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Biomedical subjects

C E Wade

Publications and source records attributed to C E Wade.

At least 73 records · Page 4Linked to original sources
PubMed1993

Further evaluation of the effects of 7.5% sodium chloride/6% Dextran-70 (HSD) administration on coagulation and platelet aggregation in hemorrhaged and euvolemic swine.

In previous studies, we determined that incubation of high concentrations of the 7.5% saline (HS) component of HSD with human blood, in vitro, significantly prolonged prothrombin time (PT), and reduced platelet aggregation. Considering the rapid plasma volume expansion following HSD infusion, the present study tested the hypothesis that any HS-induced effects on coagulation would have no clinical significance when HSD was infused for the treatment of hemorrhagic hypotension. Conscious, splenectomized pigs, either euvolemic (n = 11) or bled 27 ml/kg over 60 min (n = 9), were treated with the proposed therapeutic dose of 4 ml/kg HSD. Blood samples were withdrawn prior to and at the end of the hemorrhage and 0.5, 1, 2, 3, 4, 24, 48, 72, and 168 hr following HSD infusion, and PT, activated partial thromboplastin time (APTT), and platelet aggregation were determined. HSD did not significantly affect PT, APTT, or platelet aggregation in either group of swine at any time measured. In other studies, HSD did not prolong bleeding times after 1 or 2 hr in euvolemic pigs. These data further support the premise that a single dose of HSD for the prehospital treatment of hemorrhagic hypotension will not adversely affect blood coagulation.

Animals↗
PubMed1992

Acute and subacute toxicity of 7.5% hypertonic saline/6% dextran-70 (HSD) in dogs. 1. Serum immunoglobulin and complement responses.

Clinical use of modern dextran solutions has been limited by concerns of anaphylactoid reactions. To assess the short-term antigenic response to 7.5% hypertonic saline in 6% Dextran-70 (HSD), sera were obtained from dogs involved in the acute and subacute toxicology testing of HSD and its individual components, and analyzed for IgG, IgM and C3 complement. In separate studies, beagles were infused i.v. with a single dose of HSD or its components at 20 ml kg-1 (the maximum tolerated dose; MTD), or the MTD daily for 14 days, and serum was obtained prior to and at various times after infusion up to 14 days. In both studies, despite serum dextran concentrations exceeding 2000 mg dl-1, no induction of IgG, IgM or C3 complement concentrations were observed. In addition, serum IgG immunoelectrophoretic patterns were of normal curvature, position and intensity; the immunoprecipitin bands were not displaced, bowed, inhibited or thicker than the normal preinfusion immunoelectrophoretograms. The data suggest that single or multiple HSD i.v. injections, as much as five times the proposed therapeutic level for the treatment of hypovolemia, evoked no increase in antibody titers in dogs. Therefore, therapeutic use of HSD in the treatment of hemorrhagic shock should not be associated with widespread concomitant allergic complications.

Animals↗
PubMed1992

Effect of dehydration on cardiovascular responses and electrolytes after hypertonic saline/dextran treatment for moderate hemorrhage.

STUDY OBJECTIVE: To determine if hypertonic saline/dextran (HSD) is effective in treating hemorrhage in the presence of dehydration. DESIGN: After surgical preparation, swine were euhydrated or dehydrated for 24 or 48 hours. Animals were bled 25 mL/kg over 60 minutes and treated with HSD. SETTING: Laboratory. PARTICIPANTS: Seventeen immature Yorkshire pigs. INTERVENTIONS: 4 mL/kg HSD (7.5% NaCl in 6% dextran-70) administered over one minute. MEASUREMENTS AND MAIN RESULTS: All euhydrated animals survived; 100% of the pigs survived 180 minutes after treatment. Two animals dehydrated for 24 hours and three animals dehydrated for 48 hours died within three hours of HSD treatment. In all groups, plasma potassium was reduced significantly and equally; cardiac output was increased; mean arterial pressure rose rapidly within first five minutes, but was sustained only in euhydrated animals; hematocrit, hemoglobin, and plasma total protein levels were reduced; and plasma glucose increased with persistent between-group differences. RESULTS: HSD immediately rectified the decreases in mean arterial pressure and cardiac output incurred during hemorrhage; over time, however, the improvement in pressure was not sustained in dehydrated pigs. Parallel increases in plasma osmolality and sodium concentrations were offset by the initial group differences resulting from dehydration. CONCLUSION: Dehydration does not compromise the efficacy of HSD as a resuscitation treatment for hemorrhagic shock.

Animals↗
PubMed1992

Use of hypertonic saline/dextran versus lactated Ringer's solution as a resuscitation fluid after uncontrolled aortic hemorrhage in anesthetized swine.

STUDY OBJECTIVE: We tested the hypothesis that following aortotomy, administration of hypertonic saline/dextran increases hemorrhage and mortality. We also compared hypertonic saline/dextran with the standard therapy of attempting to replace three times the amount of lost blood with lactated Ringer's solution. DESIGN: In this model of uncontrolled arterial hemorrhage resulting from aortotomy, 24 anesthetized Yorkshire swine underwent splenectomy, stainless steel wire placement in the infrarenal aorta, and instrumentation with Swan-Ganz and carotid artery catheters. The wire was pulled, producing a 5-mm aortotomy and spontaneous intraperitoneal hemorrhage. INTERVENTIONS: The animals were randomly assigned to one of three study groups: control; hypertonic saline/dextran group in which six minutes after aortotomy a 4-mL/kg mixture of IV 7.5% NaCl and 6% Dextran-70 was given over one minute; or lactated Ringer's group in which six minutes after aortotomy 80 mL/kg IV lactated Ringer's was given over nine minutes. MEASUREMENTS AND MAIN RESULTS: The volume of hemorrhage and the mortality rate in hypertonic saline/dextran-treated animals were significantly greater than in the nonresuscitated controls (1,340 +/- 230 mL versus 783 +/- 85 mL and five of eight versus zero of eight, respectively; P less than .05). Although the mortality rate in the lactated Ringer's group was not significantly different from the hypertonic saline/dextran group, survival time was significantly shorter than in the hypertonic saline/dextran group. CONCLUSION: In this model of uncontrolled hemorrhage, immediate IV administration of hypertonic saline/dextran significantly increased hemorrhage volume and mortality. However, the accentuation of hemorrhage and reduction in survival were not as great as that produced by the standard practice of attempting to replace the lost blood with three times that volume of lactated Ringer's.

Anesthesia↗
PubMed1992

Measurement of glomerular filtration rate in ICU patients using 99mTc-DTPA and inulin.

Improved and reliable methods for assessing glomerular filtration rate (GFR) in intensive care patients are needed in light of known deficiencies using creatinine clearance. We compared simultaneous two-hour clearances of inulin (CIn), creatinine (CCr), and 99mTc-diethylenetriaminepentaacetic acid (CDTPA) in 18 medical or surgical intensive care patients (range, 49 to 92 years old) with blood urea nitrogen (BUN) levels greater than 17.9 mmol/liter (0.5 mg/ml), serum creatinine levels greater than 150 mumol/liter (0.02 mg/ml), or estimated Cockcroft clearance less than 60 ml/min. Patients had severe renal dysfunction with average GFR of 35 ml/min (range, 2 to 69 ml/min). CDTPA and CCr correlated significantly with CIn, although CDTPA tended to provide a closer approximation. Cockcroft clearance (32 +/- 4 ml/min) was grossly similar to CDTPA and CIn and correlated significantly, especially when weight was calculated using actual as opposed to ideal body weight. In a subset of 13 patients with CIn less than 30 ml/min, only CDTPA was significantly correlated with CIn. In patients in the intensive care unit, CDTPA provides a rapid, accurate, and inexpensive clinical assessment of GFR, even at very low GFRs.

Aged↗
PubMed1992

The effects of 7.5% NaCl/6% dextran 70 on coagulation and platelet aggregation in humans.

The combination solution of 7.5% NaCl/6% dextran 70 (HSD) administered IV gives hemodynamic improvement in the treatment of hemorrhagic hypotension. Since earlier dextran solutions were reported to interfere with blood coagulation, the effects of HSD on the prothrombin time (PT), the activated partial thromboplastin time (APTT), platelet aggregation, and platelet concentration were studied. The HSD mixed with human plasma (1:5 and 1:10) slightly prolonged PT, but had no effect on the APTT, compared with saline controls. The HSD also decreased human platelet aggregation at the 1:5 dilution. In separate mixing studies, the hypertonic saline component of HSD was associated with the prolongation of PT and decreased platelet aggregation. The data from these studies indicate that at its proposed therapeutic dose, HSD is expected to have minimal effect on blood coagulation.

Adult↗
PubMed1992

Effect of leg exercise training on vascular volumes during 30 days of 6 degrees head-down bed rest.

Plasma and red cell volumes, body density, and water balance were measured in 19 men (32-42 yr) confined to bed rest (BR). One group (n = 5) had no exercise training (NOE), another near-maximal variable-intensity isotonic exercise for 60 min/day (ITE; n = 7), and the third near-maximal intermittent isokinetic exercise for 60 min/day (IKE; n = 7). Caloric intake was 2,678-2,840 kcal/day; mean body weight (n = 19) decreased by 0.58 +/- 0.35 (SE) kg during BR due to a negative fluid balance (diuresis) on day 1. Mean energy costs for the NOE, and IKE, and ITE regimens were 83 (3.6 +/- 0.2 ml O2.min-1.kg-1), 214 (8.9 +/- 0.5 ml.min-1.kg-1), and 446 kcal/h (18.8 +/- 1.6 ml.min-1.kg-1), respectively. Body densities within groups and mean urine volumes (1,752-1,846 ml/day) between groups were unchanged during BR. Resting changes in plasma volume (ml/kg) after BR were -1.5 +/- 2.3% (NS) in ITE, -14.7 +/- 2.8% (P less than 0.05) in NOE, and -16.8 +/- 2.9% (P less than 0.05) in IKE, and mean water balances during BR were +295, -106, and +169 ml/24 h, respectively. Changes in red cell volume followed changes in plasma volume. The significant chronic decreases in plasma volume in the IKE and NOE groups and its maintenance in the ITE group could not be accounted for by water balance or by responses of the plasma osmotic, protein, vasopressin, or aldosterone concentrations or plasma renin activity. There was close coupling between resting plasma volume and plasma protein and osmotic content.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Resuscitation of intraoperative hypovolemia: a comparison of normal saline and hyperosmotic/hyperoncotic solutions in swine.

BACKGROUND AND METHODS: We compared a hypertonic saline-dextran solution (7.5% NaCl/6% dextran-70) with 0.9% NaCl (normal saline) for treatment of intraoperative hypovolemia. Fourteen anesthetized pigs (mean weight 36.3 +/- 2.1 kg) underwent thoracotomy, followed by hemorrhage for 1 hr to reduce mean arterial pressure to 45 mm Hg. A continuous infusion of either solution was then initiated and the flow rate was adjusted to restore and maintain aortic blood flow at baseline levels for 2 hrs. RESULTS: Full resuscitation to initial values of aortic blood flow was achieved with both regimens, but the normal saline group required substantially larger volumes and sodium loads to maintain stable hemodynamic values. Normal saline resuscitation produced increases in right ventricular preload (central venous pressure) and afterload (pulmonary arterial pressure and pulmonary vascular resistance), resulting in increased right ventricular work. CONCLUSIONS: Hypertonic saline-dextran solution resuscitation of intraoperative hypovolemia is performed effectively with smaller fluid and sodium loads, and is devoid of the deleterious effects associated with fluid accumulation induced by a conventional isotonic solution regimen.

Animals↗
PubMed1992

Traumatic brain injury attenuates the effectiveness of lactated Ringer's solution resuscitation of hemorrhagic shock in rats.

Traumatic brain injury suppresses spontaneous cardiovascular compensation for hemorrhage, prompting us to examine the possibility that trauma to the brain modifies hemodynamic response to therapy in hemorrhage. Thirty rats that were anesthetized were randomly assigned to four groups--hemorrhagic shock (H), hemorrhagic shock after brain trauma (TH), hemorrhagic shock treated with lactated Ringer's (LR) solution (HR), and hemorrhagic shock after brain trauma treated with LR (THR). After hemorrhage, group TH had significantly lower mean arterial pressure (MAP), cardiac index (CI) and stroke volume index (SVI) than group H. Throughout the postresuscitative period, group HR had significantly higher MAP, CI, SVI and central venous pressure than group H. At 50 and 70 minutes after the start of hemorrhage, group THR showed significantly lower MAP, CI and SVI than group HR. This difference in hemodynamics is not because of transcapillary refill effect, because brain trauma did not cause changes in hematocrit and plasma protein levels. As heart rate, preload and afterload were not significantly different between groups THR and HR, the attenuation of fluid resuscitation can be attributed mainly to a depressed cardiac function. Furthermore, neither brain trauma nor fluid replacement altered the content of water in the brain in hemorrhaged rats. These data indicate that brain trauma not only suppresses spontaneous hemodynamic recovery from hemorrhage, but also impedes the efficacy of LR resuscitation. The results of the current study suggested that a more aggressive fluid replacement may be needed to treat hemorrhagic shock in individuals with brain injury.

Animals↗
PubMed1991

Effects of 7 successive days of unaccustomed prolonged exercise on aerobic performance and tissue damage in fitness joggers.

The effects of 7 successive days of prolonged jogging on aerobic performance and biochemical markers of muscle and red blood cell damage were examined in 10 moderately fit men, ages 27 +/- 2 yr (mean +/- SE). The subjects jogged for 2 h per day at 78 +/- 4% of maximal heart rates and covered a total of 129 +/- 2 km, nearly eight times their regular weekly training distance. At baseline, maximal oxygen uptake (VO2max) during treadmill tests averaged 3.45 +/- 0.24 L/min, or 44.7 +/- 1.4 ml/kg/min. On follow-up tests 2d after the week of increased training, VO2max (3.56 +/- 0.17 L/min) and treadmill performance were not significantly improved. Body weight declined from 79.5 +/- 4.6 kg to 77.8 +/- 4.4 kg (p less than 0.05) because of reduced body fatness (16.8 +/- 2.3% to 13.6 +/- 1.7%, p less than 0.05). Weight-adjusted VO2max increased to 46.4 +/- 2.0 ml/kg/min (p less than 0.05). However, heart rate and systolic blood pressure were not significantly changed at rest, or during submaximal and maximal treadmill exercise. Mean hemoglobin concentration at treadmill testing declined from 14.9 +/- 0.3 g/dl to 13.3 +/- 0.3 g/dl (p less than 0.05). Leg muscle soreness, especially in the thigh region, persisted in all subjects after 3 d. Soreness was accompanied by chronic elevations (p less than 0.05) in serum levels of myoglobin, creatine kinase (CK), lactic dehydrogenase (LD), aminoaspartate, and the isoenzymes CK-MB and LD1,2. Serum haptoglobin levels after jogging fell from 86 +/- 9 mg/dl to 60 +/- 8 mg/dl (p less than 0.05), suggestive of footstrike hemolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Development of runner's anemia during a 20-day road race: effect of iron supplements.

Intense training for long-distance running has been associated with reduced hemoglobin (Hb) levels and low iron stores. Whether iron supplementation helps prevent this "runner's anemia" remains controversial. To determine the relationship between iron status and the early stage of reduced Hb levels in male runners, we examined hematologic variables in 15 healthy men (ages 25 to 47 yrs) who ran twice their regular training distance in 20 days during a 500-km road race. Nine of the runners took iron-containing tablets which provided an average of 36 mg/d of iron, while the other six did not take iron supplements. Only one of the 15 subjects had a low Hb concentration (less than 14 g/dl) before the race. After 10 days (285 km), low Hb levels (p less than 0.001) were found in 12/15; six of these runners took iron supplements. However, following a 2-day rest period and five more days of running, only 5/15 and 7/15, respectively, had low Hb levels. Serum iron, ferritin, total iron binding capacity, and percent transferrin saturation values remained within normal limits and did not change significantly. Reticulocyte counts progressively increased, becoming 8-fold higher than at baseline (p less than 0.001), irrespective of the use of iron supplements. "Runner's anemia" developed in 11/15 (73%) of the subjects, independently of their iron status and iron intake. The reductions in Hb were accompanied by parallel decreases in RBC count and hematocrit, and by a significant reticulocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Immediate hypertensive response to fluid percussion brain injury may be related to intracerebral hemorrhage and hypothalamic damage.

Fluid percussion brain injury is associated with an immediate rise in mean arterial pressure (MAP). However, the cerebral morphologic basis for this response is still not clear. Thirty-four anesthetized rats were injured using a lateral craniotomy preparation. In 19 rats, impact level was set at 1.73 +/- 0.04 atm, and impact duration was kept at 25 msec to examine the relationship between postinjury hypertensive response and cerebral lesions. MAP was monitored for 1 hour after impact. Fluid percussion produced an increase in MAP from 99 +/- 3 to 134 +/- 4 mm Hg (p less than 0.001), with an increment range of -2 to 87 mm Hg (36 +/- 5 mm Hg) or 0 to 96% increase. The MAP peak occurred at 15 +/- 2 seconds and then rapidly returned to the preimpact level. Histopathological findings, principally hemorrhage, were graded and ranked from 1 to 19 according to relative severity and hypothalamic involvement. There was a significant correlation between MAP rise and the injury ranking (r = 0.52, p = 0.02). No appreciable damage was observed in the brainstem caudal to the diencephalon. Fifteen rats were subjected to higher injury levels. The overall impact magnitude ranged from 1.3 to 3.5 atm. A linear relationship was found between impact magnitude (X, atm) and increment in MAP (Y, mm Hg) (Y = 28.1*X - 14.0, r = 0.62, p less than 0.001). Our study indicates that the immediate postinjury hypertensive response is closely correlated with the impact magnitude and may be related to intracerebral hemorrhage and hypothalamic damage but not necessarily to caudal brainstem damage.

Animals↗
PubMed1991

Filtration-assisted exchange transfusion using alpha alpha Hb, an erythrocyte substitute.

A method for improving the efficiency of exchange transfusion to evaluate hemoglobin- (Hb) based erythrocyte substitutes is described. The method uses a continuous-flow hollow-fiber plasma separation filter to remove the erythrocytes while returning 75% of the plasma. The removed volume was replaced with a 14-g/dl solution of human Hb cross-linked between the alpha-chains with bis(3,5-dibromosalicyl)fumarate (alpha alpha Hb). Filtration of 2.76 blood vol in anesthetized swine resulted in a 95% reduction of hematocrit and produced a plasma Hb concentration of 7.63 g/dl. Hyperoncotic Hb solutions cause volume expansion, which reduces the efficiency of exchange but provides hemodynamic stability in the face of decreasing blood viscosity and subsequent intravascular volume loss with Hb redistribution. Filtration-assisted exchange transfusion is rapid, conserves valuable modified Hb, and ensures continuous adequate oxygen delivery.

Animals↗
PubMed1991

Suppression by traumatic brain injury of spontaneous hemodynamic recovery from hemorrhagic shock in rats.

The effects of brain trauma on cardiovascular and endocrine responses to hemorrhage were investigated. Forty anesthetized rats were randomly assigned to one of four groups of 10 rats each: a control group (Group C): a group with induction of hemorrhage at 16.2 ml/kg/10 min (Group H); a group with fluid-percussion brain injury at a peak pressure of 1.7 atm and an impulse duration of 25 msec (Group T); and a group receiving hemorrhagic shock following brain trauma (Group TH). Group C and T rats showed no significant alterations in cardiovascular function. At the end of hemorrhage there were no significant differences between Groups TH and H in the nadirs of mean arterial blood pressure (MABP) (mean values +/- standard error of the mean: 42 +/- 2 vs. 40 +/- 4 mm Hg) and stroke volume index (SVI) (0.61 +/- 0.11 vs. 0.66 +/- 0.10 ml/bt/kg); however, 1 hour post-hemorrhage recovery was blunted in Group TH compared to Group H (MABP 56 +/- 4 vs. 65 +/- 3 mm Hg; cardiac index 182 +/- 15 vs. 220 +/- 15 ml/min/kg; and SVI 0.71 +/- 0.06 vs. 0.81 +/- 0.06 ml/bt/kg). Since the two groups showed no significant differences in heart rate, preload (central venous pressure), and afterload (systemic vascular resistance), the reduced cardiac index recovery in Group TH is believed due to the attenuation of cardiac contractile performance. The Group TH preparation potentiated hormonal responses to hemorrhage with significantly higher epinephrine and aldosterone levels than in Group H. Brain trauma enhanced the norepinephrine response to hemorrhage, even at an injury level that by itself did not result in an increase in this hormone. Group TH rats also had significantly lower blood pH and HCO3 levels. The data suggest that brain trauma suppresses MABP and cardiac index recovery after hemorrhage mainly by inhibiting cardiac contractile performance, probably due to high catecholamine levels and severe metabolic acidosis.

Adrenal Cortex Hormones↗
PubMed1991

Neuroendocrine abnormalities in patients with traumatic brain injury.

This article provides an overview of hypothalamic and pituitary alterations in brain trauma, including the incidence of hypothalamic-pituitary damage, injury mechanisms, features of the hypothalamic-pituitary defects, and major hypothalamic-pituitary disturbances in brain trauma. While hypothalamic-pituitary lesions have been commonly described at postmortem examination, only a limited number of clinical cases of traumatic hypothalamic-pituitary dysfunction have been reported, probably because head injury of sufficient severity to cause hypothalamic and pituitary damage usually leads to early death. With the improvement in rescue measures, an increasing number of severely head-injured patients with hypothalamic-pituitary dysfunction will survive to be seen by clinicians. Patterns of endocrine abnormalities following brain trauma vary depending on whether the injury site is in the hypothalamus, the anterior or posterior pituitary, or the upper or lower portion of the pituitary stalk. Injury predominantly to the hypothalamus can produce dissociated ACTH-cortisol levels with no response to insulin-induced hypoglycemia and a limited or failed metopirone test, hypothyroxinemia with a preserved thyroid-stimulating hormone response to thyrotropin-releasing hormone, low gonadotropin levels with a normal response to gonadotropin-releasing hormone, a variable growth hormone (GH) level with a paradoxical rise in GH after glucose loading, hyperprolactinemia, the syndrome of inappropriate ADH secretion (SIADH), temporary or permanent diabetes insipidus (DI), disturbed glucose metabolism, and loss of body temperature control. Severe damage to the lower pituitary stalk or anterior lobe can cause low basal levels of all anterior pituitary hormones and eliminate responses to their releasing factors. Only a few cases showed typical features of hypothalamic or pituitary dysfunction. Most severe injuries are sufficient to damage both structures and produce a mixed endocrine picture. Increased intracranial pressure, which releases vasopressin by altering normal hypothalamic anatomy, may represent a unique type of stress to neuroendocrine systems and may contribute to adrenal secretion by a mechanism that requires intact brainstem function. Endocrine function should be monitored in brain-injured patients with basilar skull fractures and protracted posttraumatic amnesia, and patients with SIADH or DI should be closely monitored for other endocrine abnormalities.

Brain Injuries↗
PubMed1991

Modification of pituitary-adrenal axis responses to hemorrhage by handling techniques in conscious swine.

Responses of the pituitary-adrenal axis to hemorrhagic hypotension were compared in chronically instrumented swine that were allowed to move freely in a holding cage (n = 11) and swine trained to accept physical restraint in a Pavlov sling (n = 14). Seven to ten days after surgical preparation, each animal was hemorrhaged (37.5 ml/kg over 60 min) while confined to its environment. Before hemorrhage, control values for ACTH, cortisol, heart rate, and mean arterial pressure were at near-basal levels in both groups, and during hemorrhage both groups showed similar decrements in blood pressure. Hemorrhage in the sling animals, however, led to increases in plasma ACTH and cortisol concentration much greater than those seen in caged animals. Log-linear plots of ACTH against mean arterial pressure revealed similar response characteristics in the two groups but significant rightward shift of the response curve in sling-restrained animals. Our results indicate that sling restraint, even in highly trained animals, potentiates pituitary-adrenal responses to hemorrhage by some as yet unknown mechanism.

Adrenocorticotropic Hormone↗
PubMed1991

Neuroendocrine responses to hypertonic saline/dextran resuscitation following hemorrhage.

The neuroendocrine responses to resuscitation with 7.5% hypertonic saline/6% Dextran-70 (HSD) following hemorrhagic hypotension were evaluated in conscious swine. Following hemorrhage (37.5 ml/kg/60 min) animals received 4 ml/kg of HSD (n = 6) or 0.9% saline (n = 8). Administration of normal saline did not alter cardiovascular function nor attenuate an increase in hormones. HSD rapidly improved cardiovascular function and acutely decreased ACTH, plasma renin activity (PRA), cortisol, norepinephrine (NE), epinephrine (E), aldosterone, and lysine vasopressin levels (LVP). The initial decreased in ACTH, cortisol, and aldosterone levels was due primarily to hemodilution associated with the expansion of plasma volume. The reductions in NE, E, LVP, and PRA were greater than those attributed to hemodilution alone. Values for LVP, NE, and E remained at values below those at the end of hemorrhage, but greater than basal levels, while PRA returned to values similar to these at the end of hemorrhage. The decrease in LVP, NE, and E following HSD resuscitation for the treatment of hemorrhagic hypotension may result from and contribute to the rectification of cardiovascular and metabolic function.

Adrenocorticotropic Hormone↗