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Biomedical subjects

D E Carlson

Publications and source records attributed to D E Carlson.

At least 55 records · Page 3Linked to original sources
PubMed1992

Resting energy expenditure in patients with thermal injuries.

Resting energy expenditures (REE) were measured using indirect calorimetric techniques in 62 patients with burn injuries admitted during 1987 to 1989 and compared with similar measurements made during 1972 to 1973. Energy requirements were related to burn size in both populations, but were greater in the earlier population. In the present study, data from some patients were obtained using a canopy system and from others during mechanical ventilation and were analyzed separately. The regression of REE on burn size was linear for the canopy measurements (r = 0.724) and for the ventilator measurements (r = 0.579). REE data were corrected for the expected basal metabolic rate (BMR) for each patient, with appropriate adjustment for age and sex. The regression of REE per BMR on burn size was linear (r = 0.724), differing from the curvilinear relationship found during 1972 to 1973. These data suggest a change in postburn energy requirements, probably related to differences in patient management. Predictive equations based on older data can be expected to overestimate energy requirements in patients receiving modern burn therapy.

Adolescent↗
PubMed1991

Fetal choroid plexus cysts in the second trimester of pregnancy: a cause for concern.

Controversy surrounds the issue of recommending cytogenetic studies in second-trimester fetuses with fetal choroid plexus cysts. To assist in clarifying this issue, a prospective study was designed to describe the association between fetal choroid plexus cysts and aneuploidy in a large population. During a 3-year period 7350 women at 15 to 22 weeks' gestation underwent an ultrasonographic evaluation. Fetal choroid plexus cysts were diagnosed in 71 (0.96%) of these pregnancies. Sixty-two of the 71 patients elected to undergo amniocentesis. An abnormal karyotype was identified in four (6.4%) of these fetuses. One fetus had trisomy 21, and three fetuses were diagnosed with trisomy 18. These data indicate that it is reasonable to offer genetic counseling and cytogenetic studies in those patients identified as having a fetal choroid plexus cyst.

Aneuploidy↗
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

Prenatal diagnosis: ultrasound advances.

This article reviews the uses of sophisticated ultrasound technology in a wide range of situations including chorionic villus sampling, the prenatal diagnosis of common fetal syndromes and fetal aneuploidies.

Congenital Abnormalities↗
PubMed1991

Implementing nutritional therapy in the thermally injured patient.

Providing adequate nutritional support is an important adjuvant therapy in the management of thermal injuries. Technological advances in both enteral and parenteral nutrition have enabled clinicians to administer large amounts of essential nutrients to critically ill patients who frequently cannot or will not take these nutrients orally. The use of any method of nutritional support requires careful administration and scheduled monitoring to ensure its safety and efficacy. Critical care nurses have an integral role in assuring that appropriate nursing care and monitoring measures are performed.

Burns↗
PubMed1990

Prognostic indicators of the resolution of nonimmune hydrops fetalis and survival of the fetus.

To delineate any possible prognostic indicators, we reviewed the ultrasonographic and nonmorphometric findings in 19 antenatally diagnosed cases of nonimmune hydrops fetalis in which it was chosen to continue the pregnancy. Thirteen fetuses died and six survived. Of all parameters examined, including associated anomalies, abnormal karyotype, location of serous fluid, anemia, and possible cause of nonimmune hydrops fetalis, the most sensitive prognostic indicator was the real-time-directed M-mode echocardiographic measurement of the biventricular outer dimension in diastole. All fetuses with biventricular outer dimensions greater than 95% died, whereas all but one with normal biventricular outer dimensions had resolution of nonimmune hydrops fetalis and survived. This was highly significant (p less than 0.001) with the predictive value of a normal biventricular outer dimension being 86% and the predictive value of an enlarged biventricular outer dimension being 100%.

Chromosome Aberrations↗
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

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↗
PubMed1990

Quantifiable polyhydramnios: diagnosis and management.

Little has been written regarding the ultrasonographic quantification of polyhydramnios or its subsequent management. Therefore, we designed this study to define polyhydramnios using the amniotic fluid index of greater than 2 SDs above the mean for late second- to third-trimester pregnancies, or 24 cm or greater. One hundred twelve nondiabetic women referred to Women's Hospital, Los Angeles County/University of Southern California Medical Center with the descriptive diagnosis of polyhydramnios made by experienced ultrasonographers were included in the study. There was poor correlation between these descriptions and fetal outcome. Twenty-six were qualitatively described as having severe, 29 as moderate, and 57 as mild polyhydramnios. Forty-nine of the 112 patients met our definition of significant polyhydramnios by having an amniotic fluid index of 24 cm or more. This particular definition allowed the inclusion of all fetuses with serious structural defects and/or death. Seven patients had an amniotic fluid index less than 24 cm, but with the traditional quantitative definition of one pocket of 8 cm or more; none of these patients had poor fetal outcome. These data appear to suggest that the use of descriptive definitions of polyhydramnios or a single fluid pocket of 8 cm or greater should be discarded in favor of using an amniotic fluid index of 24 cm or more. Once the diagnosis of polyhydramnios is made, the patient should have a detailed sonographic evaluation, be offered cytogenetic studies, and have antepartum surveillance.

Congenital Abnormalities↗
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↗
PubMed1988

Thioredoxin from Rhodospirillum rubrum: primary structure and relation to thioredoxins from other photosynthetic bacteria.

Thioredoxin was isolated from a photosynthetic purple nonsulfur bacterium, Rhodospirillum rubrum, and its primary structure was determined by high-performance tandem mass spectrometry. The sequence identity of R. rubrum thioredoxin to Escherichia coli thioredoxin was intermediate to those of the Chlorobium thiosulfatophilum and Chromatium vinosum proteins. The results indicate that R. rubrum has an NADP-thioredoxin system similar to that of other photosynthetic purple bacteria.

Amino Acid Sequence↗
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↗