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Biomedical subjects

R M Jackson

Publications and source records attributed to R M Jackson.

At least 73 records · Page 4Linked to original sources
PubMed1988

Neutrophils in reexpansion pulmonary edema.

This study investigated the possible contribution of neutrophils to development of reexpansion pulmonary edema (RPE) in rabbits. Rabbits' right lungs were collapsed for 7 days and then reexpanded with negative intrathoracic pressure for 2 h before study, a model that creates unilateral edema in the reexpanded lungs but not in contralateral left lungs. Two hours after lung reexpansion, significant increases in lavage albumin concentration (17-fold), percent neutrophils (14-fold), and total number of neutrophils (7-fold) recovered occurred in the reexpanded lung but not in the left. After 2 h of reexpansion increased leukotriene B4 was detected in lavage supernatant from right lungs (335 +/- 33 pg/ml) compared with the left (110 +/- 12 pg/mg, P less than 0.01), and right lung lavage acid phosphatase activity similarly increased (6.67 +/- 0.35 U/l) compared with left (4.73 +/- 0.60 U/l, P less than 0.05). Neutropenia induced by nitrogen mustard (17 +/- 14 greater than neutrophils/microliters) did not prevent RPE, because reexpanded lungs from six neutropenic rabbits were edematous (wet-to-dry lung weight ratio 6.34 +/- 0.43) compared with their contralateral lungs (4.97 +/- 0.04, P less than 0.01). An elevated albumin concentration in reexpanded lung lavage from neutropenic rabbits (8-fold) confirmed an increase in permeability. Neutrophil depletion before reexpansion did not prevent unilateral edema, although neutrophils were absent from lung sections and alveolar lavage fluid from neutropenic rabbits.

Acid Phosphatase↗
PubMed1988

Superoxide dismutase and cytochrome oxidase in collapsed lungs: possible role in reexpansion edema.

This study examined the effects of lung collapse, a condition that causes relative hypoxia in lung tissues, on superoxide dismutase (SOD), cytochrome oxidase (cyt ox), and pyruvate kinase (py ki) activities in rabbits. Cyanide-insensitive respiration measurements were done in collapsed and contralateral lungs, as an index of intracellular free radical production. Rabbits' right lungs were collapsed for 7 days after which the animals were killed. We found that control rabbit lungs contained approximately 25 SOD units/mg DNA measured with 10(-5) M KCN (total SOD) and approximately 11 SOD units/mg DNA measured with 10(-3) M KCN (mitochondrial or MnSOD). Right lung collapse caused a 25% decrease in mitochondrial SOD activity after 7 days (P less than 0.05), whereas no significant changes occurred in right or left lungs' total SOD activity. In control rabbits cyt ox activity averaged approximately 0.009 mumol ferrocytochrome c.min-1.mg DNA-1. Right lung collapse caused a greater than 40% decrease in cyt ox activity after 7 days of collapse (P less than 0.05), whereas cyt ox activity in contralateral left lungs did not change. Pyruvate kinase activity, a marker for anaerobic glycolysis resulting from tissue hypoxia, increased 49% in collapsed right lungs (P less than 0.01). Cyanide-insensitive respiration was 83% higher in 7 day-collapsed lungs (2.28 +/- 0.66 microliters O2.min-1.g-1) compared with contralateral lungs (1.24 +/- 0.34, P less than 0.05), indicating increased O2-. and H2O2 production in this tissue after homogenization at normoxic PO2 (approximately 150 Torr).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis.

Re-expansion pulmonary edema (RPE) has been attributed to decreased lung interstitial pressures from a variety of mechanisms. Because some recent studies have implicated mechanisms that increase microvascular permeability in RPE, we tested whether the edema were due to free radical generation during re-expansion and reoxygenation of the collapsed lung. We used a rabbit model of RPE to test the effects of intracellular (dimethylthiourea) or extracellular (catalase) oxygen metabolite scavengers. Allopurinol was administered separately to determine whether xanthine oxidase was an important source of superoxide in this model. Edema was quantitated both gravimetrically and histologically, and lung xanthine oxidase activity was measured using a sensitive fluorometric assay with pterin as substrate. The results suggest indirectly that OH. or H2O2 (derived from O2-) contribute to the well-documented increase in lung permeability in RPE because dimethylthiourea, dimethylthiourea plus catalase, or catalase alone inhibited the edema to various degrees. Further, we observed histologically that increased numbers of neutrophils were present in re-expanded lungs and that neutrophil infiltration appeared to be diminished by antioxidant administration. Allopurinol did not decrease the edema, because xanthine oxidase activity in rabbit lung tissue is extremely low. We speculate that free radical generation in lung tissue contributes to the pathogenesis of RPE, although reinitiation of lung perfusion and ventilation requires a rapid change in intrathoracic pressure.

Allopurinol↗
PubMed1988

Hypoxia-induced oxygen tolerance: maintenance of endothelial metabolic function.

Hypoxia (10%-12% O2) preadaptation for 4-7 days effectively protects rats from oxygen toxicity. The present study was designed to investigate the hypothesis that the lung's microvascular endothelium shares in development of oxygen tolerance and therefore that endothelial metabolic function would be protected from oxygen toxicity by prior adaptation to hypoxia. Since pulmonary oxygen toxicity decreases lung capillary angiotensin converting enzyme (ACE) activity, we assayed converting enzyme active sites in an isolated perfused rat lung preparation as a marker for the development of oxygen toxicity and tolerance. Rats were exposed to air, hypoxia (10% O2 for 4 days), hyperoxia (greater than 95% O2 for 2 days) alone, or hypoxia followed immediately by hyperoxia. Lung vascular ACE content was quantitated by measuring the single pass binding of an iodinated-converting enzyme inhibitor, 125I-MK351A, a derivative of lisinopril. Hypoxia adaptation per se had no effect on ACE content reflected in normal 125I-MK351A binding, whereas hyperoxia exposure caused a significant decrease in lung vascular ACE. Hyperoxia-induced decreases in ACE content were prevented partially by hypoxia adaptation, indicating that ACE content on luminal endothelial surfaces was protected from oxygen toxicity. In isolated perfused lungs 125I-MK351A binding reflects development of oxygen tolerance after hypoxia preadaptation and suggests that lung endothelial metabolic function is protected from oxygen toxicity.

Adaptation, Physiological↗
PubMed1988

Effects of leukotriene B4 on permeability, prostacyclin and thromboxane release by normal and oxygen-preexposed isolated, perfused rat lungs.

This study assessed the hemodynamic and permeability effects of exogenous, synthetic leukotriene B4 (LTB4) on normal rat lungs and lungs from rats preexposed to oxygen for 48 h, which were isolated and perfused at constant flow in vitro. Adult, Sprague-Dawley rats were exposed to air or greater than 97% O2 for 48 h. After exposure, their lungs were removed from the thorax, ventilated with normoxic gas, and perfused at 12 ml/min with Krebs-Ringer bicarbonate buffer which contained 5 mM glucose and 3 mg/ml albumin. A total of 5.55 micrograms of synthetic LTB4 was infused in three separate boluses over 15 minutes. Perfusion and airway pressures were monitored, and the lungs release of 6-ketoprostaglandin F1 alpha and thromboxane B2 (TXB2) into the effluent from the pulmonary vasculature was measured by radioimmunoassay. The LTB4 had no measureable effects on pulmonary vascular pressures. LTB4 infusion caused a pronounced increase in permeability, indicated by increased albumin concentrations in alveolar lavage fluid from O2-preexposed lungs. Release of TXB2 from both air- and O2-preexposed lungs was increased after LTB4 infusion, while the change in 6-ketoprostaglandin F1 alpha release was not statistically significant. Both the increase in permeability enhanced TXB2 released after LTB4 infusion were inhibited by 10 microM indomethacin in the perfusate. These data indicate that exogenous LTB4 increases microvascular permeability in O2-exposed lungs in association with increased release of TXB2 into the pulmonary vascular effluent.

Animals↗
PubMed1987

Hypoxia-induced inhibition of converting enzyme activity: role in vascular regulation.

Systemic and pulmonary vascular reactivity to graded doses of angiotensin I (ANG I), angiotensin II (ANG II), and, as a control, phenylephrine were examined in 14- or 28-day hypoxia-exposed and air control rats. Hypoxic rats exhibited pulmonary hypertension that was reversible on return to room air, but systemic arterial pressure was not altered by hypoxia. Systemic pressor responses to ANG I and ANG II were significantly less in the hypoxic rats than in the control rats at 14 and 28 days but returned to control levels in hypoxic animals that were then returned to room air, demonstrating reversibility of the hypoxia-induced changes in vascular reactivity. Pulmonary pressor responses to ANG I were significantly less at 14 days, whereas responses to ANG II were significantly greater at 28 days, in hypoxic rats than in controls. There were no significant differences in systemic and pulmonary pressor responses to phenylephrine between the hypoxic and air control animals. The altered systemic and pulmonary pressor responsiveness to ANG I and ANG II in hypoxic rats is probably related to mechanisms specific to the renin-angiotensin system, such as inhibition of intrapulmonary angiotensin-converting enzyme activity and down regulation of ANG II receptors in the systemic circulation. Further study is needed to elucidate these mechanisms.

Angiotensin I↗
PubMed1987

Acute bacterial sinusitis and diabetes mellitus.

Diabetes mellitus has deleterious effects on the immune system which may lead to infection that is more serious and difficult to treat. Fifteen diabetic patients with acute bacterial sinusitis are reviewed. Diabetic pathophysiology and its relationship to infection are discussed. A protocol for treatment is outlined, with emphasis on the importance of intravenous antibiotics.

Adult↗
PubMed1986

Fractionation of rat alveolar macrophages by isopycnic centrifugation: morphological, cytochemical, biochemical, and functional properties.

Studies on alveolar macrophages have usually been performed on a single cell suspension obtained by lung lavage. However, recent evidence on the diversity of functions of the alveolar macrophage suggests that the macrophage is not a single population, but one composed of several subpopulations of macrophages. One approach toward determining if alveolar macrophages are heterogeneous would be to separate subpopulations based on density. To accomplish this, we developed a continuous gradient of iso-osmotic colloidal silica (Percoll) that separated alveolar macrophages from Fischer 344 rats into 18 density-defined subpopulations. The density-defined alveolar macrophage subpopulations were then characterized and were shown to be significantly different based on morphological, cytochemical, biochemical, and functional analysis. The results of this study suggest that alveolar macrophages are heterogeneous and that a continuous iso-osmotic gradient of colloidal silica is an efficient and reproducible method for separating subpopulations.

Animals↗
PubMed1986

Coins in the esophagus. What is the best management?

In order to compare esophagoscopy to the Foley catheter method of removing coins from the esophagus, we reviewed our results with 136 esophagoscopies performed to remove coins during a 15-year period. Fifty-two percent of the patients were under two years of age and 29% were under one year. One hundred and twenty-seven patients had no problems from the anesthesia or the esophagoscopy. Complications related to the endotracheal tube and exacerbations of pre-existing respiratory illnesses occurred in 9 patients. There were no deaths or esophageal perforations. Our results are compared to the published results from the Foley catheter method. In our opinion, esophagoscopy is the procedure of choice for all children with coins in the esophagus.

Catheterization↗
PubMed1986

Impaired pulmonary conversion of angiotensin I to angiotensin II in rats exposed to chronic hypoxia.

The effects of exposing rats to hypoxia at normal atmospheric pressure for periods of 21-24 days on intrapulmonary conversion of angiotensin I (ANG I) to angiotensin II (ANG II) were examined using an isolated rat lung preparation perfused at constant flow. 125I-ANG I (160 fmol) was injected alone and with graded doses (0.1, 1.0, and 100 nmol) of unlabeled ANG I into the pulmonary artery, and the effluent was collected for measurement of ANG I, ANG II, and metabolites. At low doses of injected ANG I (125I-ANG I alone or with 0.1 or 1.0 nmol unlabeled ANG I), the percent conversion of ANG I to ANG II was 67.5 +/- 2.1 (SE), 65.1 +/- 2.0, and 62.5 +/- 1.6 in 21-day hypoxia-exposed animals and 83.8 +/- 2.7, 81.4 +/- 3.9, and 79.6 +/- 2.3 (P less than 0.01) in control rats maintained under normoxic conditions. At the highest dose (100 nmol) of injected ANG I, percent conversion was reduced in both hypoxic and control groups to 46.8 +/- 5.0 and 64.0 +/- 6.0, respectively (P less than 0.05). Mean transit times of labeled material through the pulmonary circulation were not significantly different in hypoxic vs. normoxic lungs at any ANG I load, suggesting that the decreased conversion seen in hypoxic lungs was not related to altered kinetics of substrate exposure. Thus chronic hypoxia is associated with significant inhibition of transpulmonary ANG I conversion that is independent of perfusate flow. We postulate that this phenomenon is due to alterations at the endothelial membrane level.

Angiotensin I↗
PubMed1986

Production of arachidonic acid metabolites by endothelial cells in hyperoxia.

This study investigated the response of bovine pulmonary artery endothelial cells to incubation in hyperoxia (95% O2-5% CO2). Changes in cell number and morphology, release of lactate dehydrogenase, and production of arachidonic acid metabolites were assessed during continuous exposure of confluent endothelial monolayers to air (air-5% CO2, "controls") or O2 (95% O2-5% CO2, "O2-exposed") for periods of 12-72 h. Control monolayer cell numbers remained constant (approximately 2,000,000 cells/flask), whereas the number of cells in O2-exposed monolayers decreased progressively to 30% of controls (P less than 0.01) by 72 h. As assessed by radioimmunoassay, both control and O2-exposed cells produced the prostacyclin metabolite, 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and prostaglandin F2 alpha (PGF2 alpha), but no thromboxane metabolite (TxB2) was detected. The O2-exposed cells released significantly more 6-keto-PGF1 alpha and PGF2 alpha than control cells when apparent net production rates over the entire 72-h period were compared. In addition, both control and O2-exposed (48 h) endothelial monolayers released immunoreactive leukotriene B4 (LTB4) on stimulation with calcium ionophore (10 microM A23187). As with the cyclooxygenase products, O2-exposed cells released more immunoreactive LTB4 than did controls. Both cyclooxygenase and lipoxygenase metabolites of arachidonic acid are released by cultured endothelial cells during the development of O2 toxicity.

Animals↗
PubMed1986

Studies of membrane receptors and phagocytosis in subpopulations of rat alveolar macrophages.

Recent data suggest that alveolar macrophages may be a heterogeneous group of cells with several subpopulations. This study was undertaken to determine if there is heterogeneity among rat alveolar macrophages with respect to receptors for zymosan, immunoglobulin, and complement. In addition, avidity for the immunoglobulin IgG was defined by opsonizing sheep red blood cells (SRBC) with different amounts of IgG. Alveolar macrophages were harvested by bronchoalveolar lavage and separated into 18 density-defined fractions by centrifugation through a continuous isosmotic gradient of colloidal silica. All density-defined alveolar macrophages exhibited similar abilities to attach zymosan and SRBC opsonized with a high level of IgG. In contrast, macrophages of a density of 1.046 g/ml to 1.075 g/ml exhibited high receptor activity capable of attaching and phagocytizing SRBC opsonized with small amounts of IgG. Similarly, attachment indices for complement-coated SRBC exhibited a peak activity among fractions exhibiting similar high avidity receptors for IgG. These results demonstrate the functional heterogeneity with respect to IgG and complement receptors among density-defined rat alveolar macrophage subpopulations.

Animals↗
PubMed1986

Malignant schwannoma of the cervical vagus nerve in a patient with neurofibromatosis (von Recklinghausen's disease).

A patient with malignant schwannoma arising from the cervical vagus nerve has been described. Treatment consisted of wide en bloc resection of the tumor and adjacent carotid artery. A subclavian-middle cerebral arterial bypass procedure, using a saphenous vein graft, was performed. A course of postoperative radiotherapy was administered. The patient remains without evidence of disease 11 months following therapy.

Adult↗
PubMed1985

The effect of bleomycin on lung metabolism of prostaglandin E2 in hamster.

Lung is a major site of prostaglandin synthesis and degradation. One site of metabolism has been shown to be the endothelial cell. Metabolism of prostaglandins has been shown to be influenced by both physiological and pathological mechanism. Furthermore, it has been suggested that a relationship might exist between pulmonary disease and the lung's ability to synthesize and/or degrade prostaglandins. Therefore, we evaluated if bleomycin-induced fibrosis, a model of human pulmonary fibrosis, affects the ability of lung to metabolize prostaglandins. Single pass metabolism of prostaglandin E2 was evaluated in an isolated, perfused and ventilated lung of hamsters at 5 and 500 nM concentrations 4,7,14,21 and 28 days after intratracheal bleomycin. The metabolism of prostaglandin E2 was not changed at the 5 nM level, but was significantly decreased at 500 nM level on day 14 and day 28 after intratracheal bleomycin. The results suggest that intratracheal bleomycin causes alterations in prostaglandin metabolism; the mechanism(s) is unknown but may be related to endothelial cell damage and possible changes in alveolar-capillary surface area.

Animals↗