Spring viraemia of carp.
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Aeromonas hydrophila↗
Biomedical subjects
A M Roberts
Publications and source records attributed to A M Roberts.
A novel method to assess reactivities of retinal microcirculation.
This study introduces a novel method of bovine retinal microcirculation preparation to assess reactivities of retinal microvessels in ex vivo. This preparation is perfused intraluminally through the retinal artery. Effects of vasoactive hormones on these microvessels can be studied by perfusion or topical application to muscle bath. Effects of these compounds on the retinal microvessels of 1A (180- to 200-microns diameters), 2A (50- to 60-microns diameter), and 3A (20- to 30-microns diameter) can be assessed simultaneously using video microscopy. In this study, the water-soluble compound endothelin-1, when applied topically, caused dose-dependent vasoconstriction of all microvessels but had no effect when perfused intraluminally. On the other hand, lipid-soluble prostaglandin F2 alpha (PGF alpha) caused dose-dependent vasoconstriction when administered either intra- or extraluminally. Furthermore, preconstricted retinal arterioles (by PGF alpha) were dilated in a dose-dependent manner when acetylcholine was perfused through the retinal artery. This vasodilation was attenuated by atropine or N3-monomethyl arginine, a nitric oxide synthase inhibitor. Topical potassium chloride also caused dose-dependent vasoconstriction of all retinal microvessels. Fluorescein angiography showed no breakdown of the blood-retinal barrier. Thus, in this ex vivo perfused bovine retinal microcirculation preparation, the water-soluble compounds may not cross the blood-retinal barrier to affect microcirculation while lipid soluble can affect this circulation. Additionally this study shows that endothelial-derived compounds, endothelin and nitric oxide, caused vasoconstriction and dilation, respectively.
Acetylcholine↗
Nucleotide sequence of cDNA encoding the group II allergen of cocksfoot/orchard grass (Dactylis glomerata), Dac g II.
Cocksfoot/orchard grass (Dactylis glomerata) anther cDNA clones encoding the group II allergen Dac g II were previously isolated on the basis of immunoreactivity of human, rabbit, and murine antibodies with a 24-kDa protein expressed as a fusion protein with beta-galactosidase. Nucleotide sequencing reveals an open reading frame predicting expression of a 98-amino-acid (11-kDa) polypeptide exhibiting > 90% homology with the group II allergen of Lolium perenne, Lol p II. In vitro translation of different sized clone fragments generated by polymerase chain amplification confirms eukaryotic expression of a 10-12-kDa polypeptide by SDS-PAGE and the position of a translational stop apparently unrecognized during expression of lambda gt11 in E. coli. The unusual characteristics of the prokaryote-expressed fusion proteins may be exerting conformational alterations in Dac g II, as reflected by previous demonstrations of differences in human IgE immunoreactivity. Northern blot analysis using PCR-generated partial and full-length probes suggests that group II allergens may be encoded by a different family or families of temporally expressed genes from those encoding group I major allergens, although a group I gene may have been the progenitor.
Allergens↗
Arteriolar dilation mediated by capsaicin and calcitonin gene-related peptide in rats.
In addition to altering vascular tone by stimulating primary afferent nerves and acting through reflex pathways, capsaicin acts locally. We examined effects of topically applied capsaicin on arteriolar diameter in striated muscle and tested the hypothesis that capsaicin can alter microvascular tone by releasing substance P (SP) or calcitonin gene-related peptide (CGRP). In anesthetized rats, the right cremaster muscle was exposed and suspended in a tissue bath filled with a physiological salt solution. Diameters of third-order arterioles were displayed and measured using in vivo video microscopy. In 17 of 20 rats, addition of capsaicin (3 x 10(-7) M) to the bath dilated arterioles (85 +/- 14% above control). Failure of a second administration of capsaicin to produce a sustained dilation in 6 of 7 arterioles that had previously dilated to capsaicin is consistent with the hypothesis that this agent causes depletion of an endogenous vasodilator. Pretreatment with an SP inhibitor did not alter capsaicin-induced dilation. CGRP (1 x 10(-10) to 2 x 10(-8) M) caused dilation similar to that caused by capsaicin. Pretreatment with a CGRP inhibitor to the bath prevented capsaicin-induced dilation, but not constriction. These results suggest that capsaicin can dilate microvessels by releasing CGRP, which can modulate tone.
Animals↗
Isolation and amplification of human IgE Fd encoding mRNA from human peripheral blood lymphocytes.
In order to establish the feasibility of applying recombinatorial library technologies to investigate human in vivo IgE responses, and as a pre-requisite of recombinatorial library construction, we have attempted to determine workable peripheral blood sample volumes required for isolation of mRNA for polymerase chain reaction (PCR) amplification of human IgE Fd encoding sequences. Cells secreting chimeric human IgE monoclonal antibody specific for the hapten NIP were used to establish the conditions for specific amplification of C epsilon 1 domain and Fd encoding sequences, as determined by Southern hybridisation. Amplification of C epsilon 1 domain sequences could be achieved using as few as ten cultured cells as the source of RNA. Specific IgE+ B cell enrichment using immuno-magnetic particles prior to RNA extraction was, however, required to obtain amplification of IgE C epsilon 1 and Fd fragments from lymphocytes prepared from 40 ml human peripheral blood. IgG1+ B cell enrichment from similar samples was not required for detectable amplification of human C gamma 1 cDNA sequences. However, this procedure improved amplification efficiency. Optimisation of methods to separate specific B cell populations, or specific RNA/cDNA sequences, will facilitate in vitro generation of human IgE Fab fragments from peripheral blood.
B-Lymphocytes↗
Neuralgia-inducing cavitational osteonecrosis (NICO). Osteomyelitis in 224 jawbone samples from patients with facial neuralgia.
A somewhat obscure etiologic theory for facial neuralgias presumes a low-grade osteomyelitis of the jaws that produces neural degeneration with subsequent production of inappropriate pain signals. Animal investigations and treatment successes with human patients based on this theory lend it credence. The present study examined 224 tissue samples removed from alveolar bone cavities in 135 patients with trigeminal neuralgia or atypical facial neuralgia. All tissue samples demonstrated clear evidence of chronic intraosseous inflammation. The most common microscopic features included dense marrow fibrosis or "scar" formation, a sprinkling of lymphocytes in a relative absence of other inflammatory cells (especially histiocytes), and smudged, nonresorbing necrotic bone flakes. Very little healing or new bone formation was visible. These lesions were able to burrow several centimeters to initiate distant cavities. The present preliminary investigation cannot prove etiology, but the presence of intraosseous inflammation in every single jawbone specimen in these patients and certain clinical and treatment aspects of these lesions (to be reported later) has led the authors to recommend the term neuralgia-inducing cavitational osteonecrosis or NICO for these lesions.
Adult↗
N-terminal amino acid sequence homologies of group V grass pollen allergens.
In an earlier study, we presented data regarding the immunoaffinity purification and N-terminal sequencing of a major pollen allergen from orchard/cocks-foot grass (Dactylis glomerata), now identified as the group V allergen Dac g V. In this paper, we have extended our investigations to include group V allergens from other grass species. Our data confirm the presence of group V-restricted characteristic N-terminal amino acid sequences containing a high alanine and hydroxyproline (P') rather than proline (P) content, and based upon two conserved elements (ADAGY and TPA/TP'A).
Allergens↗
Recombinant pollen allergens from Dactylis glomerata: preliminary evidence that human IgE cross-reactivity between Dac g II and Lol p I/II is increased following grass pollen immunotherapy.
We previously described the isolation of three identical complementary DNA (cDNA) clones, constructed from Orchard/Cocksfoot grass (Dactylis glomerata) anther messenger RNA (mRNA), expressing a 140,000 MW beta-galactosidase fusion protein recognized by IgE antibodies in atopic sera. Partial nucleotide sequencing and inferred amino acid sequence showed greater than 90% homology with the group II allergen from Lolium perenne (Lol II) indicating they encode the group II equivalent, Dac g II. Western blot immunoprobing of recombinant lysates with rabbit polyclonal, mouse monoclonal and human polyclonal antisera demonstrates immunological identity between recombinant Dac g II, Lol p I and Lol p II. Similar cross-identity is observed with pollen extracts from three other grass species: Festuca rubra, Phleum pratense and Anthoxanthum odoratum. Recombinant Dac g II was recognized by species- and group-cross-reactive human IgE antibodies in 33% (4/12) of sera randomly selected from grass-sensitive individuals and in 67% (14/21) of sera from patients receiving grass pollen immunotherapy, whilst 0/4 sera from patients receiving venom immunotherapy alone contained Dac g II cross-reactive IgE. Cross-reactive IgG4 antibodies were detectable in 95% of sera from grass pollen immunotherapy patients. These preliminary data suggest that conventional grass pollen allergoid desensitization immunotherapy may induce IgE responses to a cross-reactive epitope(s) co-expressed by grass pollen groups I and II (and possibly group III) allergens.
Allergens↗
Nicotine impairs reflex renal nerve and respiratory activity in deoxycorticosterone acetate-salt rats.
Smoking exacerbates the increase in arterial pressure in hypertension. The effect of nicotine on the baroreceptor-mediated reflex responses of renal nerve activity (RNA), heart rate, and respiratory activity (minute diaphragmatic activity [MDA]) after bolus injections of phenylephrine was compared in deoxycorticosterone acetate (DOCA)-salt sensitive and normotensive rats. Osmotic minipumps that dispensed either nicotine (2.4 mg/kg/day) or saline were implanted in DOCA and normotensive rats for 18 days. Anesthetized DOCA-nicotine, DOCA-saline, control-nicotine, and control-saline rats had mean arterial pressures (MAP) of 117 +/- 3, 110 +/- 9, 90 +/- 3, and 89 +/- 5 mm Hg, respectively. Nicotine decreased the sensitivity (p less than 0.05) of baroreceptor reflex control of RNA (% delta RNA/delta MAP) in the DOCA-nicotine rats (-0.92 +/- 0.08) compared with the DOCA-saline (-1.44 +/- 0.16), control-nicotine (-1.45 +/- 0.08), or control-saline (-1.45 +/- 0.21) rats. The reflex decrease in respiratory activity (% delta MDA/delta MAP x 100) was impaired (p less than 0.01) in both control-nicotine (-24.5 +/- 3.3) and DOCA-nicotine (-18.2 +/- 4.6) rats compared with control-saline (-59.2 +/- 9.1) and DOCA-saline (-52.5 +/- 9.9) rats. The reflex decrease in heart rate (absolute delta HR/delta MAP) in both DOCA-nicotine (1.56 +/- 0.17) and control-nicotine (1.54 +/- 0.24) rats was augmented compared with DOCA-saline and control-saline rats (0.91 +/- 0.12 and 0.97 +/- 0.14).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Indirect effects of histamine on pulmonary rapidly adapting receptors in cats.
We did experiments to determine the relative importance of lung mechanical changes during histamine induced activation of pulmonary rapidly adapting receptors (RARs). In anesthetized, open-chest, artificially ventilated cats, we recorded RAR activity and injected histamine (25-50 micrograms/kg) into the right atrium. Histamine initially increased RAR activity from 1.1 +/- 0.2 to 3.6 +/- 0.6 imp/sec (n = 30) at 15.6 +/- 0.8 sec when dynamic lung compliance (CDYN) was decreased by 29.1 +/- 1.5%. The firing pattern of RARs changed from a relatively irregular pattern to a pronounced respiratory modulation. RAR activity reached its peak (5.6 +/- 0.8 imp/sec) at 36.3 +/- 3.3 sec. The firing pattern further changed to a cardiac modulation, and the activity closely correlated with cardiac output. Comparing the initial response of RARs to histamine with the response to mechanically decreasing CDYN, we found that the activities were similar when CDYN was decreased by the same amount. Our experiments suggest that in cats the initial increase of RAR activity in response to histamine is related to lung mechanical changes, but the later increase is related to cardiovascular functions.
Action Potentials↗
Shock, transfusion, and pneumonectomy. Death is due to right heart failure and increased pulmonary vascular resistance.
To determine the physiologic cardiopulmonary abnormalities leading to death when pneumonectomy is required to stop bleeding in patients in hemorrhagic shock, we compared cardiopulmonary responses to resuscitation in pigs undergoing hemorrhagic shock alone, pneumonectomy alone, and hemorrhagic shock plus pneumonectomy. Four shock-plus-pneumonectomy pigs died acutely from right heart failure. When the five remaining shock-plus-pneumonectomy pigs were compared to the two control groups, pulmonary vascular resistance (PVR) increased to significantly higher levels than would be expected from the increase in PVR noted with resuscitation from shock alone and pneumonectomy alone. Right ventricular compensation maintained cardiac index in the hemorrhage-alone group and the pneumonectomy-alone group but could not maintain cardiac index in the shock-plus-pneumonectomy group, despite maximal increases in right ventricular systolic pressure, heart rate, and right ventricular end diastolic volume. These data indicated that resuscitation from shock plus pneumonectomy cannot be effectively accomplished because increased PVR leads to right ventricular failure, which limits left ventricular preload to levels that are insufficient to maintain cardiac index.
Animals↗
Reflex inotropic responses to distension of left atrium or pulmonary veins.
Previous investigators demonstrated that distension of the left atrium (LA) or pulmonary veins (PV) evokes reflex changes in heart rate (HR) and mean arterial blood pressure (MABP). This study was designed to determine whether stimulation of receptors in these areas could evoke reflex changes in left ventricular (LV) maximum contractility (Vmax) in anesthetized dogs. Balloons were placed in the left atrial appendage or in two right pulmonary veins to stimulate mechanoreceptors in these regions without directly altering other cardiorespiratory pressures. Distension of either the LA or PV increased LV contractility and decreased MABP. LA distension evoked a vagally mediated increase in HR when predistension HR was less than 140 beats/min but did not change HR when predistension HR was greater than 140 beats/min. Reflex changes in inotropic state and MABP were not altered by bilateral vagotomy or carotid sinus denervation. In dogs with stellate ganglia and sympathetic chains sectioned and vagi intact, PV or LA distension decreased LV contractility and MABP. Responses were eliminated when both vagal and sympathetic pathways were cut. We conclude that distension of the LA or the PV and LA junction evokes a sympathetically mediated increase in LV contractility.
Animals↗
Lung inflation evokes reflex dilation of microvessels in rat skeletal muscle.
Lung inflation can reflexively decrease peripheral resistance, but effects on the microcirculation have not been determined. In this study, we examined the effects of lung inflation on microvessels in skeletal muscle. In anesthetized spontaneously breathing rats, the right cremaster muscle with intact circulation and innervation was exposed and suspended in a tissue bath filled with a physiological salt solution. Diameters of third-order arterioles (3As) were displayed by television microscopy and measured as an index of microcirculatory resistance. In other experiments, sympathetic activity (in the genital femoral nerve) to the cremaster was recorded. Lung inflation decreased systemic blood pressure by 32 +/- 3 mmHg and increased 3A diameter by approximately 23% (P less than 0.05, n = 17). The increase was abolished by cutting the cervical vagus nerves or the right genital femoral nerve. Furthermore, inflation decreased sympathetic nerve activity by 47.6 +/- 11.3% (P less than 0.05, n = 5) before vagotomy but not after. Dilation in response to inflation was also abolished by phentolamine or guanethidine. These results suggest that stimulation of vagal afferents by inflation reflexively decreases microvascular resistance by withdrawal of sympathetic tone.
Animals↗
Postanesthesia care of the biliary lithotripsy patient.
Alabama Lithotripsy Services is a consortium of Baptist Medical Centers in Birmingham, Montclair, and Princeton, Druid City Regional Medical Center in Tuscaloosa, and Huntsville Hospital in Huntsville, AL. This consortium is the first of two mobile lithotripsy services currently involved in the Food and Drug Administration investigational study using the Medstone (Medstone International, Inc, Irvine, CA) STS Lithotripter in the treatment of biliary gallstones. This procedure is a safe and effective alternative to abdominal surgery. Postanesthesia nurses need to know the population and criteria for selecting patients, how the lithotripter operates, postanesthesia care, possible complications, advantages, and disadvantages, as well as the future consideration of biliary lithotripsy using the Medstone STS Biliary Lithotripter.
Cholelithiasis↗
Attenuation of pulmonary afferent input by vagal cooling in dogs.
In open chest, artificially ventilated, anesthetized dogs, we examined the effect of vagal cooling on the pulmonary afferent input evoked by hyperinflating the lungs to 3 VT, recording the activity of slowly adapting pulmonary stretch receptors (PSRs), rapidly adapting receptors (RARs) and pulmonary C fibers rostral to the cooling platform. At 15 degrees C and below, input in all three types of fiber was significantly reduced, attenuation being least marked in C fibers. Between 12 degrees C and 7 degrees C, attenuation of RAR input was significantly less than that of PSRs. At 7 degrees C, virtually none of the hyperinflation-evoked increase in PSR activity and only 10% of that in RARs passed the cooling platform--indeed RAR input was less than during normal ventilation at 37 degrees C; by contrast, 40% of the hyperinflation-evoked increase in C fiber activity was still transmitted. Cooling had similar effects on C fiber input evoked by capsaicin. If reflexes are attenuated in proportion to the attenuation of afferent input, our results suggest that a hyperinflation-evoked reflex that survives vagal cooling below 6 degrees C is almost certainly triggered by C fibers.
Afferent Pathways↗
Reciprocal action of pulmonary vagal afferents on tracheal smooth muscle tension in dogs.
Tracheal smooth muscle usually relaxes when the lungs are transiently inflated, an effect attributed to inhibitory input from pulmonary stretch receptors (PSRs). Relaxation is often followed by contraction, however, and occasionally contraction is the sole response. We attempted to identify the afferents responsible for this reflex contraction. In anesthetized, artificially ventilated dogs with open chest we recorded transverse tension in an upper tracheal segment innervated only by the superior laryngeal nerves and periodically hyperinflated the lungs as the cervical vagus nerves were cooled. Hyperinflation usually evoked tracheal relaxation when vagal temperature was 37 degrees C, but contraction became more frequent as temperature decreased and was the sole response below 8 degrees C. We hypothesise that above 6 degrees C contraction was triggered by rapidly adapting receptors and lung C fibers, whereas below 6 degrees C only C fibers were involved. Contraction, which appeared to represent the bronchomotor counterpart of Head's paradoxical reflex, was abolished below 2 degrees C. Cooling alone without periodic hyperinflation increased baseline tracheal tension to a maximum at 7-8 degrees C; further cooling often decreased tension, sometimes to control levels. Cutting the pulmonary vagal branches abolished these effects. Our results indicate that PSRs and C fibers act reciprocally, one causing bronchodilation, the other bronchoconstriction, and that background activity in C fibers may contribute to bronchomotor tone, an effect unmasked by selectively blocking A fibers.
Animals↗
Aortic wall creep and acute baroreceptor resetting.
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Animals↗
Stimulation of pulmonary vagal afferent C-fibers by lung edema in dogs.
In anesthetized, open-chest dogs we examined the effect of pulmonary edema on the firing frequency of afferent vagal fibers arising from the lung. We recorded impulses from slips of the cervical vagus nerves and infused isotonic Krebs-Henseleit solution (20% of body weight) intravenously to increase net filtration pressure in the lung microvasculature. Measurement of extravascular lung water (6.0 +/- 0.4 g/g dry lung), and morphological examination of lung tissue (revealing various degrees of perivascular and peribronchial cuffing) confirmed that edema was present. At the end of the infusion when the lungs were congested (lung microvascular pressure, 37 cm water) and edematous, the impulse frequency of pulmonary and bronchial C-fibers and rapidly adapting receptors had increased 5-6 times. The only significant change in slowly adapting receptor activity was an increase during deflation. When lung water was still elevated but lung microvascular pressure had been restored to control by withdrawal of blood, impulse activity of rapidly and slowly adapting receptors reverted to or below control. Pulmonary C-fiber activity, although less than during congestion, remained significantly above control, several C-fibers being stimulated by interstitial edema in the absence of alveolar edema. Bronchial C-fibers were stimulated in severely edematous lung showing pronounced peribronchial cuffing and alveolar edema, but were not stimulated in milder grades of edema. Our results support the hypothesis (Paintal, 1969) that pulmonary C-fibers (J-receptors) are stimulated by an increase in interstitial pressure secondary to edema.
Action Potentials↗