 ± 5 pg/ml; cortisol: 21.2 ± 1 μg/dl; x̄ ± se). A second CRF bolus injection at the end of the infusion did not lead to a significant further increase of ACTH and cortisol levels. This shows that there is no desensitisation or depletion of a ready releasable pool, as it is observed with other pituitary hormones after releasing hormone stimulation. Pulsatile administration of CRF in 2 patients with secondary adrenal insufficiency due to previous cortisol or glucocorticoid excess, respectively, revealed a blunted response to the first pulse which became normal after the following pulses. The latter could not be sustained until the next morning without CRF given overnight. These findings point to a hypothalamic defect being the cause of hypocortisolism after long-term cortisol suppression.


1972 ◽  
Vol 70 (1) ◽  
pp. 196-208 ◽  
Author(s):  
Bengt Karlberg ◽  
Sven Almqvist

ABSTRACT The effects of the administration of normal saline in four normal subjects and the single iv injections of synthetic pyroglutamyl-histidyl-proline amide (TRH) in doses of 6.25, 12.5, 25, 50, 100, 200 and 400 μg in 12 healthy subjects were evaluated by clinical observations and serial measurements from −10 to + 360 minutes of serum TSH, PBI, STH, cholesterol, glucose and insulin. Normal saline and TRH 6.25 μg iv did not change the serum TSH level. The minimum iv dose of TRH increasing serum TSH within 10 minutes was 12.5 μg. Nine of 12 subjects gave maximal increases of serum TSH after TRH 100 μg and all after 200 and 400 μg. The time for the peak response varied with the dose from 15 to 60 minutes. The dose-response curves, average and individual, were complex and not linear. This was interpreted as a varying degree of stimulation of both pituitary synthesis and release of TSH by TRH. PBI changes were measured at 2 h and 6 h. Minimum dose for a significant increase of PBI was 12.5 μg and 6.25 μg of TRH for the respective times. No change in basal STH-levels occurred in 53 of 65 TRH-stimulation tests. Nine of the 12 changes in serum STH occurred in four subjects with varying basal STH-levels. No changes were found in serum cholesterol, glucose or insulin. Our results show that 50 μg of TRH can be used as a standard dose for the single iv stimulation of pituitary release of TSH. TRH stimulated both TSH and STH release in 18% of our tests.


1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.


2009 ◽  
Vol 106 (3) ◽  
pp. 893-903 ◽  
Author(s):  
Z. Ghanim ◽  
J. C. Lamy ◽  
A. Lackmy ◽  
V. Achache ◽  
N. Roche ◽  
...  

The vestibular responses evoked by transmastoid galvanic stimulation (GS) in the rectified soleus electromyogram (EMG) in freely standing human subjects disappear when seated. However, a GS-induced facilitation of the soleus monosynaptic (H and tendon jerk) reflex has been described in few experiments in subjects lying prone or seated. This study addresses the issue of whether this reflex facilitation while seated is of vestibulospinal origin. GS-induced responses in the soleus (modulation of the rectified ongoing EMG and of the monosynaptic reflexes) were compared in the same normal subjects while freely standing and sitting with back and head support. The polarity-dependent biphasic responses in the free-standing position were replaced by a non-polarity-dependent twofold facilitation while seated. The effects of GS were hardly detectable in the rectified ongoing voluntary EMG activity, weak for the H reflex, but large and constant for the tendon jerk. They were subject to habituation. Anesthesia of the skin beneath the GS electrodes markedly reduced the reflex facilitation, while a similar, although weaker, facilitation of the tendon jerk was observed when GS was replaced with purely cutaneous stimulation, a tap to the tendon of the sternomastoid muscle, or an auditory click. The stimulation polarity independence of the GS-induced reflex facilitation argues strongly against a vestibular response. However, the vestibular afferent volley, insufficient to produce a vestibular reflex response while seated, could summate with the GS-induced tactile or proprioceptive volley to produce a startle-like response responsible for the reflex facilitation.


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