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Biomedical subjects

G Hogan

Publications and source records attributed to G Hogan.

10 recordsLinked to original sources
PubMed2003

Resistance of the pulmonary epithelium to movement of buffer ions.

Exposure of the apical surfaces of alveolar monolayers to acidic and alkaline solutions has been reported to have little influence on intracellular pH compared with basolateral challenges (Joseph D, Tirmizi O, Zhang X, Crandall ED, and Lubman RL. Am J Physiol Lung Cell Mol Physiol 282: L675-L683, 2002). We have used fluorescent pH indicators and a trifurcated optical bundle to determine whether the apical surfaces are less permeable to ionized buffers than the membranes that separate the vasculature from the tissues in intact rat lungs. In the first set of experiments, the air spaces were filled with perfusate containing FITC-dextran (mol wt 60000) or 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Air space pH fell progressively from 7.4 to 6.61 +/- 0.03 (mean +/- SE, n = 11, air space buffers at 10 mM). Perfusion for 2 min with 2 mM NH4Cl increased air space pH by 0.142 +/- 0.019 unit, without a subsequent acidic overshoot. Infusions of NaHCO3 and sodium acetate reduced pH without a subsequent alkaline overshoot. In the second set of experiments, cellular pH was monitored in air-filled lungs after perfusion with BCECFAM. Injections of NH4Cl caused a biphasic response, with initial alkalinization of the cellular compartment followed by acidification after the NH4Cl was washed from the lungs. Subsequent return of pH to normal was slowed by infusions of 1.0 mM dimethyl amiloride. These studies suggest that lung cells are protected from air space acidification by the impermeability of the apical membranes to buffer ions and that the cells extrude excess H+ through basolateral Na+/H+ exchangers.

Acid-Base Equilibrium↗
PubMed2001

Protection of the lungs from acid during aspiration.

Unlike the thick mucosa that normally covers the upper gastrointestinal tract, the membranes that cover the distal surfaces of the lungs are remarkably attenuated. This permits rapid exchange of gases between the airspaces and pulmonary vasculature, and may make the lungs more susceptible to acid challenges associated with acid reflux and aspiration. Any injury to the alveolar epithelium could result in the movement of solute and water into the airspaces (chemical pneumonia) and impair gas exchange. In this study, we used a fluorescent approach to compare the relative permeability of the apical basolateral surfaces of the lungs to the exchange of the ionic forms of acids and bases. The apical membranes proved to be much less permeable to NH(4)(+) and HCO(3)(+) than the basolateral membranes. This asymmetry in permeability should enhance resistance of the epithelium to inspired acidic challenges by slowing entry of acid into the cells and by linking the intracellular pH of the alveolar cells to that of the plasma, which is a relatively large, well-buffered compartment. Evidence also was obtained that the acid is secreted by the membranes covering the lungs.

Ammonium Chloride↗
PubMed2001

Relationship of ultrafiltration and anastomotic flow in isolated rat lungs.

OBJECTIVE: When arterial and venous pressures are increased to equal values in "stop-flow" studies, perfusate continues to enter the pulmonary vasculature from the arterial and venous reservoirs. Losses of fluid from the pulmonary vasculature are due to ultrafiltration and flow through disrupted anastomotic (bronchial) vessels. This study compared the relative sites of ultrafiltration and anastomotic flows at low and high intravascular pressures. METHODS: Isolated rat lungs were perfused for 10 minutes with FITC-dextran, which was used to detect ultrafiltration. Arterial and venous catheters were then connected to reservoirs containing radioactively labeled dextrans at 20 or 30 cm H2O for 10 minutes. The vasculature was subsequently flushed into serial vials, and ultrafiltration and vascular filling during the equal-pressure interval were calculated. RESULTS: Ultrafiltration equaled 0.43 +/- 0.11 mL at 20 cm H2O and was similar to the volume of fresh arterial and venous perfusate which entered and remained in the pulmonary vasculature during the equal-pressure interval (0.45 +/- 0.10 mL). At 30 cm H2O, 0.80 +/- 0.23 mL entered and remained in the vasculature during the equal-pressure interval, replacing the original perfusate, and calculated transudation (0.56 +/- 0.09 mL) was not significantly more than at 20 cm H2O. Fluid also entered the airspaces at 30 cm H2O but not at 20 cm H2O. CONCLUSIONS: At 20 cm H2O, flow through anastomotic vessels occurs at sites that are at the arterial and venous ends of the microcirculation. Flow in exchange vessels remains minimal, permitting measurements of ultrafiltration and exchange. Losses of perfusate from the pulmonary vessels complicate measurements of ultrafiltration at 30 cm H2O.

Animals↗
PubMed1989

Induction of tumour hypoxia by a vasoactive agent. A combined NMR and radiobiological study.

The effect of hydralazine treatment on 3 murine tumours (RIF-1, KHT and 16/C) was monitored using 31P-NMR. Changes in the 31P-NMR spectrum are compared with measurements of radiobiological hypoxic fraction (RHF) in the RIF-1 and KHT. Hydralazine is known to reduce temporarily blood flow in experimental tumours, and thus cause a transient increase in the RHF to 100% (in RIF-1 and KHT). This correlates with a decline in energy status as measured by 31P-NMR (i.e. there was an increase in Pi in all three tumours). Time-course data from the RIF-1 and KHT tumours show that maintenance of anaesthesia prolongs the hypoxia induced by hydralazine.

Animals↗
PubMed1986

Human papillomavirus types 16 and 18 sequences in early cervical neoplasia.

A total of 100 colposcopic biopsies from patients with abnormal Papanicolau's tests were surveyed for the presence of human papillomavirus (HPV) types 16 and 18 sequences by spot-blot hybridization. HPV 16 and 18 DNA sequences were detected in 58% of the biopsies. None of the cervical intraepithelial neoplasia grade I (CIN I) contained HPV 16 while 50% of the CIN III lesions (carcinoma in situ, CIS) contained HPV 16. HPV 18-related sequences were equally represented in CIN I, II, and III. Southern-blot hybridization of total undigested cellular DNA revealed the presence of HPV DNA sequences only in an episomal form. While the restriction enzyme patterns in HPV 16-positive samples were mostly identical to the originally cloned sequence, the restriction enzyme pattern for HPV 18-positive samples were different from that of HPV 18 but identical to each other. Furthermore, this DNA hybridized more strongly to HPV 18 under nonstringent conditions, suggesting a new type.

Colposcopy↗