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Levels of nicotinamide adenine dinucleotide in extracellular body fluids of pigs may be growth-limiting for Actinobacillus pleuropneumoniae and Haemophilus parasuis.

During infection, nutrient deprivation can alter bacterial phenotype. This, in turn, may have implications for pathogenesis and prophylaxis. Actinobacillus pleuropneumoniae (biotype 1) and Haemophilus parasuis, respiratory tract pathogens of swine, are both V-factor-dependent. The concentrations of V factor in the extracellular fluids of pigs are unknown and may limit the growth of these bacteria in vivo. The aim of this study was to determine the concentrations of nicotinamide adenine dinucleotide (NAD) in select porcine body fluids and to compare the availability of NAD in vivo with the affinities of the organisms for this compound. Levels in plasma, tissue fluids (peritoneal, pleural, synovial, and cerebrospinal), and laryngeal, tracheal, and lung washings were determined with an enzymatic cycling assay. We concluded that, although the NAD supply in the respiratory tract is probably not growth-limiting, it may become limiting if the organisms are disseminated.

Actinobacillus Infections↗

Investigation of intake-output as a means of assessing body fluid balance.

This study has demonstrated a mean error in I-O figures of 799.50 cc per day when compared with daily weight calculations. There was no statistically significant correlation between the two values. It is suggested that a change be made in nursing practice. If recording of intake-output is to continue as a nursing practice, then it must be coupled with daily weighings and used only in cases where intake must be limited and/or output carefully monitored. Then the two figures, weight loss and gain and fluid balance, loss or gain, must be compared and causes sought for any variances greater than +/- 250 cc.

Adult↗

Ultrasensitive determination of phencyclidine in body fluids by surface ionization organic mass spectrometry.

Gas chromatography (GC)/surface ionization organic mass spectrometry (SIOMS) has been found to give much higher sensitivity for measurements of phencyclidine (PCP) than the conventional GC/electron impact (EI)-mass spectrometry (MS). Thus, we have established a detailed procedure for measurements of PCP in body fluids by both mass chromatography and selected-ion monitoring (SIM) of SIOMS using pethidine as an internal standard (IS). Good linearity was found in the range of 0.25-10 ng/mL of whole blood or urine, when measured by mass chromatography, and in the range of 0.025-1.0 ng/mL of whole blood by SIM. The recoveries of PCP and IS spiked to whole blood were 106 +/- 17% at 1 ng/mL and 113 +/- 11% at 5 ng/mL; that of IS was 97.8 +/- 10.4% at 5 ng/mL. The detection limits (signal-to-noise ratio = 3) were estimated to be 0.05 ng/mL of whole blood or urine by mass chromatography and 0.01 ng/mL of whole blood by SIM. The coefficients of intraday and interday variations were not greater than 10.3%. We could detect PCP from rat whole blood 2 h after subcutaneous injection of PCP (1 mg/kg) by mass chromatography. The mean PCP concentration in rat blood was 47.7 +/- 6.2 ng/mL (mean +/- SD, n = 4).

Animals↗

Nickel-, chrom- and cobalt-concentrations in human tissue and body fluids of hip prosthesis patients.

The world-wide experience with millions of metallic implantations suggests the biocompatibility of modern alloys, commonly made of cobalt, chromium and nickel. There is, however, little information available on the internal metal exposure resulting from implants. In this study we assessed the metal concentrations in body fluids and tissue samples (muscle, bone) of patients who had undergone total hip replacement. Our patients were divided up into two groups. One group had firmly fixed implants two years after surgery. The other group had loose implants of the same Co-Cr-Mo alloy. Urine analyses revealed an increased renal elimination of nickel, chromium and cobalt. Cobalt and nickel exceeded the upper normal value. In serum the concentrations of nickel and chromium were normal or slightly elevated, the cobalt concentrations were significantly elevated. In some cases tissues adjacent to the implant showed extremely high concentrations of chromium and cobalt. This finding was also obtained in tissues that had no direct contact with the arthroplasty. The findings suggest that alloys of prostheses can undergo corrosion and release metal ions.

Aged↗

Role of angiotensin in body fluid homeostasis of mice: fluid intake, plasma hormones, and brain Fos.

CD1 mice injected peripherally with either ANG I or ANG II failed to drink substantial amounts of water or NaCl, yet showed strong Fos immunoreactivity (ir) in subfornical organ (SFO). Mice injected with furosemide showed modest stimulation of NaCl intake either 3 or 24 h later, were hypovolemic, and showed elevated plasma renin activity (PRA). The pattern of Fos-ir in the brain after furosemide was similar to that seen after peripheral injection of ANG II. Mice became hypovolemic after subcutaneous injection of polyethylene glycol (PEG), showed large increases in PRA, aldosterone, and water intake, but did not show sodium appetite. PEG-treated mice had strong activation of SFO as well as other brain regions previously shown to be related to ANG-associated drinking in rats. ANG II appears to have a modified role in the behavioral response to fluid loss in mice compared with rats.

Aldosterone↗

Acute and long-term effects of acebutolol on systemic and renal hemodynamics, body fluid volumes, catecholamines, active renin, aldosterone, and lymphocyte beta-adrenoceptor density.

Acebutolol is a relatively new beta-adrenoceptor blocking antagonist, possessing both beta 1-adrenoceptor selectivity and partial agonist activity (PAA). Its acute (24 h, 400 mg, twice daily) and long-term effects (3 weeks) on systemic and renal hemodynamics, body fluid volumes, hormones, and beta-adrenoceptor density on lymphocytes were studied in a single-blind placebo-controlled trial, in 10 hypertensive patients. The initial response to acebutolol (1-2 h) was a fall in heart rate (HR) (-9.6 +/- 2.7%), cardiac output (-16.0 +/- 3%), and stroke volume (SV) (-10.7 +/- 0.2%), and an increase in systemic vascular resistance (SVR) (18.0 +/- 3.9%). Mean arterial pressure (MAP) began to fall 2-3 h after dosing in parallel with a decrease in SVR. At the end of the acute study, MAP and SVR were decreased by 18.1 +/- 2.7% and 15.6 +/- 5.6%, respectively. By that time, HR and SV had returned to control values despite blockade of beta-adrenoceptors. After 3 weeks of treatment (mean dose of acebutolol 480 mg twice daily), the fall in MAP was 10.1 +/- 2.7% and HR was decreased by 13.0 +/- 2.3%. Renal blood flow and glomerular filtration rate did not change. Acute and long-term treatment had no effect on the density of lymphocyte-membrane beta-adrenoceptors. This could be explained by acebutolol's beta 1 selectivity or, alternatively, this could be due to the drug's PAA.

Acebutolol↗

Arsenic concentrations in tissues and body fluids of dogs on chronic low-level dietary sodium arsenite.

Twenty-four female Beagle dogs, 7-8 months old, were assigned to 4 groups. Control, low-dosage, medium-dosage, and high-dosage groups were offered 0, 1, 2, and 4 mg of sodium arsenite per kilogram of body weight per day (mg/kg/day), respectively, in their feed (equivalent to 0.0, 33.4, 66.7, and 133.4 micrograms/g in feed). On day 59, the dosage was doubled for the rest of the experiment, which ended on day 183. In general, arsenic concentrations in tissues and body fluids reflected arsenic levels in feed. Arsenic caused a dose-related decrease in food intake. Statistically significant differences in blood, liver, and kidney arsenic were detected, in most cases, between the 2 higher dosage groups and controls. The greatest differences in arsenic concentrations between groups were present in urine and hair. Results indicate that urine and hair would be the most useful specimens for chemical analysis when attempting to confirm low-level dietary inorganic arsenic exposure or poisoning.

Animal Feed↗

A sandwich enzyme immunoassay for the determination of neutrophil lipocalin in body fluids.

Human neutrophil lipocalin was purified from human buffycoat. A polyclonal antibody was obtained by immunisation of rabbits. The antibody reacted with the free lipocalin as well as with the PMNL-gelatinase bound protein. This antibody was used to establish a sensitive sandwich-ELISA for the determination of the protein in body fluids using the biotin/streptavidin system. The mean intra-assay C.V. was 2.3% and the mean inter-assay C.V. 6.7%. The recovery in human plasma was determined to be 98.8%. The ELISA allowed the determination of the protein in the concentration range 0.2-25 micrograms/l. Measurement of the neutrophil lipocalin concentration showed that human plasma of healthy donors contained 9.7 +/- 81 micrograms/l (n = 122) and that the concentrations in serum were significantly higher (P < 0.001) with 133 +/- 90 micrograms/l (n = 122). Neutrophil lipocalin was also found in the urine of healthy donors (8.1 micrograms/l; n = 9). Very high concentrations of this lipocalin were found in the synovial fluids of patients suffering from inflammatory rheumatoid arthritis (1.7 +/- 1.4 mg/l; n = 37).

Acute-Phase Proteins↗

Body fluid expansion is not essential for salt-induced hypertension in SS/Jr rats.

To evaluate the importance of volume in the development of hypertension in inbred Dahl salt-sensitive rats (SS/Jr), we measured the changes in blood pressure (BP) that occurred with oral intake of food (salt) and water in rats whose body weight was permitted to increase versus those in which body weight was maintained constant with a servo-control system. We hypothesized that if volume expansion is essential in the development of hypertension, then BP would not increase if body weight was held constant. We found that oral presentation of chow containing 4% salt to SS/Jr rats caused BP to increase 32.2 +/- 2.9 mmHg over 4 days when body weight was controlled at its initial value. Plasma sodium increased from 142.0 to 145.2 meq/l during 4 days of high salt. Neither plasma volume, hematocrit, nor central venous pressure changed significantly on the high-salt diet. In contrast, the inbred Dahl salt-resistant rats (SR/Jr) did not increase their BP during body weight control when given 4% salt. This demonstrates that volume expansion is not an obligatory step in the pressure response to increased salt in SS/Jr rats. Our results obtained with oral presentation of salt, in contrast to intravenous, represent a physiological evaluation of the significance of volume changes in response to dietary salt because no potential regulatory reflexes have been bypassed.

Animals↗