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Biomedical subjects

D O McCarthy

Publications and source records attributed to D O McCarthy.

At least 37 records · Page 2Linked to original sources
PubMed1995

Body energy status and the metabolic response to acute inflammation.

An animal model of acute inflammation was used to examine how body energy status influences the syndrome of anorexia, negative nitrogen balance, and body weight loss typically seen in response to injury. Specifically, the metabolic response to acute inflammation was studied in rats of normal, elevated, or reduced body weights. Rats induced to overeat and gain weight prior to inflammation displayed protracted anorexia, greater subsequent weight loss, higher metabolic rates, and greater negative energy balance than rats of normal weight. Conversely, rats with reduced body weights displayed elevated food intakes, body weight gain, attenuated nitrogen loss, and normal rates of energy expenditure. Prior weight reduction did not affect postinflammation fever or levels of fibrinogen, iron, and interleukin-6-like activity, suggesting that the ability to mount an acute phase response was not impaired in weight-reduced rats. These results suggest that the usual postinflammation adjustments in body energy flux and body nitrogen are regulated components of a metabolic response to acute inflammation which renders normally protected sources of endogenous energy and substrate available for repair and recovery.

Acute Disease↗
PubMed1994

The effect of psychological stress on neutrophil superoxide release.

Stress has long been suggested to exacerbate symptom expression in people with chronic inflammatory disorders. The release of oxidative metabolites from activated PMN plays a significant role in the pathophysiology of inflammation. Thus, we examined the effects of psychological stress on release of superoxide anions from PMN of rats with or without an inflammation induced by injection of shellfish glycogen (SFG). Psychological stress was found to significantly increase PMN superoxide release in both healthy and SFG-injected animals. Total amounts of superoxide release were similar between the two groups, suggesting that PMN from animals with a mild inflammatory condition were not more susceptible to the effects of stress than PMN from healthy animals. However, this study should be repeated using an animal model of chronic inflammation, such as airway hyperactivity or rheumatoid arthritis.

Analysis of Variance↗
PubMed1994

Measurement of symptoms of interstitial cystitis. A pilot study.

The existence of a reliable and valid measure of interstitial cystitis symptoms would assist with diagnosis and the evaluation of treatment effectiveness. The purpose of this article is to report development of a scale to measure symptoms of interstitial cystitis. Data concerning the evidence of content and construct validity, as well as reliability, is provided. The findings suggest that this scale accurately measures the symptoms of interstitial cystitis.

Cystitis↗
PubMed1993

The effects of cyclooxygenase inhibitors on tumor-induced anorexia in rats.

BACKGROUND: Interleukin-1 (IL-1) and tumor necrosis factor (TNF) are potent induces of prostaglandin (PG) synthesis and injection of PGE, IL-1, or TNF decreases food intake in healthy animals, whereas the anorexigenic effects of injected IL-1 and TNF are blocked by inhibitors of PG synthesis. It has been hypothesized that host secretion of IL-1 and TNF contribute to tumor-induced anorexia. This study was undertaken to determine whether administration of PG inhibitors alters food intake in anorectic rats implanted with Walker 256 carcinoma. METHODS: Groups of six tumor-bearing rats were implanted with slow-release pellets containing ibuprofen, indomethacin, or acetylsalicylic acid. Food intake, tumor growth, and body temperature were monitored for 14 days and compared with control tumor-bearing animals implanted with placebo pellets. RESULTS: Tumor growth was associated with anorexia, fever, weight loss, and increased leukocyte secretion of IL-1 and TNF. Indomethacin and ibuprofen retarded tumor growth 30-40% and lowered body temperature compared with controls, but had no effect on food intake or body weight of tumor-bearing animals. CONCLUSIONS: Prostaglandins do not mediate tumor-induced anorexia.

Animals↗
PubMed1993

The role of cholecystokinin in interleukin-1-induced anorexia.

Anorexia is a common response to infection which is thought to be mediated, at least in part, by interleukin (IL-1), an immunoregulatory peptide secreted by activated monocytes. Cholecystokinin (CCK) is a neuropeptide that suppresses food intake and gastric emptying when injected into healthy animals. There is increasing evidence of bidirectional interactions between neuropeptides, immune cell function, and secretion of immunoregulatory cytokines. Therefore, the present study was undertaken to determine if administration of L364,718 (L364), a CCK receptor antagonist, might block the anorexigenic effects of recombinant human IL-1 alpha (IL-1 alpha) in rats. We report that injection of IL-1 alpha significantly increased plasma CCK 1 h after injection, and decreased food intake and emptying of gastric contents. Pretreatment with 1 mg/kg L364 partially blocked the decrease in food intake and gastric stasis induced by IL-1 alpha. We conclude CCK may mediate, at least in part, IL-1 alpha-induced anorexia.

Animals↗
PubMed1992

The role of gastric stasis in tumor-induced anorexia in rats.

BACKGROUND: The current study was undertaken to determine if changes in gastric emptying contribute to tumor-induced anorexia. METHODS: Rats were implanted with the Walker 256 carcinoma, and food intake was measured daily. On days 0, 8, and 15, the rats were fasted overnight, gavage fed a bolus of liquid food, and residual gastric contents were measured 3 hours later. RESULTS: Tumor growth was associated with a progressive decline in voluntary food intake. When the rats were gavage fed 2.5 or 7 ml of liquid food, the percent of gastric contents cleared in 3 hours was unchanged with tumor growth. CONCLUSIONS: Changes in gastric emptying did not contribute to decreased food intake with growth of the Walker 256 in rats.

Animals↗
PubMed1992

The effects of noise stress on leukocyte function in rats.

It has been reported that exposure to increased noise levels impairs wound healing in surgical patients and in rats. The purpose of the present study was to determine if exposure to noise stress would alter the biological function of neutrophils, macrophages, and lymphocytes, leukocytes that are involved in wound healing. Rats were exposed to 80 db of "rock" music for 24 hr, during which time the control animals were maintained in their usual environment. Leukocyte subpopulations were obtained and stimulated in vitro. Neutrophils and macrophages from noise-exposed animals secreted significantly less superoxide anion and interleukin-1 than cells from control animals. Lymphocyte function was not altered following noise stress. We conclude that short-term exposure of rats to noise stress alters some of the biological functions of leukocytes.

Animals↗
PubMed1992

The effect of diet consistency on food intake of anorectic tumor-bearing rats.

Delayed gastric emptying has been shown to occur in cancer patients complaining of anorexia and early satiety. Given that liquids are emptied from the stomach faster than solid food, the present study was undertaken to determine if diet consistency would affect food intake of hypophagic rats implanted with the Walker 256 carcinosarcoma. By Day 15 of tumor-growth, caloric intake of tumor-bearing animals was 20% less than controls. The caloric intake of tumor-bearing animals fed a liquid diet was not significantly different from animals fed a solid diet. Furthermore, a delay in gastric emptying was not seen in this animal model of tumor-induced anorexia.

Animals↗
PubMed1992

The role of prostaglandins in interleukin-1 induced gastroparesis.

Interleukin-1 is a small molecular weight peptide that is thought to mediate much of the acute phase response to infection, including fever and anorexia and gastric stasis. In the present study, we examined the effects of recombinant human IL-1 alpha (rhIL-1a) on food intake and gastric emptying, and the role of prostaglandins (PG) in IL-1 induced gastroparesis. We report that pretreatment with ibuprofen significantly improved food intake and gastric emptying in IL-1 injected rats, but did not return them to control levels. We conclude that PGs mediate, at least in part, IL-1 induced gastroparesis. The role of gastroparesis in IL-1 induced anorexia remains to be determined.

Animals↗
PubMed1991

Interleukin-1-inhibitor activity induced by respiratory syncytial virus: abrogation of virus-specific and alternate human lymphocyte proliferative responses.

Respiratory syncytial virus (RSV) infection has been shown to induce human mononuclear leukocyte (MNL) production of net interleukin-1 (IL-1)-inhibitor activity. In the current studies of IL-1-inhibitor effects, RSV-exposed cells were compared with autologous MNL that were sham-exposed or exposed to inactivated RSV or influenza virus (which induces net IL-1 activity and commonly elicits effective homotypic immunity). Exposure of MNL to influenza virus or inactivated RSV resulted in increased expression of human leukocyte antigen-DR, the IL-2 receptor, and the transferrin receptor and increased progression through the cell cycle by 3 days. In contrast, exposure to infectious RSV resulted in decreased marker expression and cell cycle arrest, with abrogation of proliferation in response to the virus or other stimuli. These data raise the possibility that a contributing mechanism for recurrence of RSV infection is early suppression of the clonal expansion of virus-specific lymphocytes due to net IL-1-inhibitor activity.

Cell Cycle↗
PubMed1989

Interleukin-1 inhibitor production by human mononuclear leukocytes and leukocyte subpopulations exposed to respiratory syncytial virus: analysis and comparison with the response to influenza virus.

Net interleukin-1 (IL-1) inhibitor activity is induced by exposure of purified human monocytes-macrophages to respiratory syncytial virus (RSV). Furthermore, IL-1 inhibitor activity was produced by monocytes-macrophages exposed to RSV in the presence of lymphocytes, that is, by unseparated mononuclear leukocytes (MNL). Purified RSV-exposed lymphocytes, as well as the lymphocytes exposed within MNL preparations, produced net IL-1 inhibitor activity. In contrast, net IL-1 activity was produced when purified monocytes-macrophages or unseparated MNL were exposed to influenza virus. The RSV-induced IL-1 inhibitors demonstrated antiproliferative effects on mitogen-stimulated human lymphocytes as well as on the mouse thymocytes used in standard assays. The results raise the possibility that such antiproliferative activity is mediated, at least in part, by monocytes-macrophages. The data also suggest that IL-1 inhibitors produced by MNL after exposure to RSV may contribute along with other factors to the recurrence of RSV infection in immune individuals.

Humans↗
PubMed1986

Effect of centrally administered interleukin-1 and endotoxin on food intake of fasted rats.

We have previously shown that interleukin-1 (IL-1), a polypeptide known to mediate many aspects of the acute phase response to infection, suppresses food intake when injected intraperitoneally into fasted rats. IL-1 acts at the level of the hypothalamus to induce fever. In view of the large number of peptides that have been shown to alter food intake as well as body temperature when injected intracerebroventricularly (ICV), we hypothesized that the receptor site for the anorexigenic activity of IL-1 would be located in a central nervous site bathed by the cerebrospinal fluid. In the present study, ICV injection of IL-1 or E. coli endotoxin (a stimulus for the synthesis of IL-1), significantly elevated body temperature, but did not affect food intake of fasted rats. We conclude that receptors mediating the anorexigenic actions of IL-1 or endotoxin are not located at a central nervous site bathed by the cerebrospinal fluid. Furthermore, fever per se is not responsible for the reduction in food intake seen following peripheral injection of IL-1 or endotoxin.

Animals↗
PubMed1985

Suppression of food intake during infection: is interleukin-1 involved?

Loss of food appetite is a common manifestation of acute infectious illness and is believed to contribute to the negative nitrogen balance and loss of body weight that is seen during infection. The frequency with which anorexia occurs with infection suggests that it may be part of the acute phase response. In the present experiments, food intake of fasted rats was suppressed following injection of interleukin-1, a polypeptide that mediates many host responses to infection. We conclude that infection-induced anorexia is, in part, due to the release of interleukin-1.

Animals↗
PubMed1984

The role of fever in appetite suppression after endotoxin administration.

In order to test the hypothesis that fever, and not some other aspect of the acute phase response, decreases food intake after administration of endotoxin, food intake of rats was studied under conditions of 1) fever, 2) antipyresis, and 3) endotoxin tolerance. Injection of endotoxin resulted in a significant elevation in rectal temperature and a significant reduction in food intake. Administration of the antipyretic drug sodium salicylate to endotoxin-injected animals lowered rectal temperatures to control levels, but food intake was still suppressed. When rats were made tolerant to endotoxin by repeated injections, an attenuated fever was observed, and food intake was not significantly different from that of control animals. We conclude that the effects of endotoxin on body temperature can be dissociated from its effects on food intake. We speculate that the failure of endotoxin to suppress food intake in endotoxin-tolerant rats may be due to a decreased production of endogenous pyrogen.

Animals↗
PubMed1978

The plasma clearance of fructose and glucose during and after surgical operation.

Fasting blood glucose is elevated and the rate of disappearance of a glucose load is reduced after major surgery. Resistance to insulin is considered to play a part in post-traumatic glucose intolerance. Fructose metabolism is partly independent of insulin. Glucose and fructose clearance were compared in two groups of 6 matched male patients with normal glucose tolerance who were studied before and after major vascular surgical operations of the same severity. Fructose or glucose (25 g) was given intravenously over a 2-min period before, during and at intervals for 8 days after surgery. The rate of clearance of fructose increased significantly during operation (P less than 0.01), but returned to the preoperative level by the first postoperative day. Glucose clearance, in contrast, was reduced during and throughout the 8 days of the study. The fructose load produced a brisk insulin response before operation which was diminished and delayed during surgery. These findings suggest that administered fructose may be removed more rapidly than glucose during and immediately after surgical operation.

Aged↗
PubMedDate not supplied

Immune responses to final exams in healthy and asthmatic adolescents.

Immune responses to an academic stressor were examined in healthy and asthmatic adolescents with regard to their illness symptom reports. Eighty-seven high school students completed a health diary for 2 weeks and provided three blood samples during midsemester, final-exam, and postexam periods. During exam week, all students showed significant immunological alterations from baseline. Natural killer cell activity was significantly lower, whereas lymphocyte proliferation and neutrophil superoxide release were significantly higher. These immune changes tended to return toward baseline during the postexam period, but the enhanced neutrophil reactivity continued to rise. Overall, immunological responses were similar between asthmatic subjects and controls. Appropriate medical management may have accounted for this similarity. However, subtle group differences in the postexam recovery pattern and a continuous activation of inflammatory cell function following a stressor may warrant further investigation.

Adolescent↗