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New Zealand male rabbits were anaesthetized with thiopental, tracheotomized, curarized by vecuronium bromide and mechanically ventilated. Six rabbits received L‐NAME 10 mg kg−1i.v., six rabbits L‐NAME 15 mg kg−1iv, and six rabbits received saline i.v. (controls), 5 min before a histamine aerosol (2% solution during 5 min). Six others rabbits received an injection of L‐NAME 15 mg kg−1iv, 5 min before the histamine aerosol, followed by an infusion of L‐arginine over a 60‐ min period. Total respiratory resistance (Rrs) and elastance (Ers) were derived by least square analysis of the relationship between tracheal pressure and flow, and computed every minute before and over a 1‐h period after the histamine aerosol. Oxygen free radicals (OFR) were measured with a luminometer, in microsomes from lung homogenates at the end of the experiment. Compared with the histamine response of the control group, the Rrs response in the L‐NAME 10 group was slightly less, while Ers changes were the same in the two groups. In contrast, L‐NAME 15 was responsible for an increased Rrs response, the difference being significant (P < 0.05) only between 15 and 40 min after the aerosol (+114% vs. + 85% in controls at the 20th min). The increase in Ers with L‐NAME 15 was stronger and significantly larger (+71% vs. +42% in controls at the 20th min after the histamine aerosol, P < 0.001). The relatively greater effect of L‐NAME on Ers than on Rrs suggests that NO predominantly modulates the response to histamine of the peripheral lung rather than that of the large airways. Furthermore, the effect of L‐NAME on Rrs was completely abolished by L‐arginine, while its effect on Ers was only partially reversed. This suggests that the changes in Ers are partly related to a hardly reversible phenomenon. Possibly, the mechanical changes are linked with the rise of OFR in the lung parenchyma, which were significantly higher in the L‐NAME 15 group compared to the control group (P< 0.05).

Glucose metabolites (lactate, pyruvate, citrate, malate), alanine, glutamate and adenosine triphosphate (ATP) were determined in the resting anterior tibial muscle of dogs. The muscle was sampled in anesthetized animals first breathing air, and secondly after an hour of breathing a hypercapnic mixture, FICO2=0.10 (experimental subjects n=6) or air (control subjects n=6). A decrease in concentration of glucose metabolites (lactate: -34%; pyruvate: -24%; Citrate: -34%; malate: -54%), glutamate (-43%), alanine (-35%) and ATP (-8%) was observed in the resting muscle during acute hypercapnic acidosis. This was not the case in control animals breathing air.

New methods of respiratory support are needed to reduce the high mortality rate of acute respiratory failure. To simplify the procedures of extracorporeal CO2elimination under apneic oxygenation, one approach is to replace the membrane lung by a hemodialyzer and to administer an alkali, since hemodialysis requires a lower blood flow rate than blood-gas exchange. This study compared the effectiveness of trishydroxymethyl aminomethane (THAM) and NaOH in this procedure. Twelve male Anglo-Poitevin dogs (25 to 33 kg) were anesthetized, curarized and mechanically hypoventilated (&Vdot;E= 41% of the control value). After not less than 15 min, a venovenous shunt was used for dialysis with blood flow of 7-10 ml. min.-1kg-1for at least 8 hours. The dialysate contained no acetate, bicarbonate or lactate, but was alkalinized to a pH of 8-9 by the addition of NaOH. A solution of THAM (0.5 N) was infused into the right heart at the rate of 0.30 ml.min.-1kg-1in six animals, and NaOH (0.15 N) was infused in the other six at the rate of 0.80 ml.min.-1kg-1. The injected volumes were compensated for by an equivalent amount of ultrafiltration. Elimination of CO2(mean †CO2= 2.3 ml.min.-1kg-1) was the same with both methods and the difference for the electrolytes and acid-base equilibrium was only very small. However, hemolysis was six times greater with NaOH than with THAM. Despite ultrafiltration, a similar marked weight gain was observed from the second hour of the experiment in the NaOH series, but only after 7 hours with THAM. It thus appears that hemodialysis combined with alkalinisation is still too complex a procedure to be safely applied in acute or chronic pulmonary failure

Total superoxide dismutase activity (SOD) was measured in the retinas obtained from 18 kittens aged 1 to 11 days born to 6 litters. Pretreatment with 100 mg of α-tocopherol acetate S.C. followed by a 72 hr exposure to 80 oxygen led to a higher (p < .06) SOD activity than in untreated animals. Retinas obtained from littermates who were not exposed to oxygen exhibited a greater (p < .01) SOD activity than those of the two hyperoxic groups.

Summary: Total superoxide dismutase activity (SOD) was measured in the retinas obtained from 18 kittens aged 1 to 11 days born to 6 litters. Pretreatment with 100 mg of α-tocopherol acetate S.C. followed by a 72 hr exposure to 80 % oxygen led to a higher (p < .06) SOD activity than in untreated animals. Retinas obtained from littermates who were not exposed to oxygen exhibited a greater (p < .01) SOD activity than those of the two hyperoxic groups.These data suggest that normobaric hyperoxia leads to a fall in SOD activity which can be partially prevented by pretreatment with a large dose of vitamin E.Speculation: The retina of the newborn kitten and of the premature human Infant are reported to be equally vulnerable to hyperoxia. The development of lesions may be related to a fall in retinal SOD activity. The observation that viLamin E administration reduced this drop suggests an explanation for the partial protection it provides agalnst retrolental fibroplasia.