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BACKGROUND We explored the ability of increased oxygen pressure to modify necrosis in an open-chest rabbit model of myocardial ischemia and reperfusion. METHODS AND RESULTS A branch of the left coronary artery was occluded for 30 minutes followed by 3 hours of reperfusion. Infarction was measured by triphenyl tetrazolium staining and expressed as a percentage of the ischemic zone. Untreated rabbits were ventilated with 100% oxygen at 1 atm absolute. Treatment animals were exposed to hyperbaric oxygen at 2.5 atm absolute. The 1.0-atm control hearts developed 41.5 +/- 4.6% infarction of the ischemic zone. Animals exposed to hyperbaric oxygen during ischemia only, reperfusion only, or ischemia and reperfusion had significantly smaller infarcts with respect to control animals (16.2 +/- 2.9%, 14.5 +/- 3.7%, and 9.8 +/- 2.7%, respectively; P < or = .01), indicating that they had been protected by the procedure. When hyperbaric oxygen was begun 30 minutes after the onset of reperfusion, no protection was seen (35.8 +/- 3.8%). CONCLUSIONS We conclude that hyperbaric oxygen limits infarct size in the reperfused rabbit heart and that the effect can be achieved when hyperbaric oxygen is begun at reperfusion.

Ischemic preconditioning renders the heart resistant to infarction by an unknown mechanism. This study tests whether preconditioning may be working through activation of ATP-sensitive potassium channels. If that were the case, then blockade of the channels should eliminate preconditioning's protection, and activation of these channels should mimic it. Thirty minutes of regional coronary ischemia followed by 3 hours of reperfusion caused 38.0 +/- 3.7% of the risk zone to become infarcted in control rabbits. Preconditioning with 5-minute ischemia followed by a 10-minute reperfusion before the 30-minute insult caused only 8.8 +/- 2.1% infarction, which was a reduction of 29.2% in infarct size by preconditioning (p < 0.01 versus control value). Pretreatment with the potassium channel blocker glibenclamide at three different concentrations significantly elevated infarct size in the nonpreconditioned hearts at all doses. Preconditioning, however, continued to limit infarct size by an amount not different from that seen in the control group at all doses of glibenclamide. Pinacidil, a potassium channel agonist, given before a 30-minute ischemic insult resulted in infarct sizes no different from that seen in nonpreconditioned control rabbits. We conclude that ATP-sensitive potassium channels are not involved in preconditioning in the rabbit heart; however, blocking those channels does exacerbate ischemia.

Continuous measurement of electron temperature and electron concentration during the great magnetic storm of Mar. 8, 1970, when the F2 peak rose as high as 800 km. Continuous measurements of the vertical component of E x B drift were made from 1130 to 1730 LT. A synthesis of the observed electron concentrations was made using a model that solved the time-dependent electron-ion continuity equation for O(+) and the molecular ions; the latter chemistry was included to improve the solutions at lower heights. It was found, using the observed values of vertical drift, that most of the observed features of the F2-region ionosphere were synthesized by the model. An interpretation of the synthesis that emphasizes the importance of horizontal diffusion at the equator is given. Observations are presented for Mar. 7, 8, and 9, 1970, including the Huancayo magnetograms, which display a close correlation with the drift measurements.

Electromagnetic drifts and neutral air winds effects on F 2 region derived from electron continuity equation, using Jacchia model atmosphere

Traveling ionospheric disturbances at magnetic equator, determining electron concentration profiles by incoherent scatter radar

Further evidence is presented to show that the interpretation of some Ogo 6 retarding potential analyzer (RPA) results in terms of ambient Fe+ ions is correct. The Fe+ ions are observed only within dip latitudes of plus or minus 30 deg, and the reason for this latitudinal specificity is discussed in terms of a low-altitude source region and F region diffusion and electrodynamic drift. It is shown that the polarization field associated with the equatorial electrojet will raise ions to 160 km out of a chemical source region below 100 km but it will do so only in a narrow region centered on the dip equator. Subsequent vertical ExB drift, coupled with motions along the magnetic fields, can move the ions to greater heights and greater latitudes. There should be a resultant fountain of metallic ions rising near the equator that subsequently descends back to the E and D layers at tropical latitudes.

Solar eclipse effects on equatorial F 2 layer by transient solutions of time dependent continuity equation, calculating electron concentrations

It is suggested that convective electric fields in the equatorial ionosphere are generated by neutral winds (zonal or meridional) which act on regions having structure in their field aligned Pedersen conductivity integrals. The conductivity structure is presumably caused by long-lived metallic ions concentrated irregularly below the F layer at altitudes where their collision and gyrofrequencies are comparable. The resulting plasma convection leads to large-scale irregularities and sets up gradients in the electric field that drive other instability mechanisms to produce small-scale irregularities. The mechanism proposed requires a different velocity above and below 200 km for winds in the magnetic east-west direction, but for winds in the magnetic meridian direction, an altitude gradient is not required.