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Biomedical subjects

F C Martin

Publications and source records attributed to F C Martin.

32 records · Page 2Linked to original sources
PubMed1989

Suppression of natural killer cell activity by high-dose narcotic anesthesia in rats.

Suppression of natural killer (NK) cell activity in the postoperative period has been reported in several clinical studies. Endogenous opioids and cerebral injection of morphine have been shown to suppress NK cell activity. Since high-dose opiates are commonly used in anesthetic practice, we sought to determine the effects of three narcotic agents on NK cell activity. Male rats were injected subcutaneously with morphine (30 mg/kg), fentanyl (0.3 mg/kg), or sufentanil (0.06 mg/kg). Three, 12, or 24 h later the cytotoxic activity of splenic NK cells was measured in a 4-h chromium-51 release assay using radiolabeled target cells. All three drugs significantly suppressed NK cytotoxicity at 3 h after administration; this effect was blocked by an opiate antagonist, naltrexone. Fentanyl and sufentanil also caused a significant suppression 12 h after drug administration. By 24 h NK activity of all groups returned to normal values. Interferon is known to augment NK cell activity. Therefore, in another experiment rats were given an interferon inducer, polyinosinic:polycytidylic acid (poly I:C), to determine if it would alter the effects of these narcotics on splenic NK activity. Poly I:C treatment increased NK cytotoxicity to above baseline; fentanyl in these animals reduced NK activity and brought it back to control levels. These findings suggest that clinically used high-dose narcotic anesthesia can suppress NK cytotoxic activity and that pretreatment with interferon can attenuate this suppression.

Anesthesia↗
PubMed1987

Effects of a single administration of morphine or footshock stress on natural killer cell cytotoxicity.

We previously reported that daily exposure for 4 days to an inescapable form of footshock stress, known to cause opioid-mediated analgesia, suppressed the cytotoxic activity of splenic natural killer (NK) cells in rats. Similarly, daily injection of high doses of morphine (greater than or equal to 30 mg/kg) for 4 days also suppressed splenic NK cell activity. We now report that a single exposure to the opioid form of footshock stress or a single high dose of morphine induces suppression of splenic NK cell cytotoxicity. This effect is evident 3 h after treatment, returning to normal by 24 h. Morphine-induced NK suppression is evident in both male and female rats, is blocked by the opiate antagonist naltrexone, and develops tolerance. Morphine-induced NK suppression is seen in cells derived simultaneously from the spleen, bone marrow, and peripheral blood, suggesting that this suppression does not result from a selective egress of NK cells from the spleen.

Animals↗
PubMed1986

Involvement of brain opiate receptors in the immune-suppressive effect of morphine.

We previously reported that a single systemic injection of a high dose of morphine (greater than or equal to 20 mg/kg) transiently suppresses splenic natural killer cell cytotoxicity in rats. The present study examined the possibility that the immune-suppressive effect of morphine is mediated by opiate receptors in the brain. Supporting this hypothesis, we found that morphine (20 or 40 micrograms) injected into the lateral ventricle suppressed natural killer cell activity to the same degree as a systemic dose higher by three orders of magnitude. This effect was blocked by an opiate antagonist, naltrexone. Natural killer cell activity was unaffected by systemic administration of N-methyl morphine, a morphine analogue that does not cross the blood-brain barrier. These data implicate opiate receptors in the brain in morphine-induced suppression of natural killer cell cytotoxicity.

Animals↗
PubMed1985

Assessment in vitro and in vivo of muscle degradation in chronic skeletal muscle myopathy of alcoholism.

1. Muscle protein breakdown in vivo has been studied by measurements of urinary 3-methyl-histidine/creatinine ratios. No differences were found between control subjects and chronic alcoholics either with or without proximal muscle wasting or cirrhosis. 2. Calculation of muscle turnover rates, with the correction of Afting et al. (1981, Biochemical Journal, 200, 449-452) for non-skeletal muscle contributions of 3-methylhistidine and creatinine, showed lower values for alcoholics compared with controls. 3. Tissue activities of a neutral protease, assayed by a novel, rapid and sensitive fluorimetric method, were similar in patients and controls. The activity did not vary with severity of atrophy or the presence of cirrhosis. 4. No evidence was therefore obtained to suggest that alcoholic myopathy is due to increased muscle breakdown.

Adult↗
PubMed1985

Stress, opioid peptides, the immune system, and cancer.

Our results indicate that a particular form of footshock stress can suppress immune function in rats and decrease their resistance to tumor challenge. These effects appear to be mediated by opioid peptides released by stress, and they can be mimicked by high doses of morphine given systemically or by a vastly smaller dose delivered intracerebroventricularly. Such findings fit well into the emerging field of behavioral neuroimmunology and reinforce continuing efforts to elucidate the neural and neurohumoral mechanisms by which the environment can affect the organism's immune system.

Animals↗
PubMed1984

Glycogen content and activities of key glycolytic enzymes in muscle biopsies from control subjects and patients with chronic alcoholic skeletal myopathy.

The capacity for glycolysis in muscle biopsies obtained from long-term heavy alcohol drinking patients has been compared with tissue from control subjects by assay in vitro of the total activities of glycogen phosphorylase, phosphofructokinase and fructose 1,6-bisphosphatase, key regulatory enzymes in the anaerobic glycolytic pathway. Biopsies from 13 of 22 patients had type II fibre atrophy, and the activities of all three enzymes were reduced in these biopsies, when expressed in terms of DNA content, the most striking reduction being in phosphofructokinase activity. The amount of glycogen in the tissue correlated closely with these enzyme activities and was slightly lower in the most atrophic tissue, when expressed in terms of DNA content. The activities of acid and neutral alpha-glucosidases were similar in biopsies from control subjects and patients with various severities of alcohol myopathy. The reduced activities are consistent with a reduced proportion of type II fibre muscle mass in these patients, and suggest that there may be a reduced capacity for glycolysis with resultant reduced lactate production. Whether the changes in enzyme activities are primary to the selective atrophy remains to be established.

Adult↗
PubMed1984

Investigation of the organelle pathology of skeletal muscle in chronic alcoholism.

The muscle abnormalities associated with chronic alcohol consumption were studied by applying histological and biochemical techniques to tissue obtained by percutaneous needle biopsy from the quadriceps muscles of 41 patients. Measurement of the fibre size showed atrophy of both type I (p less than 0.05) and type II (p less than 0.001) fibres. The degree of atrophy was more severe for type II fibres (33% reduction in median diameter) than type I (17%). Marker enzyme activities for the principal organelles were assayed. Compared with biopsy specimens from non-alcoholic controls, no differences were found in the activities of lysosomal, mitochondrial, peroxisomal, cytosolic, sarcolemmal, or sarcoplasmic reticulum enzymes, expressed per microgram DNA. A reduction in the protein to DNA ratio was evident in severely atrophic biopsies, and this was associated with a significant reduction of myofibrillary Ca2+-ATPase activity. These results suggest a selective loss of type II fibre myofibrillary protein and do not confirm earlier suggestions of specific mitochondrial damage.

Adult↗
PubMed1983

Analytical subcellular fractionation of normal human skeletal muscle by sucrose density gradient centrifugation.

The principle organelle marker enzymes and various adenosine triphosphatase (ATPase) activities were studied in human skeletal muscle. The reproducibility of each assay was established under optimal and linear assay conditions. Whole homogenates of normal human quadriceps muscle were fractionated by centrifugation on a continuous sucrose density gradient. Gradient fractions were assayed for organelle marker enzymes and frequency-density histograms were constructed for each enzyme. Good resolution of the principal organelles was obtained. Adenosine triphosphatase (ATPase) was assayed under conditions of maximal stimulation by Ca2+, or Mg2+ or Na2+, K+ + Mg2+. The distribution of these activities was compared with those of the organelle marker enzymes. Both Ca2+-ATPase and Mg2+-ATPase were distributed to both the mitochondrial and myofibrillar fractions but could be distinguished by the inhibition of mitochondrial ATPase with sodium azide. The distribution of Na+, K+-activated, Mg2+-dependent ATPase (Na+, K+ ATPase) activity suggested a sarcolemmal localization. The results of electron microscopy of gradient fractions were consistent with the organelle content of the fractions as determined by enzymic analyses. These studies provide reference information for the subsequent investigation of organelle pathology of human muscle disorders.

5'-Nucleotidase↗
PubMedDate not supplied

Simulating the effects of climatic variation on stem carbon accumulation of a ponderosa pine stand: comparison with annual growth increment data.

Simulation models of ecosystem processes may be necessary to separate the long-term effects of climate change on forest productivity from the effects of year-to-year variations in climate. The objective of this study was to compare simulated annual stem growth with measured annual stem growth from 1930 to 1982 for a uniform stand of ponderosa pine (Pinus ponderosa Dougl.) in Montana, USA. The model, FOREST-BGC, was used to simulate growth assuming leaf area index (LAI) was either constant or increasing. The measured stem annual growth increased exponentially over time; the differences between the simulated and measured stem carbon accumulations were not large. Growth trends were removed from both the measured and simulated annual increments of stem carbon to enhance the year-to-year variations in growth resulting from climate. The detrended increments from the increasing LAI simulation fit the detrended increments of the stand data over time with an R(2) of 0.47; the R(2) increased to 0.65 when the previous year's simulated detrended increment was included with the current year's simulated increment to account for autocorrelation. Stepwise multiple linear regression of the detrended increments of the stand data versus monthly meteorological variables had an R(2) of 0.37, and the R(2) increased to 0.47 when the previous year's meteorological data were included to account for autocorrelation. Thus, FOREST-BGC was more sensitive to the effects of year-to-year climate variation on annual stem growth than were multiple linear regression models.

Journal Article↗