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Biomedical subjects

D E Carlson

Publications and source records attributed to D E Carlson.

At least 91 records · Page 5Linked to original sources
PubMed1978

Effects of negative pi mesons on immune responses in mice.

Spleen cells from normal or preimmunized mice were exposed to graded doses of peak pions or 300-kVp x rays in vitro and then cultured in heavily irradiated mice to determine antibody production against sheep erythrocytes. The RBE for the primary antibody response was 1.46. Equal suppression of secondary responses was seen with both pions and x rays. When spleen cells were irradiated 1, 3, or 5 days after antigen injection, developing immune responses became less sensitive to pions than to x rays. Because T-cell activity (needed for the antibody response) is also implicated in tumor immunity, antitumor immune responses might not be more sensitive to pions than the response used; also, pions might not impair ongoing autochthonous immune responses more than conventional radiation modalities do.

Animals↗
PubMed1978

Humoral and mechanical factors modulating neural input to the renal vasculature.

The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model was only able to account for the experimental findings after the blockade of prostaglandin synthesis, and this blockade significantly increased the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.

Angiotensin II↗
PubMed1978

Organization of the medial hypothalamus for control of adrenocorticotropin in the cat.

To examine the role and interrelations of areas of the medial hypothalamus in the control of release of ACTH, we stimulated electrically (20-sec train, 200-microamperemeter amplitude at 100 Hz) 695 sites in the hypothalamus of 91 cats anesthetized with chloralose-urethane. Changes in ACTH were measured by RIA. Responses of arterial pressure could not account for changes of release of ACTH. Several ACTH-active areas were defined. The anatomical relations of these areas with known nuclei and pathways then were considered. Two ACTH facilitatory areas and one ACTH inhibitory area were identified in the lateral aspect of the medial hypothalamus. The dorsal facilitatory area appears to be an extension of the lateral division of the dorsolongitudinal fasciculus and to extend medially to join the Fields of Forel, the ventral tegmental area of Tsai, and the parvocellular, paraventricular, and periventricular nuclei. The ACTH inhibitory area appears to be an extension of portions of the central tegmental tract and to extend medially to the posterior hypothalamic area and the dorsal hypothalamic area and ventrally toward the basal hypothalamus. The ventral ACTH facilitatory area appears to be coincident with the medial forebrain bundle and to extend anteroventrally and medially through the supraoptic decussation to the suprachiasmatic, ventromedial, dorsomedial, periventricular, infundibular, and premammillary nuclei. Stimulation of the median eminence led to increased release of ACTH. The results suggest that ascending pathways from the lower brainstem mediating control of ACTH project to discrete areas of the hypothalamus and then converge on the medial basal hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1978

Therapy of the murine plasmacytoma MOPC 104E: role of the immune response.

The murine plasmacytoma MOPC 104E was susceptible to cytotoxic therapy in female inbred BALB/c mice. Palpable subcutaneous tumors (0.6--1.2 X 10(8) cells) could be cured with a single administration of cyclophosphamide (5--250 mg/kg) or localized irradiation (800--2,400 R). Clonogenic assay showed that, following minimal curative doses of cyclophosphamide or radiation, 0.5--1.5 X 10(6) tumor cells should remain viable. Control animals succumbed to progressive, invariably lethal tumor growth after they were given sc injections of 2--3 X 10(3) tumor cells. Minimal doses of cyclophosphamide, which were curative in control tumor-bearing animals, were ineffective in treating tumor-bearing animals immunosuppressed by 450 R whole-body irradiation. Subsequent experiments measured the ability of animals cured of the murine plasmacytoma to reject secondary challenge with the same tumor. These experiments demonstrated and partially quantitated the substantial role of the immune response in effecting tumor cure following radiotherapy or chemotherapy.

Animals↗
PubMed1978

Immunity against MOPC 104E plasmacytoma: effects of tumor size and time post therapy on in vivo tumor immunity.

BALB/c mice with the plasmacytoma MOPC 104E were cured of palpable tumors (6-15x10(7) cells) with a single injection of cyclophosphamide (10 mg/kg). Animals cured of tumor showed a considerable increase in their ability to reject secondary challenge with graded numbers of viable tumor cells. Mice with palpable subcutaneous tumors were cured therapeutically and rechallenged 22, 44, or 120 days post therapy. The ability of such animals to reject secondary tumor cell challenge was similar in all groups, which implied that in vivo tumor immunity remained relatively constant for at least 4 months post therapy. A second group of animals was treated therapeutically (10 mg cyclophosphamide/kg) 4, 11, or 20 days post tumor cell injection. These therapeutically treated animals were then rechallenged with various numbers of viable tumor cells 30 days post therapy. Mice given cyclophosphamide 4, 11, or 20 days post tumor injection rejected 6, 60, or 400 times as many tumor cells, respectively, as did control animals. These results implied that, over the range of tumor sizes investigated, exposure to greater amounts of tumor antigen resulted in increasing amounts of residual tumor immunity following cure.

Animals↗
PubMed1977

Neural control of ACTH release in response to hemorrhage.

A three dimensional reconstruction of the central neural pathways that appear to mediate release of ACTH in response to hemodynamic change is illustrated in Figure 11. Fibers from receptors in the right atrium and the carotid arteries project to the lateral solitary nucleus and then to the medial and the lateral nucleus intercalatus. A pathway containing projections from these nuclei then converges dominantly in the locus subcoeruleus and locus coeruleus. Multiple pathways then diverge, to travel in part directly to the hypothalamus through dorsal pathways. One pathway inhibits and another facilitates the release of ACTH. Multiple pathways also diverge, to travel in part medially, and then to the hypothalamus through ventral pathways. Again, one pathway inhibits and another facilitates the release of ACTH. The dorsal and ventral inhibitory pathways appear to converge in a region extending from just caudal and ventral to the paraventicular nucleus to the posterior hypothalamic area. Thus, after the coalescences of the various pontine-hypothalamic pathways, three principal pathways remain. These include a posterior inhibitor path, an anterodorsal facilitatory path that terminates in the paraventricular nucleus and that may be mediated through release of vasopressin, and an anteroventral facilitatory path that terminates in the suprachiasmatic and ventromedial nuclei and that is probably mediated through release of corticotropin-releasing hormone. The mode of integration of these pathways has not been defined. The pathways described herein are oligosynaptic: a signal may travel from atrium to hypothalamus over three to seven neurons. The combination of control of input hemodynamic signals and of measurement of ACTH permits quantitation of both sensory and motor events, that inevitably must be embedded in the neuronal pathways described here. The analysis of the input-output relations and their correlation with internal neural events must form the basis of a description of the physiology of the physiology of the system whose central neural anatomy has been defined in part by these studies.

Adrenocorticotropic Hormone↗
PubMed1977

Specific muscle protein-sparing postoperative dextrose-free amino acid infusions.

The protein-sparing and ketogenic effect of postoperative infusion of maintenance solutions containing either 3.5% amino acids or 5% dextrose in 0.33 normal (N) saline was compared by nitrogen balance and urinary acetone determination in 31 patients. A specific muscle protein sparing effect was determined by quantitation of excretion of 3-methylhistidine in seven patients of the amino acid group and eight patients in the dextrose group. In addition, an extensive hormone and substrate profile was determined. It was found that amino acid infusions not only produce a less negative nitrogen balance but also significantly reduce excretion of 3-methylhistidine indicating specific preservation of the muscle compartment.

Amino Acids↗
PubMed1976

Relative biological effectiveness of negative pi mesons for the immune response in mice.

Immunologically competent mouse spleen cells were exposed to negative pi mesons in the entrance plateau or at the peak of the dose distribution at a maximum dosage of 5 rads/min. or to 60Co gamma rays at 4.96 rads/min. Survival curves from cells irradiated in vitro but incubated in vivo yielded RBE values of 2.15 for the peak and 1.84 for the entrance plateau at a surviving fraction of 0.1. The dose-rate dependence of antibody-forming spleen cells for both 60Co gamma rays and the lot-LET components of the pion beam is discussed. The authors suggest that these RBE values constitute an upper limit for normal mammalian cells exposed to pions and tha the RBE with clinically useful dose rates may be significantly lower than those reported here.

Animals↗
PubMed1976

Effects of negative pi mesons on mouse bone marrow cells.

Mouse bone marrow cells exposed in vitro to graded doses of negative pi mesons at 3.5-6.0 rads/min. gave Do values of 160 rads in the plateau (0.6 and 12.0 cm), and 130 rads in the peak (16.5 and 18.4 cm). Survival curve shoulders were narrow, with Dq values of 25 and 15 rads for plateau and peak positions. Gamma rays from 60Co at 4.5 rads/min. produced a curve with wider shoulder but steeper slope such that the RBE was essentially 1 for single doses between 100-400 rads.

Animals↗
PubMed1975

Inhibition of renal vasoconstriction by elevated ureteral pressure.

These experiments were prompted by the observation that elevated ureteral pressure inhibited renal vasoconstrictions elicited by electrical stimulation of "defense regions" of the central nervous system (DNS) in cats. Experiments were designed to detect the relative contributions to this inhibition of CNS reflexes and interactions between autoregulatory and neural controls of the renal circulation. Cats were anesthetized with either chloralose or pentobarbital. Renal blood flow was measured electromagnetically. Elevated ureteral pressure lowered prestimulus renal vascular resistance. Renal vasoconstrictions elicited by electrical stimulation of the CNS or the peripheral renal nerves and by infusion of catecholamines into the renal artery were equally inhibited by elevated ureteral pressure. Equal inhibition of CNS and renal nerve-evoked vasoconstrictions suggested that a reflex was not involved. Equal inhibition of vasoconstrictions elicited by renal nerve stimulation and by catecholamine infusions suggested that elevated ureteral pressure acted primarily at a postsynaptic site. Inhibition of prostaglandin synthesis by indomethacin diminished, but did not abolish, the ureteral pressure-induced inhibition of neurogenic vasoconstrictions.

Animals↗