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When retinal ischemia is produced by elevating the intraocular tension, normal vision persists for about 4 sec in healthy subjects breathing air at atmospheric pressure. Persistence times were determined at alveolar oxygen pressures up to 4 atm abs (3,000 mm Hg), obtained by oxygen breathing in a high-pressure chamber. Below an alveolar Po2 of 2 atm the rise in persistence time is relatively small. Above that level the time increases in direct proportion to the increase in alveolar Po2 and may exceed 50 sec at 4 atm. The rise of persistence time follows a pattern similar to that of computed blood oxygen pressure assuming an oxygen extraction of about 3 vol%. high pressure; blood oxygen tension; tissue oxygenation; intraocular tension; retinal circulation; visual blackout Submitted on February 7, 1964

The similarity between spontaneous "pistol-shot" sounds heard over large vessels and the Korotkoff sounds heard distal to a partially inflated blood pressure cuff suggests that a similar mechanism is responsible for their occurrence. Simultaneous records of intravascular pressures and of the sounds demonstrate that the sounds generally precede the major rise in intravascular pressure.These observations cannot be explained by the existing theories of sound production. A possible mechanism based on rapid changes in flow pattern is advanced.D ESPITE continued interest in the nature of sounds that occur along the course of an artery distal to a segment compressed by an inflated cuff at a pressure between systolic and diastolic (Korotkoff sounds),'-" little consideration has been given to the spontaneously occurring "pistol-shot" sounds heard under certain circumstances over the larger arteries. That these spontaneous vascular sounds may be related to the sounds elicited by the cuff is suggested by the occasional indirect blood pressure recording of 'zero diastolic pressure," which implies that sounds continue to be heard distal to the cuff even when the cuff has been completely deflated. This

No abstract

Circulatory, chemical, and ventilatory response factors in Cheyne-Stokes respiration (CSR) were studied by experimental procedures and by mathematical analysis. Hemodynamic, ventilatory, and blood gas patterns in 16 patients with heart disease and CSR (group A) and 16 patients with congestive heart failure (CHF) without CSR (group B) were compared. CO2 and oxygen were administered to group A. The phenomena exhibited by patients with CSR were simulated by a mathematical model.The following conclusions were drawn: (1) Reduced blood flow and respiratory alkalosis were similar in both groups; (2) circulation times, lung to artery, were 29 sec greater than normal in patients with CSR but only 8 sec greater than normal in group B patients; (3) the abnormal CO2 response in CSR, a reduction in threshold and sensitivity, was similar to that in CHF, suggesting that abnormal respiratory mechanics were responsible; (4) mathematical simulation of CSR was possible by appropriate prolongation of circulation time alone; the CO2 response (reduction in threshold and sensitivity) had no significant effect on stability; (5) damping of oscillatory ventilation by CO2 inhalation could be efficiently simulated; (6) CSR with cycle periods less than 50 sec suggests increased neural or chemoreceptor excitability, anemia, or hypoxemia as contributory factors, whereas longer periods suggest primary circulatory factors.