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Biomedical subjects

D S Gann

Publications and source records attributed to D S Gann.

At least 55 records · Page 3Linked to original sources
PubMed1990

A new characterization of injury severity.

ASCOT (A Severity Characterization of Trauma) is a physiologic and anatomic characterization of injury severity which combines emergency department admission values of Glasgow Coma Scale, systolic blood pressure, respiratory rate, patient age, and AIS-85 anatomic injury scores in a way that obviates ISS shortcomings. ASCOT values are related to survival probability using the logistic function and regression weights reaffirm the importance of head injury and coma to the prediction of patient outcome. The ability of TRISS and ASCOT to discriminate survivors from non-survivors and the reliability of their predictions, as measured by the Hosmer-Lemeshow statistic, were compared using Major Trauma Outcome Study (MTOS) patient data. ASCOT performance matched or exceeded TRISS's for blunt-injured patients and for penetrating-injured patients. ASCOT performance gains were modest for blunt-injured patients. The Hosmer-Lemeshow statistics suggest that ASCOT reliably predicts patient outcome for penetrating-injured patients and nearly so for blunt-injured patients. Statistically reliable predictions were not achieved by TRISS for either set. ASCOT provides a more precise description of patient physiologic status and injury number, location, and severity than TRISS. The ASCOT patient description may be useful in relating to other important outcomes not highly correlated with TRISS or the Injury Severity Score (ISS) such as disability, length of stay, and resources required for treatment.

Adolescent↗
PubMed1990

Progress in characterizing anatomic injury.

A three-valued description of anatomic injury is presented. Anatomic profile (AP) components A, B, and C summarize serious injuries (greater than AIS 2) to the head/brain or spinal cord; to the thorax or front of the neck; and all remaining serious injuries. Relationships between AP components and survival rate reaffirm the seriousness of head injury. Logistic function models relating AP components and the Injury Severity Score (ISS) to survival probability were based on 20,946 Major Trauma Outcome Study (MTOS) patients (9.2% mortality rate) submitted through 1986. Model performance comparisons were based on 5,939 MTOS patients (7.8% mortality rate) submitted during 1987. The AP better discriminated survivors from nonsurvivors and provided a 31% increase in sensitivity when compared with the ISS. Neither the ISS nor the AP alone reliably predict patient outcome. The predictive power of methods for estimating patient survival probability which include physiologic indices or profiles, patient age, and an anatomic profile should be compared with current methods. The AP, which is based on the severity and location of all serious injuries, provides a more rational basis for comparing patient samples than the ISS.

Humans↗
PubMed1990

Neural control of ANF release in hypoxia and pulmonary hypertension.

Hypoxia causes the release of atrial natriuretic factor (ANF), but the mechanisms are not yet understood. This study examined the relative contribution of pulmonary arterial hypertension, neural pathways, increased heart rate, or increased atrial size to the ANF response. Alveolar hypoxia [fractional concentration of O2 in inspired gas (FIo2) = 0.1] or pulmonary arterial hypertension (25-45 mmHg) was induced for 10 min in four series (n = 4-12 each) of anesthetized, mechanically ventilated pigs. During hypoxia, plasma ANF concentrations increased by 129 +/- 52 (SE) pg/ml (or 271 +/- 105%) over baseline (35 +/- 7 pg/ml; P less than 0.01) (series 1). There was also a significant increase of pulmonary arterial pressure, heart rate, central venous pressure, and pulmonary capillary wedge pressure. Repeated pulmonary hypertension induced by intravenous air infusion caused a repeated and reversible 125 +/- 14% increase (P less than 0.001) of plasma ANF, and this response was totally abolished by lesion of the cervical vagosympathetic trunks (series 2). Lesion of these nerves 1 h before hypoxia also decreased the ANF response to hypoxia by 45-58% (P less than 0.01), whereas responses of heart rate and atrial pressures were unchanged (series 3). The ANF response to hypoxia, expressed in percent of baseline, was not affected by 0.2 mg/kg propranolol (PR) (no PR: 145 +/- 63%; PR: 151 +/- 82%; not significantly different from series 1 and control, series 3), although the increase in heart rate (no PR: 61 +/- 15 beats/min) was almost abolished (PR: 17 +/- 5 beats/min) (series 4). Hypoxia caused no significant changes in right and left atrial peak volume regardless of propranolol, as measured with an electrical conductance catheter. The results indicate that a new neural reflex of probably pulmonary arterial origin mediates approximately 50% of the ANF response to hypoxia. The remaining ANF response remains to be explored further and cannot be explained by conventional release mechanisms such as atrial stretch and pulsatility alone.

Animals↗
PubMed1990

Response of prolactin to hemorrhage is similar to that of adrenocorticotropin in swine.

Prolactin (PRL) responds to several stimuli that elicit release of adrenocorticotropin (ACTH), but does not increase in response to hemorrhage in fetal animals. To determine whether PRL increases after hemorrhage in older animals, 11 immature female swine were prepared chronically under halothane and conditioned behaviorally to lie in a sling. They were bled 14 ml/kg over 5 min. PRL, ACTH, cortisol (F), lysine vasopressin (LVP), and pressure renin activity (PRA) were measured by radioimmunoassay. Epinephrine (EPI) and norepinephrine (NE) were separated by high-performance liquid chromatography. Arterial PRL increased at 0.75 and 1 h (P less than 0.01) and paralleled ACTH and F that peaked at 0.75 h (P less than 0.05 and P less than 0.01, respectively). All three hormones recovered significantly by 4 h. In contrast, PRA and LVP peaked transiently at 0.25 h after hemorrhage and recovered by 1.5 h (P less than 0.05, in each case). EPI and NE did not change significantly. In individual pigs, ACTH and F each showed correlations (Spearman) with PRL that were positive in 10 pigs and significant in six and five pigs, respectively. The pig with the smallest ACTH change (8.4 pg/ml peak) showed no increase in PRL. Peaks in PRL were simultaneous with (five pigs) or delayed by 15 min (four pigs) or 30 min (one pig) from peaks in ACTH. Significant correlations of PRL with PRA and with LVP occurred in only two pigs and in one pig, respectively. A common pathway may contribute to other independent mechanisms controlling the release of ACTH and PRL after hemorrhage.

Adrenocorticotropic Hormone↗
PubMed1990

Pituitary-adrenal and adrenomedullary responses to noise in awake dogs.

Experiments characterized the dynamics of the pituitary and adrenocortical response to noise in awake dogs to determine if a dissociation exists between changes in plasma bioactive (bio) adrenocorticotropic hormone (ACTH) and immunoreactive (ir) ACTH. In addition, experiments determined the temporal relationship between cardiovascular, adrenomedullary, and adrenocortical responses induced by the acute presentation of noise. Trained dogs were prepared chronically with adrenal venous and femoral arterial cannulas. Experiments were done 48-96 h postsurgery and consisted of presentation of noise (75 dB; 0.25-8 kHz) for 3 min (n = 6) or of blood sampling alone (n = 5). In response to noise, mean arterial pressure and heart rate increased at 30 s and returned to base line at 4 min. Adrenal secretion of epinephrine and norepinephrine increased at 1 min and remained elevated until 4 min. Adrenal blood flow increased from 2 to 4 min as the result of a parallel increase in adrenal vascular conductance. Plasma bioACTH increased from 6 to 15 min in parallel with that of plasma irACTH. Before noise, the ratio of bioACTH to irACTH was 0.2-0.3, but the absolute change in bioACTH and irACTH after noise was not different. The increase in plasma ACTH occurred concomitant with or preceded an increase in cortisol secretion. Blood sampling alone caused no change in any variable. These data show that unexpected noise evokes a sequence of responses with rapid onset that includes tachycardia, hypertension, and increases in adrenomedullary secretion and adrenal vascular conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1990

Continuous measurement of atrial volume with an impedance catheter during positive pressure ventilation and volume expansion.

Right atrial volume (RAV) and other hemodynamic parameters were measured in ten anesthetized swine with an impedance catheter in the right atrium during ventilation and increasing levels of positive end-expiratory pressure (PEEP) to determine the effects of PEEP on right atrial dynamics. RAV and cardiac output (CO) decreased progressively during ventilation with 5, 10 and 15 centimeters of water PEEP, whereas central venous pressure and pulmonary capillary wedge pressure increased. Despite this decrease in RAV, atrial ejection fraction increased significantly and active atrial output (AAO equals stroke volume times heart rate) was maintained. Thus, the decrease in CO resulted from a decrease in the passive component of ventricular filling. Compensatory increases in AAO helped to minimize the fall in CO in some swine (r = 0.73, p less than 0.01). Peripheral adenocorticotropin (ACTH) increased from 14.0 +/- 4.5 picograms per milliliter at zero centimeters of water PEEP to 46.8 +/- 18.3 picograms per milliliter at 10 centimeters of water PEEP (p less than 0.05). Volume expansion that restored CO to control levels despite PEEP led to a significant increase in RAV and in passive ventricular filling, as well as a decrease in ACTH to 11.2 +/- 1.5 picograms per milliliter (p less than 0.05). Changes in the ACTH levels correlated with changes in the RAV (r = 0.58, p less than 0.05), but did not correlate with changes in CO, arterial pressure or central venous pressure. The data herein suggest that the decrease in CO with PEEP results from decreased venous return, RAV and passive ventricular filling, whereas a compensatory increase in right atrial contractility helps to maintain CO. Ventilation with PEEP stimulates hormonal secretion that can be terminated by adequate volume expansion.

Adrenocorticotropic Hormone↗
PubMed1989

Substance P and GABAergic effects on adrenal and autonomic function evoked by microinjections into trigeminal subnucleus caudalis in the cat.

To assess the contribution of putative neurotransmitters in mediating changes in adrenal and autonomic function evoked by activation of medullary dorsal horn neurons, microinjections of substance P, bicuculline methiodide, or muscimol were directed at various laminac of trigeminal subnucleus caudalis in the anesthetized cat. Injections of substance P (35.6 pmol) into the superficial layers (lamina I-II) of subnucleus caudalis increased the adrenal secretion of epinephrine (+8.3 +/- 2.3 ng/min, P less than 0.01), arterial pressure (+11 +/- 5.3 mm Hg, P less than 0.01), and heart rate (+19.4 +/- 4.9 beats/min, P less than 0.01) by 1 min, and increased the plasma concentration of adrenocorticotropin (+26 +/- 10 pg/ml, P less than 0.01) by 3 min. Substance P injections into the magnocellular layers (lamina III-IV) or deep magnocellular layers (lamina V-VI) had no significant effects. Microinjections of the GABAA antagonist, bicuculline methiodide (62.4 pmol), into the superficial layers of subnucleus caudalis increased the adrenal secretion of epinephrine (+4.5 +/- 3.2 ng/min, P less than 0.01) by 1 min, whereas injections of the GABAA agonist, muscimol (280 pmol), decreased the secretion (-5.8 +/- 2.8 ng/min, P less than 0.05) by 6 min. Arterial pressure increased after bicuculline (+17.8 +/- 8.2 mm Hg, P less than 0.01) and decreased after muscimol (-6.3 +/- 2.9 mm Hg, P less than 0.01) injections into the superficial layers. Injections of bicuculline or muscimol into the magnocellular layers or into the deep magnocellular layers had no effect on adrenal secretion of catecholamines or on systemic cardiovascular function. Peripheral venous concentrations of adrenocorticotropin were not affected significantly by microinjections of GABAergic agents regardless of the laminar site of injection within subnucleus caudalis. Equivalent volume injections of artificial cerebrospinal fluid into the superficial laminae of subnucleus caudalis had no significant influence on any measured variable. Substance P-evoked changes in the adrenal secretion of epinephrine were not correlated with changes in adrenal venous blood flow, whereas bicuculline- and muscimol-evoked changes in adrenal secretion of catecholamines were positively correlated with changes in adrenal blood flow (P less than 0.01). The results indicate that substance P and GABA contribute significantly to the trigeminal control of adrenal and autonomic function by acting on neurons in the superficial layers of subnucleus caudalis, a brainstem region that processes nociceptive sensory information.

Adrenal Glands↗
PubMed1989

The effect of endotoxin on glucose metabolism in skeletal muscle requires the presence of plasma.

The administration of endotoxin in vivo results in an increase in glucose utilization through an as yet undetermined mechanism. This study evaluated (1) the contribution of blood to the increased glucose utilization noted following endotoxemia, (2) the direct action of endotoxin on skeletal muscle glucose uptake in an isolated hindlimb perfusion system and in incubated muscle, and (3) the possibility that the increased glucose uptake in skeletal muscle mediated by endotoxin requires the presence of plasma. Incubation of blood with 50 and 100 mg/L of endotoxin increased glucose uptake and lactate production in a dose-dependent manner. Muscle incubations and perfusions in the absence of plasma and white blood cells showed that glucose uptake and lactate production were not affected by the presence of 50 to 250 mg/L of endotoxin, while 500 mg/L of endotoxin produced a 26.2% decrease in glucose uptake. In contrast, incubation of muscle in the presence of plasma and endotoxin increased glucose uptake by 37%. These findings suggest that (1) the increased glucose utilization of endotoxemia is only partially explained by increased glucose metabolism by blood, (2) endotoxin does not have a direct effect on the glucose uptake of skeletal muscle, and (3) an interaction of endotoxin with a component of plasma is required for an endotoxin-mediated increase in glucose utilization by skeletal muscle.

Animals↗
PubMed1989

Evidence of a plasma-mediated "window" of immunodeficiency in rats following trauma.

The etiology of immunodeficiency following trauma was investigated. Plasma collected from Fischer rats 1-8 hr following a 40% surface area thermal injury (TI) displays immunosuppressive activity (ISA). Peak ISA (4 hr) exceeded 90% inhibition of Con A3-induced proliferation of normal spleen cells. Splenic macrophage IL-1 secretion and NK activity are also inhibited by 4-hr TI plasma. Most importantly, these same cellular immune functions decline in rats by 4 hr following TI. After a further decline by 16 hr (IL-1 = 19.8% and NK activity = 40% of normal), these cellular immune functions rebound toward normal values by 2 days following TI. Thus, ISA in plasma is both temporally and functionally linked to the cellular immune defects observed. Sham-treatment rats display a similar, although less marked, pattern of plasma-linked transient cellular immune defects indicating a role for stress in these responses. ISA is abolished by mild heat (56 degrees C for 30 min) and wholly contained in the greater than 10-kD fraction of plasma. Together, these results provide evidence that previously unrecognized molecules in plasma induce a "window" of immunodeficiency early following trauma.

Animals↗
PubMed1989

Hormone and catecholamine responses accompanying the antinatriuresis of glucose ingestion.

The purpose of this study was to determine the importance of various neurohormonal systems in mediating the sodium retention associated with glucose ingestion. Eight normotensive men were randomized to receive, after an overnight fast, glucose (1 mg/kg po) in water, and water alone, during two studies seven to ten days apart. Sodium excretion declined 38 +/- 5% from baseline one to two hours after glucose ingestion (P less than .005), but did not change significantly on the control day. Urinary norepinephrine and dopamine did not change during glucose or control studies. Peak serum insulin levels after glucose correlated inversely with the decline in sodium excretion (r = .67, P less than .10). Plasma renin activity (PRA) increased after glucose ingestion (P less than .01), but changes in PRA did not correlate with changes in sodium excretion. We conclude that the antinatriuresis following glucose ingestion does not result from alterations in noradrenergic-dopaminergic activity or changes in the renin-angiotensin-aldosterone axis. Insulin may modulate renal sodium metabolism directly, or through a yet unknown mechanism.

Adult↗
PubMed1989

Hypertonic saline attenuates the hormonal response to injury.

We reported previously in a randomized double-blinded study in 20 postoperative coronary bypass patients that hypertonic saline (1.8% NaCl, HS) provides early hemodynamic benefits, increased osmolality and net negative fluid balance compared to 0.9% NaCl (NS). To investigate the effects of HS on the hormonal response to injury, we measured ACTH, cortisol, angiotensin II (AII), aldosterone, vasopressin (AVP), and atrial natriuretic factor (ANF) in these patients. ACTH and cortisol concentrations increased in the NS group but were suppressed in the HS group (p less than 0.05). Aldosterone increased in NS patients, but was suppressed in HS patients (HS: delta Aldosterone 13.0 +/- 3.0 vs. NS: delta Aldosterone 26.0 +/- 7.0 ng/dl, p less than 0.05). The AII response was suppressed at six and eight hours (p less than 0.05) in patients receiving HS but did not change in patients receiving NS. ANF did not change significantly for either group. The significant increases in AVP were similar in both groups (p less than 0.05), but correlated with increases in osmolality only in the NS group (r = 0.8, p less than 0.009). Other than AVP, HS suppressed the responses of some of the hormones that normally increase in response to injury, relative to NS. Attenuation of the neuroendocrine response and other previously reported effects of HS suggest that HS may be an efficacious solution for resuscitation in the postoperative and postinjury period.

Adrenocorticotropic Hormone↗
PubMed1989

A revision of the Trauma Score.

The Trauma Score (TS) has been revised. The revision includes Glasgow Coma Scale (GCS), systolic blood pressure (SBP), and respiratory rate (RR) and excludes capillary refill and respiratory expansion, which were difficult to assess in the field. Two versions of the revised score have been developed, one for triage (T-RTS) and another for use in outcome evaluations and to control for injury severity (RTS). T-RTS, the sum of coded values of GCS, SBP, and RR, demonstrated increased sensitivity and some loss in specificity when compared with a triage criterion based on TS and GCS values. T-RTS correctly identified more than 97% of nonsurvivors as requiring trauma center care. The T-RTS triage criterion does not require summing of the coded values and is more easily implemented than the TS criterion. RTS is a weighted sum of coded variable values. The RTS demonstrated substantially improved reliability in outcome predictions compared to the TS. The RTS also yielded more accurate outcome predictions for patients with serious head injuries than the TS.

Blood Pressure↗
PubMed1989

Hypertonic saline fluid therapy following surgery: a prospective study.

Successful resuscitation of the injured may be achieved more rapidly and with less fluid using hypertonic crystalloid solutions than with isotonic solutions. This randomized, double-blind study compared 0.9% normal saline (NS) to 1.8% hypertonic saline (HS) in 20 postoperative coronary artery bypass patients suffering uniform injury. Study solutions were administered to maintain physiologic endpoints: heart rate, blood pressure, and pulmonary capillary wedge pressure. The groups were similar with respect to age, body surface area, operative procedure, intraoperative fluid status, and intraoperative and postoperative red cell transfusion requirements. HS patients required 30% less fluid than NS patients and were in negative fluid balance during the study (-1,715 +/- 732 ml/24 hr, HS, vs. +266 +/- 825 ml/24 hr, NS; p less than 0.01). In contrast, NS patients were in positive fluid balance after 8 hours. Moreover, HS patients experienced less chest tube drainage than NS patients (981 +/- 88 ml, HS, vs. 1,700 +/- 285 ml, NS; p less than 0.01). Systemic and pulmonary hemodynamic measurements, oxygen delivery, oxygen consumption, and shunt fraction did not differ between the two groups. Serum sodium and osmolality increased in the HS group and peaked at 12 hours (145.4 +/- 1.4 mEq/L and 308.7 +/- 2.0 mOsm/kg, respectively) and correlated with the volume of HS infused (correlation coefficient = 0.81). No deaths occurred and no complication was attributed the hypertonicity of the solution. We conclude that 1.8% hypertonic saline is a safe alternative to isotonic crystalloid therapy in the fluid management of postoperative patients. Decreased third-space losses may occur with HS as suggested by the lower thoracic losses in the HS group; 1.8% NaCl may be the preferred solution in situations where excess free water administration is not desired, and where interstitial edema is detrimental to function and/or survival.

Clinical Trials as Topic↗
PubMed1989

Behavioral and hormonal influence on blood volume restitution after hemorrhage in swine.

Hemorrhage of 14 ml.kg-1.5 min-1 was done in two groups of chronically prepared, splenectomized Yorkshire pigs that were conditioned behaviorally to lie in a Panepinto sling. In group 1 the conditioning included early use of active restraint. It was done before the preparative surgery and on postoperative day 3 before the experiment on day 4. In group 2 the use of active restraint was minimized during conditioning that was extended to postoperative days 4 and 5 before the experiment on day 6. Before hemorrhage, core temperature and plasma catecholamines, cortisol, adrenocorticotropin, vasopressin, and renin were greater in group 1 than in group 2; but blood volume, hematocrit, and body weight were identical. Peak hormonal concentrations were greater or more sustained during the 1st h after hemorrhage in group 1 than in group 2. Restitution of blood volume was greater in group 1 than in group 2 at 4 and 7 h. Greater total peripheral resistance at 2 h after hemorrhage and greater restitution of plasma protein by 7 h in group 1 contributed to its accelerated volume restoration. Comparison of arterial pressure and of right atrial volume (conductance catheter) between groups suggested that a greater response of arterial or right atrial stretch receptors in group 1 could not account for the results. We suggest that the method and duration of behavioral conditioning and the time for recovery from surgery are important determinants of the hemodynamic and hormonal responses to hemorrhage and their subsequent influence on the restitution of blood volume.

Adrenocorticotropic Hormone↗
PubMed1989

Atrial peptide release after hemorrhage in unanesthetized swine.

Hemorrhage of 14 ml/kg in 5 min was done in two groups of chronically prepared, splenectomized Yorkshire pigs. Group 1 was studied on post-operative day 4 and was conditioned behaviorally with "active restraint", whereas group 2 was studied on postoperative day 6 and was conditioned with behavioral "shaping." The peak decrease in blood volume occurred by 0.25 h after hemorrhage in both groups. However, plasma atrial natriuretic factor (ANF) as measured by radioimmunoassay did not decrease significantly until 2 h in group 1 and 0.5 h in group 2 even though the recovery of blood volume was significantly more rapid in group 1 than in group 2. The responses of ANF differed significantly between groups, suggesting that ANF release after hemorrhage is influenced by prior handling and the time for recovery from surgery. In both groups, some pigs showed increases in ANF during the 1st h after hemorrhage, and changes in ANF were unrelated to decreases in central venous pressure or absolute right atrial volume determined with a conductance catheter. In contrast, changes in ANF after hemorrhage correlated positively with several variables including atrial rate and changes in vasopressin. Multiple regression suggested that the effect of reduced atrial volume on ANF release was opposed by these latter variables or related factors. Furthermore, known actions of ANF do not appear to account for the observed hemodynamic and hormonal responses to hemorrhage.

Animals↗
PubMed1989

Potentiated cortisol response to paired hemorrhage: role of angiotensin and vasopressin.

Potentiated adrenocorticotropin (ACTH) and cortisol responses occur after the second of two small hemorrhages (hems) spaced 24 h apart in the dog. To test whether increased responses of other hormones might be associated with this effect, we examined plasma renin activity (PRA), angiotensin II (ANG II), and vasopressin after paired 10% hem (H1 and H2) spaced 5 h apart in chronically prepared conscious dogs. Cortisol secretion increased after each hem, and the response to H2 was larger (P less than 0.05; H1 peak at 6.8 +/- 1.3 micrograms/min vs. H2 peak at 18.3 +/- 5.3 micrograms/min). ACTH did not change after H1 but increased after H2, and the H2 response was larger (P less than 0.01). Vasopressin increased after each hem, and the H2 response was larger (P less than 0.01). The time courses of ACTH and vasopressin responses were similar after H2 (significant increases by 8 min). PRA and ANG II increased by 4 min after each hem, and although the difference was small the early PRA and ANG II responses were greater after H2. Blood volume and hem volume did not differ between hems. Hemodynamic responses to the hems were not different. We conclude that, although the PRA and ANG II respond rapidly enough after hem to influence pituitary responses, the slightly greater responses of these factors to H2 are not responsible for greatly increased pituitary-adrenal responses to H2. On the other hand, the markedly potentiated vasopressin response to H2, which parallels that of ACTH, suggests that vasopressin may mediate the increased ACTH responses to H2.

Adrenocorticotropic Hormone↗
PubMed1989

Catecholamine activity in paraventricular hypothalamus after hemorrhage in cats.

Temporal changes in catecholamine activity within the paraventricular nucleus (PVN) of the hypothalamus were assessed using in vivo voltammetry after moderate hemorrhage in chloralose-anesthetized cats. Oxidation current was measured with carbon microelectrodes, and the change at +250 mV was used as an estimate of catecholamine activity. The magnitude and directional change in catecholamine activity was assessed for each site during the initial 3 min of blood loss. Of 62 recording sites, 45 sites were located along the rostrocaudal extent of the medial PVN. Fifteen of these 45 sites exhibited an increase, 15 others exhibited a decrease, and the remaining 15 sites exhibited no change in catecholamine activity. The magnitude of change in oxidation current was independent of the magnitude of the decrease in arterial pressure after hemorrhage. Twelve of the 15 sites that exhibited increases in catecholamine activity were located in the caudal PVN along its dorsomedial aspect, whereas the location of sites that exhibited decreases in catecholamine activity were more widely distributed throughout the nucleus. These data are consistent with the hypothesis that an increase in the release of catecholamines within the caudal PVN in response to hemorrhage is facilitatory for the release of adrenocorticotropin and/or vasopressin.

Adrenocorticotropic Hormone↗