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Biomedical subjects

D E Carlson

Publications and source records attributed to D E Carlson.

At least 73 records · Page 4Linked to original sources
PubMed1988

Fetal foot length: relationship to menstrual age and fetal measurements in the second trimester.

The purpose of this study was to describe the ultrasonic measurement of fetal foot length and to develop mathematical models to quantify the relationships between menstrual age and commonly measured fetal structures. We evaluated 120 patients with known last menstrual periods and normal pregnancies to develop a cross-sectional study population. All patients had ultrasonic measurement of the fetal foot length, biparietal diameter, head circumference, abdominal circumference, and femur length. Least-squares estimation of linear models was used to select the best mathematical models to describe the relationship between menstrual age and fetal foot length. A similar evaluation of the relationship between fetal foot length and the other measured parameters was performed. All models were best described by a linear equation. An R2 value of 0.94, with a standard error of the estimate of 0.204, was obtained for menstrual age versus fetal foot length. When the model for fetal foot length and menstrual age was compared with published anatomical data, close agreement was seen over the time interval studied. Our results suggest that the measurement of fetal foot length with ultrasound gives a reliable assessment of anatomical fetal or neonatal foot length and is highly correlated to the menstrual age of the fetus.

Female↗
PubMed1987

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

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

Adrenocorticotropic Hormone↗
PubMed1987

Factors from paraventricular nucleus mediating adrenocorticotropin release in cats.

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

Adrenocorticotropic Hormone↗
PubMed1986

Hormonal responses associated with early hyperglycemia after graded hemorrhage in dogs.

Trained, awake, splenectomized dogs (n = 17) were studied to examine potential mechanisms for early hyperglycemia after hemorrhage (H). Animals were surgically prepared under halothane-nitrous oxide 3 days before the experiment. Chronic catheters were placed aseptically in the portal vein (PV), femoral vein, and femoral artery. Electromagnetic flow probes were placed around the PV and hepatic artery. After an overnight fast, dogs were hemorrhaged 10, 20, or 30% of their estimated blood volume in 3 min. Flow measurements and blood samples for glucose (G), immunoreactive insulin (IRI), immunoreactive glucagon (IRG), catecholamines (C), and cortisol (F) were taken prior to H and from 5 min to 8 h post-H. Plasma IRI, IRG, and F were measured by radioimmunoassay, plasma C by high-pressure liquid chromatography, and G by a glucose oxidase method. Peripheral G did not change after 10% H but increased significantly after 20 and 30% H from 10 min to 2 h. Similarly, peripheral C did not change after 10% H but increased significantly from 10 min to 2 h after 20 and 30% H. In contrast, the portal venous delivery of IRG did not increase significantly until at least 1 h after any magnitude of H. Peripheral IRI did not change after any magnitude of H. However, portal venous delivery of IRI decreased significantly from 20 min to 6 h after 10% H. Plasma F increased significantly in peripheral blood after all magnitudes of H. These results indicate that an increase in the release of IRG occurs too late to account for the early hyperglycemia that occurs during the 1st h following H.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Right atrial volume during hemorrhage in the dog.

Atrial B receptors elicit reflex changes after hemorrhage and respond to changes in atrial volume, but the latter have not been measured after hemorrhage. An impedance catheter that was originally designed to measure ventricular volume was advanced into the atrium from the femoral vein in each of 10 splenectomized dogs that were anesthetized with alpha-chloralose. The rate of hemorrhage and reinfusion was 2% of the estimated blood volume per min. Cardiac output (CO) was measured with dye dilution. The components of the atrial volume signal that were most sensitive to hemorrhage were the filling that occurred during late ventricular systole (Vs) and the absolute volume at the end of ventricular systole, (Vabs). Both variables were significantly less than base line (P less than 0.05) after 10% hemorrhage. The rate of change of Vs decreased significantly after 20% hemorrhage. However, the volume ejected with each atrial beat (Ve) decreased significantly (P less than 0.05) only after 30% hemorrhage. Atrial output (AO) as computed by multiplying Ve by heart rate (HR) did not change after hemorrhage. The ratio of AO to CO increased in direct proportion to HR (P less than 0.01) so that after 30% hemorrhage, for which HR was high, the decreases in CO from base line in individual dogs correlated significantly with the changes in AO (P less than 0.01). Since the B receptors are known to fire at the end of the ventricular systole at a rate that is dependent on blood volume, their firing may be a function of the concomitant atrial signals, Vs and Vabs, that are most sensitive to blood volume, and these atrial signals may serve as indexes of B fiber activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Neural interaction in control of adrenocorticotropin.

Multiple afferent pathways underlie the control of adrenocorticotropin (ACTH). The variety of sensory stimuli that elicit ACTH release indicate that neural interaction and convergence within the central nervous system contribute to this control system. The site and nature of neural interactions contributing to ACTH release are unknown. However, recent evidence suggests that some of the sensory convergence and temporal plasticity within the system that controls ACTH release may exist at the brain-stem level. Within the hypothalamus, different areas may preferentially activate the release of different releasing factors so that additional convergence and interaction may occur within the median eminence or the pituitary.

Action Potentials↗
PubMed1984

Effects of vasopressin antiserum on the response of adrenocorticotropin and cortisol to hemorrhage.

To determine if arginine vasopressin (AVP) is involved in the response of ACTH and cortisol (F) to hemorrhage, we examined the effect of injections of AVP-antiserum into the third ventricle in chronically prepared awake cats. Cats were trained to remain unrestrained in a cardboard box. Cats were prepared under halothane and nitrous oxide with aseptic technique. Two to 3 days later, experiments began. Antiserum (5 microliters) to AVP or to oxytocin (OXY) as a control was given 26 min before hemorrhage conducted over 3 min. Thirty minutes after hemorrhage, reinfusion was conducted over 3 min. Each cat received each antiserum in randomized sequence 2-3 days apart. Plasma ACTH and F were measured by RIA. Data were analyzed statistically by analysis of variance. In 12 experiments in 6 cats, ACTH and F increased significantly with 10 ml/kg hemorrhage (P less than 0.01) and to the same extent (P greater than 0.1) after either antiserum. In 20 additional experiments in 10 cats, a submaximal dose of dexamethasone was administered sc 2-3 h before hemorrhage of 15 or 17.5 ml/kg. Under this circumstance, ACTH increased significantly (P less than 0.05) after anti-OXY, but not after anti-AVP (P greater than 0.2) so that during hemorrhage the values of ACTH differed significantly (P less than 0.025). F increased significantly more after anti-OXY than after anti-AVP (P less than 0.025). Changes in arterial pressure, heart rate, and plasma glucose with or without pretreatment with dexamethasone did not differ between groups. Changes in F and ACTH in cats receiving sham injections did not differ from those after anti-OXY. These findings suggest that normally a corticotropin-releasing factor (CRF) or factors act independently of AVP to mediate the response to hemorrhage. However, in the presence of steroid feedback by dexamethasone, the release or action of this CRF(s) is suppressed so that AVP is necessary for a full response. As has been proposed previously by others, AVP could potentiate the action of other CRFs, stimulate their release, or act as a CRF.

Adrenocorticotropic Hormone↗
PubMed1984

Hypothalamic neurons responding to hemodynamic input and to stimulation in the pons may influence adrenocorticotropin release.

Experiments were designed to identify hemodynamically sensitive neurons in the mediodorsal hypothalamus and to determine if they were also sensitive to electrical stimulation of areas in the dorsal rostral pons that were implicated previously in the control of adrenocorticotropin (ACTH) release. Cats were anesthetized with chloralose and urethane, immobilized with gallamine, and artificially respired. Hemodynamic stimuli included constriction (CC) of the supradiaphragmatic inferior vena cava to reduce venous return and sinusoidal volume pulsation (RA) of the right atrium (1 ml peak at 1 Hz). Previously, CC was shown to facilitate and RA was shown to inhibit ACTH release. Electrical stimulation in the pons consisted of single shocks (500 microA DC, 0.05 msec, negative-to-tip) delivered on each of an array of three or four bipolar co-axial electrodes in the pons. Twenty-three neurons were tested with only RA. Of these, two were inhibited, two were facilitated, and 19 did not respond. Thirty-two neurons were tested with CC. Of these, nine were inhibited, nine were facilitated, and 14 did not respond. Seventeen neurons that responded either to RA or to CC were tested with stimulation in the pons. Of these, three were orthodromically activated and two were inhibited from a total of eight pontine sites. Six of the eight sites were within 300 microns of an area shown previously to contain neurons that responded to CC. Of 31 additional sites that were stimulated, but at which stimulation did not drive neurons that responded to hemodynamic stimuli, 26 were located more than 300 microns from this area (p less than 0.01, X2 test). The data suggest that some hypothalamic neurons involved in the hemodynamic control of ACTH release receive a projection from or through the dorsal raphe nucleus medially, and the ventral locus ceruleus, locus subceruleus, and underlying reticular formation laterally. However, other neurons may receive projections that bypass these regions.

Adrenocorticotropic Hormone↗
PubMed1983

Surgical treatment of aneurysms of the descending thoracic aorta: an analysis of 85 patients.

We have reviewed our experience with resection of 85 aneurysms of the descending thoracic aorta during a ten-and-one-half year interval ending in June, 1980. There were 39 arteriosclerotic aneurysms, 35 aneurysms associated with chronic aortic dissection, and 11 posttraumatic aneurysms. During repair, a temporary shunt was used in 56 patients (66%), partial (venoarterial) cardiopulmonary bypass (CPB) in 19 patients (22%), and simple aortic cross-clamping in 10 patients (12%). Hospital mortality was 11.8%, and was unrelated to the type of aneurysm or operative method. Spinal cord injury developed in 3 of the 83 patients surviving operation (3.6%), and occurred once with each of the three operative methods. Among the 82 operative survivors without preoperative renal failure, postoperative renal failure requiring hemodialysis occurred in 2 of the 10 patients who had simple aortic cross-clamping (20%), 2 of the 54 who had a shunt (3.7%), and in none of the 18 who underwent partial CPB (p = 0.049). Postoperative renal dysfunction (a rise in the preoperative blood urea nitrogen and creatinine levels of 50% or more) occurred in 27 of the 53 patients (51%) who had preoperative and postoperative determinations. Age, intraoperative hypotension, and the use of simple aortic cross-clamping were significant (p less than 0.05) independent predictors of postoperative renal dysfunction. Intraoperative blood loss and the incidence of reoperation for bleeding did not differ significantly among the three operative methods. We conclude that the aneurysm resection technique and the development of intraoperative hypotension have an important effect on postoperative renal function. Partial CPB may represent the optimal method for preservation of renal function, and may also be the method of choice for elderly patients with preexisting renal dysfunction.

Adult↗
PubMed1983

Secretory response of glucagon to hemorrhage.

Glucagon has been implicated in the hormonal-metabolic response to injury and in the restitution of blood volume. Evidence for this has been obtained largely from observations of peripheral glucagon concentrations. The secretory response to mild or moderate hemorrhage remains undefined. Experiments have been conducted in conscious dogs surgically prepared with indwelling catheters in the portal vein (PV), femoral artery (FA), and femoral vein (FV). In addition, electromagnetic flow probes were placed about the PV and the hepatic artery (HA). Animals were subsequently subjected to either a 10% (7.5 ml/kg), 20% (15 ml/kg), or 30% (22.5 ml/kg) 3-min hemorrhage. The portal venous delivery rate (PVDR) of immunoreactive plasma glucagon (IRG), portal venous IRG concentration (PVIRG), and peripheral arterial IRG (AIRG) demonstrated variable changes following hemorrhage. When hemorrhage resulted in marked deterioration in PVBF, then PVDR did not correlate with either changes in PVIRG or AIRG. These preliminary results suggest that inferences regarding changes in PVDR of IRG cannot reliably be based solely on changes in hormonal concentrations, especially when measured only in the periphery. Moreover, since marked increases in peripheral plasma glucose levels were observed at times when PVDR of IRG was severely depressed following 20% and 30% hemorrhage it is suggested that glucagon may not play the dominant role in the early hyperglycemic response to hemorrhage.

Animals↗
PubMed1983

Role of solute in the early restitution of blood volume after hemorrhage.

We examined the putative roles of decreased capillary pressure and increased transcapillary osmolar gradient in mediation of the early restitution of blood volume after hemorrhage by comparing the degree of restitution of plasma volume and protein and comparing changes in capillary pressure and osmolality in awake dogs with those in dogs anesthetized with pentobarbital. Decreases in estimated capillary pressure and increases in plasma osmolality were greater in anesthetized than in awake dogs. However, early restitution of plasma volume and of protein was greater in awake animals. Analysis of the Starling forces indicated that interstitial hydrostatic pressure was greater in awake animals than in anesthetized animals, suggesting that interstitial volume increases more rapidly in awake animals. Selective venous sampling in anesthetized dogs indicated that the splanchnic and renal vascular beds release solute to the circulation following hemorrhage. However, rather than promoting the restitution of blood volume by production of a transcapillary osmolar gradient, the data suggest that the solute is delivered to the peripheral tissues, where it mediates the movement of water from cells to the interstitium more rapidly in awake than in anesthetized dogs. It thus appears that the early metabolic changes after hemorrhage, resulting in increased solute production, are important for the early restitution of blood volume and plasma protein.

Analysis of Variance↗
PubMed1982

Vasopressin-dependent and -independent control of the release of adrenocorticotropin.

We tested the possibility that vasopressin mediates the responses of adrenocorticotropin (ACTH) to electrical stimulation of various areas of the hypothalamus. Thirty-three cats were anesthetized with chloralose-urethane, immobilized with gallamine, and respired artificially. Plasma ACTH was measured by RIA. Intraventricular administration of antiserum to vasopressin blocked the release of ACTH induced by electrical stimulation of the paraventricular nucleus (PVN), suggesting a role for the vasopressinergic projection from PVN to the external zone of the median eminence. In contrast, the release of ACTH induced by stimulation of areas ventral to PVN was unaffected by the antiserum. Thus, there is at least one corticotropin releasing factor released from nuclei other than PVN that is distinct from vasopressin.

Adrenocorticotropic Hormone↗
PubMed1981

Impaired restitution of blood volume after large hemorrhage.

Previous studies have suggested that increases in extracellular osmolality mediate a shift of intracellular fluid into the interstitium following 10% hemorrhage. This unidirectional fluid movement is required for full restitution of blood volume (BV) and for cardiovascular stabilization. The extent to which this mechanisms acts in larger hemorrhages was examined in these studies. Forty-two dogs were studies 3 weeks after splenectomy. Twenty were anesthetized with pentobarbital, the others were studied awake. Hemorrhages of 10% (7.5 ml/kg, 15 dogs), 20% (15 ml/kg, 13 dogs), and 30% (22.5 ml/kg, 15 dogs) were carried out over 3 minutes. Patterns of changes in osmolality, total plasma protein content, and blood volume were identical in the two groups, although osmolality was significantly greater during the first 2 hours in anesthetized dogs. Osmolality increased with increasing degrees of hemorrhage, providing an increasing driving force for fluid shifts. Restitution of BV was significantly greater after 20% hemorrhage than after 10% hemorrhage. However, restitution of BV after 30% hemorrhage was no greater than after 10% hemorrhage. Patterns of protein restitution paralleled changes in BV. Cunningham, Shires, and Wagner (7) reported fluid shifts into cells after a 30% hemorrhage associated with a fall in membrane potential. It thus appears likely that a fluid shift out of cells in response to increased osmolality is offset by shifts into cells as the magnitude of hemorrhage becomes large. This failure of homeostatic restoration of BV with consequent failure of cardiovascular stabilization may represent an early event in the development of hemorrhagic shock.

Animals↗
PubMed1981

Control of release of adrenocorticotropin and vasopressin by the supraoptic and paraventricular nuclei.

To determine the relative roles of the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei in the control of the release of vasopressin and of ACTH, we have examined the hormonal responses to electrical stimulation (200 microA, 0.2 msec, 100 Hz, 20 sec) of these regions. Cats were anesthetized with chloralose-urethane. Blood samples were taken 30 sec before stimulation and 1.5 min poststimulation. ACTH and vasopressin were measured by RIA. Electrical stimulation of the caudal pole of the SON increased vasopressin in plasma (1.82 +/- 0.41 microU/ml, n = 17, P less than 0.01) and decreased ACTH (-26 +/- 4 pg/ml, n = 13, P less than 0.01). In contrast, stimulation of the PVN increased vasopressin (2.01 +/- 0.60 microU/ml, n = 7, P less than 0.001) and increased ACTH (107 +/- 20 pg/ml, n = 32, P less than 0.01). Previous work has shown that vasopressinergic neurons of PVN, but not of SON, project to the zona externa of the median eminence. Other have suggested that the retrograde flow of blood from the neural lobe to the median eminence and thence to the anterior lobe would allow vasopressin to influence the release of ACTH. The present results indicate that both SON and PVN facilitate the release of vasopressin. However, PVN facilitates, but SON inhibits the release of ACTH. These findings suggest that the projection from PVN to the zona externa of the median eminence mediates the release of ACTH and that retrograde flow from the neural lobe is not important in the control of ACTH release during modest and transient increases in the release of vasopressin.

Adrenocorticotropic Hormone↗
PubMed1981

Dissection of the aorta.

Recent experience indicates that the treatment of acute aortic dissection is satisfactory in about 75 percent of cases. Most centers have moved to early operations for those dissections involving the ascending aorta and a combination of anti-impulse therapy and expectant operative treatment for those dissections involving only the descending aorta. Physicians seeing acute circulatory problems should be aware of catastrophic nature of aortic dissection and of the available methods for its diagnosis and treatment.

Aortic Dissection↗
PubMed1980

Organization of the lateral hypothalamus for control of adrenocorticotropin release in the cat.

Regions in the ventral midbrain that project to the lateral hypothalamus have been implicated in the control of ACTH release. To define further those areas in the lateral hypothalamus through which afferent signals might pass, we electrically stimulated 188 sites in the lateral hypothalamus of 20 cats anesthetized with chloralose-urethane. Stimulations were monophasic pulses of DC (200 microA; 0.2 msec; 100 Hz; 20 sec). Venous samples were drawn over 30 sec 0.5 min before and 1.5 min after stimulation. Equal volumes of warmed isoncotic dextran were infused during sampling to prevent hypovolemia. ACTH was assayed by RIA. Areas were defined in which stimulation led to increased, decreased,, or unchanged ACTH. Mean changes in ACTH were tested by analysis of variance. The present data indicate that the ACTH-active areas defined previously in the midbrain may join the medial forebrain bundle in the subthalamic area and nucleus to traverse the lateral hypothalamus. At the level of the mammillary bodies, a facilitatory area occupied the ventral portion of the medial forebrain bundle. This area extended rostrally and medially to join the medial aspect of the medial forebrain bundle. Continuity with the mediobasal hypothalamus was seen only anteriorly in the area of the supraoptic decussations. An inhibitory area occupied the dorsal extent of the medial forebrain bundle at the level of the mammillary bodies. It extended rostrally and laterally around the caudal pole of the supraoptic nucleus and then medially at the level of the optic chiasm. There appear to be no other medial projections of the lateral lying ACTH-active areas to the mediobasal hypothalamus. The lateral hypothalamus may serve as a site of passage and/or of processing of information that ascends from the midbrain and descends from the limbic system.

Adrenocorticotropic Hormone↗