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Biomedical subjects

D S Gann

Publications and source records attributed to D S Gann.

At least 73 records · Page 4Linked to original sources
PubMed1989

Splanchnic nerve stimulation modulates steroid secretion in hypophysectomized dogs.

To test whether or not splanchnic neural input to the adrenal gland affects secretion of steroids from the adrenal cortex, the thoracic splanchnic nerve was electrically stimulated in pentobarbital-anesthetized dogs after hypophysectomy and replacement with physiological concentrations of ACTH. An adrenal vein cannula was placed to permit measurement of cortisol, corticosterone, 11-deoxycortisol, epinephrine and norepinephrine secretion rates and adrenal blood flow. Plasma ACTH was measured and the presentation rate of ACTH was calculated as the product of plasma ACTH concentration and adrenal plasma flow. Dogs were infused initially with ACTH for 60 min at 2 ng/min followed by infusion for 60 min at 10 ng/min. Within each infusion period, the distal end of the nerve was stimulated (20 V; 0.5-ms pulse duration) at 4 and at 20 Hz for 10 min each. Nerve stimulation resulted in a frequency-dependent increase in mean arterial pressure, in epinephrine and norepinephrine secretion and in adrenal blood flow. Arterial ACTH remained constant during nerve stimulation; however, increased adrenal blood flow resulted in increased presentation rate of ACTH to the adrenal. Cortisol secretion increased in response to nerve stimulation at 4 and 20 Hz during infusion of 2 and 10 ng/min ACTH and occurred prior to changes in presentation rate of ACTH. Corticosterone secretion also increased after stimulation at both frequencies, but the response was observed only during infusion of 10 ng/min ACTH. In contrast, 11-deoxycortisol decreased after nerve stimulation at 4 Hz but showed no response after stimulation at 20 Hz during infusion of 2 and 10 ng/min ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1989

Dissociation between changes in plasma bioactive and immunoreactive adrenocorticotropin after hemorrhage in awake dogs.

The secretion of cortisol increases in awake dogs after small hemorrhage, with little or no change in plasma immunoreactive (IR) ACTH. To determined if IR-ACTH reflects bioactive (B) ACTH after hemorrhage, changes in B-ACTH and IR-ACTH were determined in awake dogs. Trained dogs were prepared with adrenal venous and femoral arterial and venous cannula. Experiments performed 48-96 h after surgery consisted of blood sampling from the adrenal vein and femoral artery before and after a 7.5-10 ml/kg hemorrhage done over 3 min. Cortisol was assayed by HPLC with UV detection, and adrenal secretory rates were calculated using adrenal blood flow. Arterial B-ACTH was assayed after extraction using rat adrenal cells dispersed with collagenase; corticosterone produced was assayed by HPLC-UV. Arterial IR-ACTH was assayed by RIA using antisera directed against ACTH-(1-24). Dogs in which hypotension occurred (change in mean arterial pressure, -31 +/- 3; n = 6) were compared to dogs in which mean arterial pressure did not change (change in mean arterial pressure, -6 +/- 2; n = 5). In the absence of hypotension, B-ACTH increased by 10 min after the onset of hemorrhage coincident with increased cortisol secretion, whereas IR-ACTH did not increase until 20 min. Resting IR-ACTH was greater than B-ACTH (11 +/- 1 vs. 2 +/- 1 pg/ml), but the peak response of B-ACTH was greater than that of IR-ACTH (13 +/- 4 vs. 8 +/- 3 pg/ml). In the presence of hypotension, B-ACTH increased by 4 min, and IR-ACTH and cortisol secretion increased by 8 min after the onset of hemorrhage. Resting IR-ACTH was greater than B-ACTH (27 +/- 5 vs. 6 +/- 1 pg/ml), and the peak response of B-ACTH was less than that of IR-ACTH (64 +/- 26 vs. 112 +/- 33 pg/ml). In dogs subjected to blood sampling without hemorrhage (n = 4), resting IR-ACTH was greater than B-ACTH (34 +/- 5 vs. 5 +/- 1 pg/ml), but there was no change in B-ACTH, IR-ACTH, or cortisol secretion. The results show that small hemorrhage elicits changes in B-ACTH that are dissociated in time and magnitude from changes in IR-ACTH, are coincident with changes in cortisol secretion, and are greater in dogs that fail to maintain arterial pressure. These data indicate that B-ACTH predicts more accurately the change in cortisol secretion than does IR-ACTH after small hemorrhage.

Adrenal Cortex↗
PubMed1989

Aldosterone secretion following non-hypotensive hemorrhage is potentiated by prior blood loss.

Aldosterone is a major regulator of fluid and electrolyte balance after hemorrhage and is released from the adrenal cortex by the action of adrenocorticotropin (ACTH) and angiotensin II (AII). Past work has shown that the hemorrhage-induced release of ACTH and cortisol is potentiated by prior hemorrhage. We therefore studied the response of adrenal aldosterone secretion to repeated hemorrhage and its control by ACTH and AII. Six awake dogs with chronic lumboadrenal vein catheters were bled 10% of measured blood volume (H1) with reinfusion at 30 minutes. The hemorrhage was repeated 5 hours later (H2). Adrenal presentation rates for AII (AII-PR) and ACTH (ACTH-PR) were calculated for each sample. Control hormonal and hemodynamic parameters before each hemorrhage were not different; hemodynamic responses to H1 and H2 did not differ. Aldosterone secretion increased significantly after each hemorrhage. The increase in aldosterone secretion after H1 was associated with an early increase in AII-PR and late increase in ACTH-PR. Aldosterone secretion following H2 was greater than that following H1 and was associated with early and larger responses of AII-PR and ACTH-PR. Aldosterone secretion following H1 correlated with the AII-PR (r = 0.75; p less than 0.001), but not with the ACTH-PR. In contrast, aldosterone secretion following H2 correlated with both the AII-PR (r = 0.54; p less than 0.01) and ACTH-PR (r = 0.71; p less than 0.001) and multiple regression analysis showed a highly significant relation with both AII and ACTH (r = 0.81; p less than 0.001). The data suggest that aldosterone secretion after initial small hemorrhage occurs as a result of increased AII, whereas both AII and ACTH may contribute to the larger aldosterone secretory response to H2. Since major trauma commonly involves at least two insults separated in time (e.g., injury followed by surgery), potentiated responses of aldosterone and other pituitary-adrenal hormones (ACTH, vasopressin, and cortisol) may have important implications for the control of fluid and electrolyte balance and metabolism in injured patients.

Adrenal Glands↗
PubMed1988

Adrenal secretion of catecholamines evoked by chemical stimulation of trigeminal nucleus caudalis in the cat.

Microinjections of the neuroexcitatory substance L-glutamate, were made directly into various laminae of trigeminal nucleus caudalis to examine the influence of medullary dorsal horn neurons on the adrenal secretion of catecholamines in the anesthetized cat. Microinjections into the marginal layers (lamina I-II) or into the deep magnocellular portion (lamina V-VI) of nucleus caudalis ipsilateral to the adrenal vein sample evoked a prompt increase in the secretion of epinephrine and a smaller, yet consistent, increase in the secretion of norepinephrine. Injections into the magnocellular layers (lamina III-IV) had no significant effect on secretion of catecholamines. Injections into nucleus caudalis, contralateral to the adrenal vein sample, had no consistent effect on secretion suggesting that the central pathway from nucleus caudalis to the spinal cord for control of adrenal secretion of catecholamines is mainly ipsilateral. Changes in the adrenal secretion of epinephrine were not correlated with changes in adrenal venous blood flow, in arterial pressure or in heart rate. Arterial pressure was transiently increased by L-glutamate injections into the marginal layers, whereas injections into other laminae had no consistent effect. Heart rate increased regardless of the laminar site injection. The results indicate that local excitation of nucleus caudalis, in laminae that contain the majority of nociceptive neurons, evokes a consistent increase in the adrenal secretion of catecholamines, whereas excitation of neurons in laminae that mainly process non-noxious sensory input has no significant effect. It is concluded that secondary trigeminal neurons that contribute to the autonomic responses to noxious trigeminal stimuli have a similar distribution within nucleus caudalis as those that underlie the sensory-discriminative aspects of nociceptive.

Adrenal Glands↗
PubMed1988

Ketoconazole prevents acute respiratory failure in critically ill surgical patients.

Effective prophylaxis against acute respiratory failure (ARDS) has not been established. This study investigated whether or not ketoconazole could prevent ARDS in critically ill surgical patients. Seventy-one Surgical Intensive Care Unit (SICU) patients without liver dysfunction received either ketoconazole (n = 35), 200 mg daily via the gastrointestinal tract, or placebo (n = 36), for 21 days or until discharge from the SICU, in a prospective, randomized, double-blind study. Patients were monitored clinically for signs of ARDS, defined as all the following: intrapulmonary shunt greater than 15%, a PaO2/FIO2 ratio less than 150, normal central venous, pulmonary capillary wedge, or left atrial pressure, no other cause of hypoxemia, and a consistent chest X-ray. Thirteen patients (18%) developed ARDS with significantly increased mortality versus non-ARDS patients (69% vs. 29%). The incidence of ARDS was decreased among ketoconazole patients compared to placebo (6% vs. 31%; p less than 0.01), as was median SICU stay (7.0 days vs. 15.5 days; p less than 0.05), and median SICU cost (+5,600. vs. +12,400.; p less than 0.05). Mortality is increased with ARDS after trauma and surgery. We conclude that ketoconazole prevents ARDS, shortens SICU stay, and lowers hospital costs.

Adolescent↗
PubMed1988

Do DRG payments adequately reimburse the costs of trauma care in geriatric patients?

The records of 82 consecutive trauma patients over age 65 years were reviewed to determine the costs of trauma care as well as the projected DRG reimbursement in the seriously injured elderly. During the period of study, 636 additional trauma patients under the age of 65 were admitted. For all trauma victims, hospital costs exceeded projected reimbursement by $2.55 million ($98,000 per month). In the elderly population, mean hospital costs dramatically exceeded mean projected reimbursement in patients over the age of 80 ($18,197 +/- 3,682 vs. $7,069 +/- 700; p less than 0.001), in patients with severe overall injury ($18,992 +/- 3,540 vs. $8,508 +/- 643; p less than 0.001), and in patients with more than one complication ($25,504 +/- 3,959 vs. $7,247 +/- 626; p less than 0.001). Hospital costs were also increased in elderly patients discharged to a nursing home ($22,811 +/- 3,664) primarily as a result of prolonged hospital stay in older patients with more severe injury and with more frequent complications. The daily cost for trauma care in elderly patients who died was a staggering $1,735 +/- 366, reflecting the aggressive care given these patients. In the elderly trauma population, the number of complications was the only factor that correlated with hospital costs (r = 0.63; p less than 0.001). There was no significant correlation between hospital costs and projected DRG reimbursement, suggesting that the current DRG system is a very poor predictor of actual costs for trauma care in this population. The data suggest that the present DRG system grossly underestimates hospital costs in patients more than 65 years old with severe injury and with complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

The temporal characteristics of the metabolic and endocrine response to injury.

The neuroendocrine and substrate responses immediately after injury have been extensively investigated in man and animals. The purpose of the present study was to examine simultaneously, the temporal, metabolic and endocrine consequences of a single uniform injury induced by the injection of lambda-carrageenan into the hindlimbs of male Sprague-Dawley rats and to compare this response to that observed in semistarved pair-fed control animals. Immediately after injury there was a decrease in the plasma hematocrit, increase in tissue water and peripheral vasoconstriction that suggested hypovolemia. This was followed by a restoration of the blood volume by 1 day as reflected in hemodilution. Alterations in insulin, glucagon, ACTH, corticosterone, epinephrine, norepinephrine, and dopamine in wounded animals occurred during the first 5 days. However, similar changes were observed in pair-fed control animals from days 1 to 5. These findings implied that the early endocrine response observed from 0 to 24 hours after injury arises, primarily as a result of hypovolemia, whereas the response observed from 1 to 5 days appeared to be the result of semistarvation. In contrast to the endocrine alterations observed, alterations in the plasma concentrations of lactate, acetoacetate and beta-hydroxybutyrate persisted for up to 15 days. The presence of these substrate alterations in the absence of hormonal stimuli suggest that nonendocrine mechanisms exist to induce these alterations. The possibility is raised that these substrate alterations may be, at least in part, the result of the inflammatory infiltrate.

3-Hydroxybutyric Acid↗
PubMed1988

Locus coeruleus monoaminergic activity and plasma corticotropin after hemorrhage in cats.

Temporal changes in monoaminergic activity in the locus coeruleus (LC) in response to hemorrhage of 10 or 20% of blood volume were assessed using normal pulse voltammetry in alpha-chloralose-urethan-anesthetized cats. Oxidation current was measured with a carbon microelectrode, and changes at 230 and 450 mV were used as estimates of catecholaminergic and indolaminergic activity, respectively. Plasma adrenocorticotropin (ACTH) was measured by radioimmunoassay. Hemorrhage of 20% blood volume caused a transient increase in the catecholaminergic activity in a compact area in the ventral LC (vLC) that preceded increases in the plasma ACTH. The increase in oxidation current at 450 mV was similar to that at 230 mV, suggesting no significant contribution from indolamines. Dorsal rostral pontine sites outside this area exhibited either sustained decreases in oxidation current or no change in response to hemorrhage. The proportion of sites that exhibited transient increases in oxidation current in the vLC after the 10% blood loss was less than that after the 20% blood loss, suggesting that this response was dependent on the magnitude of hemorrhage. Since the LC was implicated previously in the control of ACTH release, we suggest that hemodynamic signals traversing the LC activate catecholaminergic mechanisms that, in turn, participate in the regulation of ACTH release after hemorrhage.

Adrenocorticotropic Hormone↗
PubMed1988

Noradrenergic turnover increases in locus coeruleus after hemorrhage in cats.

Push-pull perfusion was used to determine monoaminergic activity in the locus coeruleus (LC) of alpha-chloralose-urethan-anesthetized cats after 20% hemorrhage. Blood was withdrawn from 0 to 3 min and reinfused from 10 to 13 min. Continuous 5-min interval samples of perfusate were collected from -5 to 15 min. Concentrations of the monoamines were determined using high-performance liquid chromatography with electrochemical detection. The perfusion sites (n = 21) were identified histologically. In a group of eight contiguous sites in the ventral LC (vLC), 4-hydroxy-3-methoxy-phenyl(ethylene)glycol (MHPG) increased significantly from 0.50 +/- 0.22 (control) to 1.19 +/- 0.42 pmol/5 min during the first 5 min after hemorrhage (P less than 0.05). This response differed significantly from that obtained at the remaining 13 sites. Other metabolites were not often detectable for many sites either within or outside vLC, and their responses to hemorrhage were not significant. The response of MHPG in the vLC indicates that norepinephrine (NE) turnover increases in this area selectively and implicates NE in the increase in the catecholamine oxidation current reported previously using in vivo voltammetry. Since the vLC was shown previously to facilitate adrenocorticotropin (ACTH) release, the increase in NE turnover after hemorrhage could induce ACTH release. This increase may also act locally to modulate the ascending hemodynamic signal.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Plasma beta-endorphin levels in silent myocardial ischemia induced by exercise.

Although silent myocardial ischemia is a well recognized phenomenon, the reasons for the lack of symptoms in patients with coronary artery disease (CAD) is unclear. Because the endogenous opioid beta-endorphin has been related to pain modulation, plasma beta-endorphin levels were studied before, during and after exercise-induced ischemia in symptomatic and asymptomatic men. Because beta-endorphin responses have been closely linked to adrenocorticotropic hormone (ACTH) and cortisol responses, these hormones also were measured. Nine symptomatic and 12 asymptomatic patients with a high probability (at least 95%) of CAD and 8 apparently healthy men completed a Bruce protocol treadmill test. Blood samples were drawn before, during and 10 minutes after exercise. During exercise the measured hormones showed no significant increases from basal levels. However, plasma beta-endorphin, ACTH and cortisol levels were significantly elevated (p less than or equal to 0.01) 10 minutes after exercise in all 3 groups. There was no significant difference in plasma beta-endorphin levels during or after exercise between the symptomatic and asymptomatic patients with CAD. Thus, differences in circulating levels of beta-endorphin, ACTH and cortisol are not associated with the presence or absence of pain during exercise-induced myocardial ischemia.

Adrenocorticotropic Hormone↗
PubMed1987

Responses of adrenocorticotropin and vasopressin to hemorrhage after lesions of the caudal ventrolateral medulla in rats.

Hormonal responses to hemorrhage were examined in urethane-anesthetized rats 48 h after electrolytic lesions of the caudal ventrolateral medulla. Bilateral A1-lesions (A1X) inhibited the response of plasma adrenocorticotropin relative either to other lesions (XX) or to sham lesions. A1X inhibited the response of plasma vasopressin relative to XX but not to sham lesions. A1X and XX destroyed similar areas that were dorsal or caudal to A1. No lesion blocked either response completely. A hemodynamic pathway controlling the release of both hormones may pass through A1. However, other pathways may bypass this area.

Adrenocorticotropic Hormone↗
PubMed1987

Potentiated hormonal responses in a model of traumatic injury.

Although major trauma often involves repeated insults, few studies have examined the endocrine response to repeated injury. In earlier work, we described potentiated responses of circulating adrenocorticotropin (ACTH) and adrenal secretion of cortisol, epinephrine, and norepinephrine to the second of two small hemorrhages separated by 24 hr. To investigate the response of other hormones to repeated hemorrhage and to examine possible hormonal interactions in a shorter, more clinically relevant time frame, we placed chronic adrenal vein cannulas in eight splenectomized, trained dogs. Each animal was bled 10% of measured blood volume with reinfusion of shed blood at 30 min. The hemorrhage was repeated 5 hr later. Initial hemorrhage led to a small but significant increase in adrenal cortisol secretion and circulating ACTH, vasopressin (AVP), angiotensin II (AII), and plasma renin activity (PRA). Although a 5-hr time interval between stimuli is commonly thought to lead to cortisol feedback, the circulating ACTH and adrenal cortisol secretory responses to the second hemorrhage were exaggerated in comparison to their initial responses. Similarly, the AVP response to the second hemorrhage was also increased. In contrast, the responses of PRA and AII to the second hemorrhage were not greater than their responses to the initial hemorrhage. No differences in measured blood volume before each hemorrhage or in the heart rate and arterial pressure responses to hemorrhage were observed that could explain the potentiated hormonal responses. Thus, potentiated responses of cortisol, ACTH, and AVP, but not of PRA and AII, were observed in a model of trauma that emphasizes repeated injury in a clinically relevant time frame.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1987

Survival after trauma in geriatric patients.

In contrast to other studies, a recent report from the authors' institution has shown a good prognosis for functional recovery in geriatric patients that survive trauma. Because most survivors regained their pre-injury function, the authors examined factors related to nonsurvival in this population of 82 consecutive blunt trauma victims older than the age of 65. Seventeen patients died (21%). Compared with survivors, nonsurvivors were older, had more severe overall injury, and had more severe head and neck trauma but did not differ in severity of trauma that did not involve the head and neck, number of body regions injured, mechanism of injury, or incidence of surgery after injury. Nonsurvivors experienced more frequent complications (82% vs. 33%, p less than 0.05), including a higher incidence of cardiac complications (53% vs. 15%, p less than 0.05) and ventilator dependence for 5 or more days (41% vs. 14%, p less than 0.05). Mortality rates were increased in patients who were 80 years of age or older compared with those ages 65-79 (46% vs. 10%, p less than 0.01), despite injury of similar severity. More frequent complications may contribute to an increased mortality rate in the older group, including an increased incidence of prolonged mechanical ventilation (36% vs. 12%, p less than 0.025), cardiac complications (54% vs. 10%, p less than 0.01), and pneumonia (36% vs. 16%, p less than 0.06). Severely injured patients (Injury Severity Score [ISS] greater than or equal to 25) older than 80 years old had a mortality rate of 80%, and the survivors required permanent nursing home care. Discriminant analysis yielded a reliable method of differentiating survivors from nonsurvivors based on age, ISS, and the presence of cardiac and septic complications. To assess the accuracy of the discriminant function, 61 consecutive patients admitted during 1985 were reviewed prospectively. Discriminant scoring predicted outcome correctly in 92% of these patients. A Geriatric Trauma Survival Score (GTSS) based on the discriminant function was calculated for each of the 143 patients studied and was highly correlated with mortality rate (r = 0.99, p less than 0.001). Thus, the GTSS may serve as a valuable tool for evaluating death in geriatric trauma victims. Furthermore, because complications are potentially avoidable and contribute to increased mortality rates, routine aggressive care for geriatric patients with moderate overall injury is indicated.

Aged↗
PubMed1987

Aggressive trauma care benefits the elderly.

Few past studies have examined the long-term functional outcome of geriatric patients who survive trauma. To evaluate factors that determine the long-term potential for recovery in this population, we studied 63 survivors of blunt trauma over age 65 years between 9 and 38 months after hospital discharge. The overall level of injury was moderate, with a mean Injury Severity Score of 15.8 +/- 1.1. Thirty-nine patients (62%) had two or more body regions injured. Forty-five patients (71%) had pre-existing cardiopulmonary disease. Surgery was required in half of the patients, one third experienced complications, and nine (14%) required ventilatory support for 5 or more days. Only two patients did not live independently before trauma. Immediately after discharge, 21 patients (33%) were independent, 23 (37%) were dependent but living at home, and 19 (30%) required nursing-home care (NH). NH patients were older, more severely injured, had more severe head and neck trauma, and required surgery more frequently after trauma than patients discharged directly home. Twelve of the 19 NH patients (63%) returned home 3.1 +/- 0.9 months after discharge, and 13 of the 23 dependent patients (57%) became independent. Ultimately, 56 patients (89%) returned home after trauma. These patients were younger, had a shorter hospital stay, and experienced fewer complications than patients who required permanent NH care. Among 12 patients 80 years old and over, eight patients eventually returned home. Overall, 38 patients (57%) returned to independent living after trauma. Aggressive support of the elderly trauma victim appears justified, since few patients require permanent NH care and the majority return to independent living after trauma.

Activities of Daily Living↗
PubMed1987

Corticotropin-releasing factor in the adrenal medulla.

Immunoreactive and bioactive corticotropin-releasing factor has been identified in the adrenal gland of dogs, rats and humans. Radioimmunoassay and immunohistochemical experiments have clearly demonstrated that localization of the peptide is confined to the adrenal medulla. CRF-containing cells have a characteristic appearance and are often found in close association with blood vessels. Electron microscopic studies suggest that CRF is secreted at blood vessels within the adrenal medullary vasculature. CRF has also been identified in pheochromocytomas. The amount of the peptide made by such tumors is highly variable as the CRF content of pheochromocytomas may be 20 to 100 times higher or lower than that of normal adrenal tissue. The pathophysiological importance of CRF in pheochromocytomas is unknown. Excessive secretion of the peptide into the peripheral circulation may cause prolonged activation of the pituitary adrenal axis. The peptide may also act within the tumor, although its role remains obscure. Studies on chronically cannulated, awake dogs have shown that CRF is secreted into adrenal venous blood. A gradient exists between adrenal venous and peripheral arterial blood, as CRF is undetectable peripherally under resting conditions. Hemorrhage, a hemodynamic stimulus known to activate a sympathetic adrenal response, increases the CRF secretory rate. The time course of CRF secretion in response to this stimulus parallels that of epinephrine secretion. The physiological significance of adrenal medullary CRF remains to be determined. Although CRF has been shown to affect catecholamine secretion, the peptide appears to be only a weak secretagogue for catecholamines. We suggest that CRF may affect local blood flow within the adrenal medulla and may modify catecholamine secretory rates via this mechanism. The localization of CRF cells in close apposition to blood vessels supports this hypothesis.

Adrenal Gland Neoplasms↗
PubMed1987

Factors from paraventricular nucleus mediating adrenocorticotropin release in cats.

Experiments were conducted in alpha-chloralose-urethan-anesthetized cats. We stimulated the hypothalamic paraventricular nucleus (PVH) electrically before and after intracerebroventricular (icv) injection of an antiserum to arginine vasopressin (AVP), one to corticotropin-releasing factor (CRF), or one to normal rabbit serum (NRS). Stimulation of the ventral portion of the dorsal PVH led to increases in arterial pressure and heart rate that did not change after any of the icv treatments. However, the effect of each agent on the increases in plasma adrenocorticotropin (ACTH) after stimulation was related to the area of the PVH that was stimulated. The response to stimulation of a rostral area that extended dorsally from the anterior PVH was blocked completely by the anti-AVP but not by anti-CRF or NRS. The response to stimulation of a caudal area located in the dorsal PVH was attenuated after anti-CRF, unchanged after anti-AVP, and augmented after NRS. The antibodies that were given icv were found immunocytochemically to enter the median eminence at sites that include some adjacent to the portal vessels. Immunocytochemical localization of AVP- and of CRF-containing neurons in the PVH showed that the anterior PVH had the highest proportion of AVP neurons in the PVH but had only a few CRF neurons. In contrast, the dorsal PVH contained the highest density of CRF neurons in the PVH as well as some AVP neurons. We suggest that, in the cat, the primary releasing factor for the anterior PVH is AVP and that for the dorsal PVH is CRF.

Adrenocorticotropic Hormone↗
PubMed1987

Comparison of corticotropin-releasing factor and acetylcholine on catecholamine secretion in dogs.

To test whether corticotropin-releasing factor (CRF) is a secretagogue for adrenal secretion of catecholamines, a preparation was developed that permits measurement of adrenal venous output in response to in vivo arterial injection into the dog adrenal gland. Dogs were prepared with catheters in the lumboadrenal vein for monitoring adrenal blood flow and secretion rate of epinephrine and norepinephrine and in the lumboadrenal and inferior phrenic arteries for adrenal injection. Under pentobarbital anesthesia 48 h after surgery, dogs received a series of intra-adrenal injections that included acetylcholine (0.2-200 nmol), CRF (2.0-20.0 nmol), and diluent. There was a log dose-response relationship before epinephrine secretion and norepinephrine secretion to acetylcholine. Adrenal injection of CRF stimulated epinephrine and norepinephrine secretion at the highest dose tested (20 nmol). The response observed was equivalent to the response to 0.2 nmol acetylcholine. A similar dose of CRF given systemically produced hypotension without stimulating catecholamine responses. Adrenal catecholamine responses to acetylcholine were not augmented by addition of CRF. These findings show that arterial injection of CRF into the intact dog adrenal stimulates secretion of epinephrine and norepinephrine. However, the low potency of CRF relative to that of acetylcholine, the lack of a synergistic effect of CRF on catecholamine responses to acetylcholine, and the high dose of CRF required to achieve a response suggest that CRF does not function in the adrenal medulla as a physiologically important secretagogue for catecholamines.

Acetylcholine↗