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D S Gann

Publications and source records attributed to D S Gann.

At least 19 recordsLinked to original sources
PubMed1992

Hypocalcemia during sepsis. Relationship to resuscitation and hemodynamics.

The ionized calcium (IC) and parathyroid hormone response to polymicrobial intra-abdominal sepsis and the relationship between IC and hemodynamic alterations with and without crystalloid resuscitation were investigated. Thirty swine underwent cecal ligation and incision (n = 19) or sham laparotomy (n = 11), with seven animals that had cecal ligation and incision administered Ringer's solution (50 mL/kg) after each set of measurements recorded on days 0, 1, 2, 4, and 8. An early decrease in mean arterial pressure and cardiac index in animals that had cecal ligation and incision reversed with resuscitation. The IC also fell early and parathyroid hormone level increased in both the unresuscitated and resuscitated septic groups. However, correlation coefficients of mean arterial pressure and cardiac index with IC ranged from .034 to .287 in the septic animals and were lower in the group that had sham laparotomy. We conclude that polymicrobial intra-abdominal sepsis results in decreased IC and an elevated parathyroid hormone level. Hemodynamics do not correlate with IC levels, and resuscitation can be achieved without calcium administration.

Animals↗
PubMed1992

The hypothalamic-pituitary-adrenal-immune axis. A critical assessment.

The hypothalamic-pituitary-adrenal (HPA) system has been a model for neuroendocrine control of responses of organisms to stressors since the turn of the century. Despite this, the pathways by which infectious insults interact with the HPA system remained poorly defined. Recently, evidence has been presented suggesting that humoral mediators released by inflammatory cells (cytokines) may participate in two-way communication between the site of inflammation and the central nervous system. In this review, we detail the current understanding of the responses of the HPA system to the classic physiologic stimuli of hypovolemia and pain, with an emphasis on the cellular mechanisms and mediators discovered in recent years. We also examine the data substantiating a role of interleukin 1, interleukin 6, and tumor necrosis factor in the direct humoral activation of the HPA system and consider the evidence favoring a physiologic negative feedback relationship between the HPA and the immune systems. Such as interaction is an exciting concept with broad clinical implications. However, we believe that the temporal and quantitative aspects of experiments designed to evaluate this interaction must be carefully evaluated to assure that true physiologic stimuli are studied and that the responses observed are not due to pharmacologic effects of inflammatory mediators acting through "classic" neuroendocrine pathways.

Afferent Pathways↗
PubMed1992

Saline resuscitation after fixed-volume hemorrhage. Role of resuscitation volume and rate of infusion.

The authors have reported previously that small-volume resuscitation (1.8 x bled volume) with 0.9% NaCl restores blood volume and attenuates hormonal responses after large hemorrhage without correction of arterial hypotension. The authors studied the role of rate of infusion in this observation in chronically prepared dogs (aortic flow probe, right atrial pressure and volume, and arterial catheters) after 30% hemorrhage (24.1 +/- 0.4 mL/kg). After 30 minutes, subjects were observed either without treatment (no resuscitation) or with infusion of 43 mL/kg 0.9% NaCl over 3 hours by one of three protocols: (1) impulse infusion over 10 minutes, (2) variable rate infusion, bolus with tapering infusion, or (3) constant rate infusion. Significant improvement in cardiac output and in blood volume and significant decreases of vasopressin and arterial catecholamines were observed in all fluid-treated groups. This benefit was relatively independent of rate of infusion, although impulse infusion produced greater early improvement, which dissipated with time, and constant rate infusion produced better late results. In none of the fluid-treated groups were these improvements reflected in improved mean arterial pressure compared with the no resuscitation group. The authors conclude that small-volume, slow-rate saline infusion produces physiologic benefits that cannot be assessed by easily measured clinical parameters. Thus, early resuscitation after trauma could aid patients even if arterial pressure is unchanged. This benefit might be even greater in patients with uncontrolled bleeding because arterial pressure, and hence bleeding, may not be increased by resuscitation of this type. A reassessment of the value of prehospital fluid resuscitation in the injured patient is warranted.

Animals↗
PubMed1992

Identification of carotid vascular receptors that control adrenal catecholamine secretion in dogs.

The role of carotid sinus and thyrocarotid mechanoreceptors in the reflex control of adrenal medullary function was assessed in anesthetized dogs with adrenal vein catheters. Dogs underwent carotid sinus, thyrocarotid junction, combined carotid sinus and thyrocarotid junction, or sham denervation. On the day after surgery, catecholamine secretion was measured after carotid occlusion proximal to the thyrocarotid junction, cervical vagotomy, and repeat carotid occlusion, each separated by 90 min. After combined carotid denervation, baseline norepinephrine secretion was increased, resulting in a decreased epinephrine-to-norepinephrine ratio. Carotid occlusion before vagotomy did not change the secretion of catecholamines or the epinephrine-to-norepinephrine ratio. After sham carotid denervation, acute vagotomy did not affect catecholamine secretion. However, after denervation of the carotid sinus or thyrocarotid junction, vagotomy resulted in small increases in catecholamine secretion without changing the epinephrine-to-norepinephrine ratio; the magnitude of the response was augmented after combined denervation. At 90 min after vagotomy in dogs with intact carotid baroreceptors, carotid occlusion increased adrenal secretion of catecholamines and decreased the epinephrine-to-norepinephrine ratio. After denervation of carotid sinus or thyrocarotid junction receptors, carotid occlusion increased secretion of catecholamines without changing the epinephrine-to-norepinephrine ratio; the response was abolished by combined denervation. These results show that both carotid sinus and thyrocarotid receptors contribute to the adrenomedullary response to carotid occlusion and to acute vagotomy. Also, reduction in the activity of carotid sinus and thyrocarotid junction receptors chronically (by denervation) or acutely (by carotid occlusion) results in preferential secretion of norepinephrine over epinephrine.

Adrenal Glands↗
PubMed1992

Hypotensive hemorrhage elevates corticotropin-releasing hormone messenger ribonucleic acid (mRNA) but not vasopressin mRNA in the rat hypothalamus.

We examined the effect of acute hypotensive hemorrhage on corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) messenger RNAs (mRNAs) in neurons of the rat hypothalamus. Sprague-Dawley male rats were cannulated (femoral artery and vein) and received a 15 ml/kg.3 min hemorrhage on the morning of the fourth day. Time controls received no hemorrhage. After light halothane anesthesia, the rats were decapitated at 1 or 4 h (six to nine rats per group). The hypothalami were removed, frozen, and sectioned at 12 microns. In situ hybridization was performed using two 48-base oligodeoxynucleotide probes for CRH and AVP message, respectively. Hemorrhage led to a fall in arterial blood pressure and heart rate that recovered by 1 h. Plasma ACTH, corticosterone, and AVP were elevated 20, 60, and 90 min after hemorrhage, but returned to near control levels by 4 h. CRH mRNA was significantly elevated 1 and 4 h after hemorrhage, as compared to time controls, in parvocellular neurons of the paraventricular nuclei. However, AVP mRNA was not different from controls at 1 or 4 h after hemorrhage in the magnocellular or parvocellular paraventricular nuclei, or in the supraoptic or accessory nuclei of the hypothalamus. AVP mRNA was also found in neurons of the suprachiasmatic nuclei, but there was no difference in the amount of mRNA between the 1-h hemorrhage and control groups. These data suggest that neural signals, originating for cardiovascular receptors activated by hemorrhage, up-regulate message for CRH but not for AVP in the paraventricular nuclei of the rat hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1992

Alpha-adrenergic input in the locus coeruleus modulates plasma adrenocorticotropin in cats.

Previous evidence suggested that noradrenergic activity in the vicinity of the ventrorostral locus coeruleus (LC) increased in response to hemorrhage. To investigate the possible role of this response in the control of ACTH release, microinjections (100 nl/min for 2 min) of several agents were made at 59 sites in 35 cats anesthetized with chloralose. Injections were as follows: vehicle (all sites); 150 mM L-glutamate (GLU; 51 sites); an alpha 2-agonist, 1 mM clonidine (19 sites); an alpha 2-antagonist, 1 mM yohimbine (32 sites); an alpha 1-agonist, 1 mM phenylephrine (PE; 42 sites); and an alpha 1-antagonist, 0.05 mM prazosin (20 sites). Plasma ACTH was measured by RIA. Responses were tested statistically by repeated measures analysis of variance. GLU at 12 sites in the region of the ventrorostral LC facilitated plasma ACTH (P less than 0.01), whereas GLU at 6 sites in the caudal LC inhibited ACTH (P less than 0.05). Clonidine at 9 sites in an area that included the ventrorostral LC inhibited ACTH (P less than 0.05), and yohimbine at 7 sites within this latter area facilitated ACTH (P less than 0.01). PE within the ventrorostral LC had no effect on ACTH. However, PE at 10 sites within the caudal LC and along the ventromedial border of the ventrorostral LC facilitated ACTH. The responses for all of these areas to the respective agents differed from those to vehicle, whereas responses from other areas to the former agents or from all areas to prazosin did not. An increase in noradrenergic turnover in the LC may provide inhibitory alpha 2 modulation to the neurons in the LC that are activated by hemorrhage. This modulation and possible alpha 1 input in areas adjacent to the ventrorostral LC may influence the hemodynamic control of ACTH release.

Adrenocorticotropic Hormone↗
PubMed1991

A circulating factor(s) mediates cell depolarization in hemorrhagic shock.

Cell depolarization in hemorrhagic shock has been attributed to hypoperfusion, but the mechanism remains unclear. Suspensions of single cell lines loaded with the potential-sensitive fluorescent dye bis-(1,3-dibutylbarbiturioc acid) trimethine oxonal (DIBAC) and exposed for 30 minutes to rat plasma drawn either before or after hemorrhagic shock (bled 20 mL/kg: mean arterial blood pressure less than 40 mmHg) were studied. Plasma drawn after, but not before, hemorrhage led to partial depolarization regardless of cell type (rat H9C2 skeletal muscle, A-10 smooth muscle, C-9 liver, adrenal, kidney, red blood cell [RBC], white blood cell [WBC]) or species (cat, dog, pig RBC; cat WBC; mouse C2C12 skeletal muscle; and human intestinal smooth muscle [HISM]). Dialysis did not remove the factor(s), suggesting a molecular weight of more than 10,000 daltons. The factor appeared within 5 minutes of shock. The depolarization amplitude increased as a function of plasma concentration and demonstrated saturation kinetics indicating specific receptor binding. Cells were equivalently oxygenated, excluding hypoperfusion as a necessary condition for depolarization. Tumor necrosis factor or platelet activating factor alone or in combination were not effective in this system. Stable measurements can be obtained with this noninvasive system that avoids cell injury consequent to cell impalement with electrodes. This system provides a sensitive in vitro bioassay that should permit identification of the plasma factors mediating cell depolarization, as well as definition of the responsible intracellular mechanisms.

Animals↗
PubMed1991

Interaction of sodium and volume in fluid resuscitation after hemorrhage.

Some measures of the efficacy of fluid resuscitation after hemorrhage are blood volume restitution (BVR) and attenuation of the neuroendocrine response. We compared the effectiveness of resuscitation with 0.9% NaCl and 3.0% NaCl in chronically prepared awake dogs after 30% hemorrhage. Each dog was bled on four occasions and resuscitated by four protocols: 1) full resuscitation (infusion to return and maintain mean arterial pressure (MAP) at control +/- 10 mm Hg) with 3.0% NaCl (HS); 2) full resuscitation with 0.9% NaCl (NS); 3) under-resuscitation with a volume of 0.9% NaCl equal to the subject's previous 3.0% NaCl requirement (SV); and 4) no fluid therapy (NR). Approximately three times more volume was needed to restore MAP with NS vs. HS, and thus the amount of Na administered was not different in these groups. Net volume balance was positive in the NS and SV groups but negative in the HS group due to marked saline diuresis. Net Na balance was positive in all three fluid-treated groups, but significantly higher in the HS group (p less than 0.01). MAP remained below baseline in the SV and NR groups (p less than 0.05). BVR exceeded 100% in NS and HS early in resuscitation, but BVR was not sustained in the HS group. Total plasma protein increased in all three fluid treated groups. Responses of all hormones were completely attenuated in the NS group. ACTH, cortisol, and AVP responses were promptly attenuated in the HS group, but remained greater than control. In the SV group, all hormone levels except renin returned to control values, but more slowly than the other groups. ACTH and cortisol correlated best with BVR; AVP, PRA, and aldosterone correlated with MAP restoration. In summary, resuscitation with either HS or NS can achieve similar MAP restoration. Hypertonic saline produces a more rapid increase in BVR and MAP, but the BVR improvement is transient. Resuscitation with HS incurs an intracellular water debt which is aggravated by a saline diuresis. Hormonal attenuation is linked either to BVR (ACTH, cortisol) or to MAP restoration (renin, AVP). Thus the optimal resuscitation regimen may consist of initial infusion of hypertonic saline followed by sufficient hypotonic solution to restore interstitial fluid volume and normal cellular hydration.

Adrenocorticotropic Hormone↗
PubMed1991

Carotid baroreceptor control of right atrial mechanics in dogs.

To investigate the influence of the carotid arterial baroreceptors on right atrial mechanics, the carotid sinus region was isolated surgically in eight dogs prepared acutely under pentobarbital. Right atrial pressure and conductance volume were measured with a strain-gauge tip catheter and a conductance catheter, respectively. Reduction of carotid sinus pressure from 225 to 50 mmHg elicited significant increases in the a wave in right atrial pressure, in atrial stroke volume, in atrial stroke work (2.5-fold), and in atrial stroke power (4-fold). Mean central venous pressure and atrial volume at the onset of each beat did not change. These responses were unchanged after bilateral cervical vagotomy. Head-up tilt was applied at carotid sinus pressures less than or equal to 150 mmHg in four dogs to oppose any contribution of decreased systemic venous capacity to the responses through increased atrial filling. Tilt did not change atrial stroke work or atrial filling during late ventricular systole before vagotomy but inhibited these variables significantly after vagotomy. The slope of the relationship between right atrial stroke work and atrial volume at the onset of contraction increased significantly with reduction of carotid sinus pressure. This response was unaffected by either vagotomy or tilt. Carotid arterial hypotension appears to augment right atrial stroke work and stroke volume through an increase in atrial contractility. A decrease in venous capacity may contribute to this response especially after vagotomy.

Animals↗
PubMed1991

Response of plasma adrenocorticotropin to injections of L-glutamate or norepinephrine in the dorsal rostral pons of cats.

Previously, electrical stimulation of several nuclei in the dorsal rostral pons of the cat was shown to modulate the release of ACTH. However, the stimulation may have activated fibers of passage. To determine if there are specific groups of neurons within the pons that modulate plasma ACTH when stimulated with glutamate, 30 cats were prepared acutely under chloralose anesthesia. Microinjections of several agents were made at each of 2 sites in the pons of each cat. ACTH was measured by RIA. Injections of 150 mM L-glutamate (100 nl/min.2 min) elicited increases in arterial pressure that were related to the loci of injection. The responses did not decrease significantly when the rate and volume of the injection were reduced by half. Eight sites in a lateral area that extended rostrally from the parabracheal nucleus elicited a significant pressor response that was greater in duration and magnitude than a second significant pressor response that was obtained from 18 sites in a medial area that included the rostral locus coeruleus. Pressor responses did not occur when 0.1 mM norepinephrine or vehicle was substituted for L-glutamate in any area. The larger, but not the smaller, dose of L-glutamate elicited changes in plasma ACTH that were related to the loci of injection. Eight sites in a caudal area that included the ventral locus coeruleus and was within the medial pressor area elicited a significant increase in ACTH. Seven sites in an area rostral to the ventral locus coeruleus that included the rostromedial locus subcoeruleus elicited a significant decrease in plasma ACTH. ACTH responses were not observed when 0.1 mM norepinephrine or vehicle was substituted for L-glutamate in any area. In conclusion, the ventral locus coeruleus and the rostrally adjacent locus subcoeruleus contain neurons with receptors for L-glutamate that can modulate plasma ACTH and arterial pressure independently of a second pathway that includes the parabracheal region and influences arterial pressure. Because the neurons in the coeruleus are known to respond to hemodynamic input, they may participate in the hemodynamic control of ACTH release.

Adrenocorticotropic Hormone↗
PubMed1991

Trauma care for the elderly?

The enormous consumption of health-care resources by bluntly injured elderly patients can be justified if their outcome after trauma is good. In this series, 89% of injured elderly patients ultimately returned to their homes, either independent of (57%) or dependent on (32%) outside help. Factors contributing to increased mortality in such patients included age, injury severity, and the presence or absence of cardiac and septic complications. A Geriatric Trauma Survival Score (GTSS) was devised that predicted the likelihood of mortality in these patients. Finally, study of reimbursement indicated that Medicare does not adequately reimburse hospitals for the enormous cost of providing elderly trauma care.

Aged↗
PubMed1990

Measurement of blood flow to the adrenal capsule, cortex and medulla in dogs after hemorrhage by fluorescent microspheres.

Changes in adrenal medullary and total cortical blood flow after hemorrhage have been described using radioactive microspheres. To assess changes in adrenal capsular and in intracortical adrenal blood flow, a method was used based on microscopic detection of non-radioactive microspheres. Injection of microspheres labelled with fluorescent dyes permitted multiple determinations of blood flow. Pentobarbital anesthetized dogs (n = 6) were prepared acutely with left ventricular and aortic catheters for injection and collection of microspheres, respectively. Adrenal denervation was done unilaterally by cutting the thoracic splanchnic nerve. Injections of 16-microns spheres were made prior to and immediately after 18 ml/kg hemorrhage done over 6 min. Dogs were killed with KCl and adrenals were removed, fixed and sectioned at 80 microns. Using fluorescence microscopy, microspheres were counted in the adrenal capsule, zona glomerulosa, inner cortex (zona facsiculata and reticularis), and the medulla. The majority (95%) of microspheres in the adrenal cortex were trapped in the zona glomerulosa, precluding an independent estimate of blood flow to the inner cortex. Thus, total cortical blood flow was determined by summing the number of 16-microns microspheres in the zona glomerulosa and inner cortex. Prior to hemorrhage, blood flow was greater in the capsule (5.4 +/- 1.6 ml/min/g) compared to the cortex (1.8 +/- 0.9 ml/min/g) and the medulla (2.9 +/- 1.8 ml/min/g). Splanchnicotomy did not change blood flow in the resting state. Following hemorrhage, in innervated glands, medullary blood flow increased to 8.6 +/- 3.1 ml/min/g, whereas blood flow to other zones was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1990

Ionized calcium, parathormone, and mortality in critically ill surgical patients.

A prospective study measured ionized calcium and parathormone sequentially at 48- to 72-hour intervals in 25 surgical intensive care unit patients. Twelve patients (48%) died at mean day 40 and median day 26. Levels of ionized calcium, parathormone, blood urea nitrogen, creatinine, albumin, magnesium, and phosphate for patients who lived were compared with levels for patients who died. The incidence of hypotension, renal failure (creatinine greater than or equal to 3.0), and bacteremia, as well as the amount of red cell, crystalloid, and colloid administration for the two groups was compared. Hypotension, bacteremia, red cells, crystalloid, and colloid were no different. On days 1 and 2 ionized calcium levels were significantly lower and parathormone levels significantly higher in nonsurviving patients; this difference persisted through days 3 and 4. Blood urea nitrogen and creatinine levels increased early in nonsurviving patients but renal failure, which occurred in nine nonsurviving patients, did not develop until mean day 14, median day 18. The phosphate level was slightly higher but still within normal range in nonsurviving patients. By days 5 and 6 ionized calcium and parathormone levels were no different in nonsurviving patients, despite there being no improvement in renal function. Magnesium and albumin levels were no different between groups. Ionized calcium levels are lower and parathormone levels higher early in nonsurviving patients. This difference is not readily explained by associated clinical conditions, including renal dysfunction. Although etiology remains unclear, low ionized calcium and elevated parathormone are early predictors of mortality in critically ill surgical patients.

Aged↗
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↗