PubMed · 7489447
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
G W Stevenson, M Tobin, S C Hall. 1995. Bubbles, bubbles, everywhere.. https://pubmed.ncbi.nlm.nih.gov/7489447/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Both the dorsomedial hypothalamic nucleus (DMH) and the paraventricular hypothalamic nucleus (PVN) have been implicated in the neural control of the cardiovascular response to stress. We used the GABAA agonist muscimol to inhibit neuronal activation and attempted to identify hypothalamic nuclei required for the cardiovascular response to air stress. Chronically instrumented rats received bilateral injections of either 80 pmol of muscimol or 100 nl of saline vehicle into the DMH, the PVN, or an intermediate area (including the rostral edge of the DMH and the region between the two nuclei) and were placed immediately in a restraining tube and subjected to 20 min of air stress. In all rats, air stress after vehicle injections caused marked increases in heart rate (137 +/- 6 beats/min) and blood pressure (26 +/- 2 mmHg). Microinjection of muscimol into the DMH suppressed the heart rate and blood pressure response by 85 and 68%, respectively. Identical microinjection of muscimol into the intermediate area between the DMH and the PVN attenuated the increases in heart rate by only 46% and in blood pressure by 52%. In contrast, similar injections into the vicinity of the PVN failed to alter the cardiovascular response to air stress. These findings demonstrate that muscimol-induced inhibition of neuronal activity in the region of the DMH blocks air stress-induced increases in heart rate and arterial pressure, whereas similar treatment in the area of the PVN has no effect.
To test the hypothesis that lung sensory C fibers protect the small distal airways and alveoli from oxidant injury, we compared the effects of inhalation of ozone (1 ppm) or filtered air for 8 h on lung injury and lung inflammation in four groups of rats: (1) normal rats exposed to filtered air; (2) normal rats exposed to ozone; (3) rats treated as neonates with capsaicin (50 mg/kg, intraperitoneally) and subsequently exposed to filtered air; and (4) rats treated as neonates with capsaicin and subsequently exposed to ozone. All rats were allowed to recover in filtered air for 0, 4, 16, and 40 h before necropsy. Rats exposed to filtered air (Groups 1 and 3) showed normal airway and parenchyma structure. Normal untreated rats exposed to ozone showed a random distribution of mild, interstitial inflammatory changes and epithelial necrosis of bronchi and bronchiolar epithelium. However, rats treated with capsaicin and subsequently exposed to ozone demonstrated severe acute interstitial inflammation and epithelial coagulate necrosis in all airways, especially in small, peripheral airways and parenchyma; all of these changes were statistically significant. These findings support our hypothesis that lung sensory C fibers protect the distal airways from oxidant injury during acute ozone inhalation.
Surface viscosities of phospholipid/steroid mixtures at the air-water interface were measured by means of an oscillating pendulum. Phospholipids studied included 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC); 1,2-dipalmitoyl-sn-glycero-3-phosphodimethylethanolamine (DPPDME); 1,2-dipalmitoyl-sn-glycero-3-phosphomonomethylethanolamine (DPPMME); 1,2-dipalmitoyl-sn-glycero-3-phosphoethanolamine (DPPE); 1,2-dipalmitoyl-sn-glycero-3-[phospho-rac-(1-glycerol)] (DPPG); 1-palmitoyl-2-elaidyl-sn-glycero-3-phosphocholine and 1-palmitoyl-2-linelaidyl-sn-glycero-3-phosphocholine. Each saturated phospholipid was studied in the presence of cholesterol, DPPC was also investigated in the presence of 5-androsten-3beta-ol; cholestanol; 5-cholestene;5alpha-cholesten-3beta-ol methyl ether; coprostanol; 7,(5alpha)-cholesten-3beta-ol; desmosterol; epicholestanol; lanosterol and lophenol. The surface viscosities of the trans-unsaturated phosphatidylcholines (PC) were undetectable by this method and in this respect they resembled cis- unsaturated PC. The surface viscosities of saturated phospholipids were very high but were reduced by low concentrations of steroids. Interpretation of the results for DPPC/cholesterol mixtures indicates that DPPC functions at the air-water interface as a one-dimensional linear aggregate. At 50 mN/m and 22 degrees C the average structure contains approximately 300 DPPC molecules. DPPDME acts similarly but DPPMME, DPPE and DPPG differ from DPPC in their response to cholesterol. All of the steroids examined except 5-androsten-3beta-ol and the lanosterol mixture paralleled cholesterol in their interaction with DPPC an indication that phospholipid/steroid interactions modifying surface viscosity have less stringent requirements for the steroid structure than interactions measured as condensation in surface area.