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J A Neubauer

Publications and source records attributed to J A Neubauer.

45 records · Page 3Linked to original sources

Correlation between ventilation and brain blood flow during sleep.

The relationships between brain blood flow (BBF) and ventilation (VI) were studied during sleep in 13 goats. Unilateral BBF was continuously measured with an electromagnetic flow probe; total and regional BBF were assessed by the radioactive microsphere technique in four animals. Interacting changes in VI and BBF occurred during both slow wave (SWS) and rapid eye movement (REM) sleep. During SWS, significant decreases in VI and increases in arterial PCO2 occurred compared to wakefulness. BBF during SWS correlated linearly with arterial CO2 tension (PaCO2); nd the relationship was similar to that for awake goats breathing CO2. During REM sleep, VI was significantly less than both the awake (W) and SWS states due principally to a decrease in tidal volume. BBF during REM sleep was significantly and substantially increased compared with both the W and SWS states; this increase was shared by all brain areas. The increase in BBF during REM sleep was greater than that predicted from changes in PaCO2. In five goats provided with chronic sagittal sinus fistulae, arteriovenous oxygen difference was measured in separate studies and found to be significantly lower during REM sleep compared with W; brain O2 consumption was similar in magnitude in the REM and W states. Thus, the high BBF of REM sleep was also unexplained by an increase of brain metabolic activity. We conclude that, during SWS, increases in BBF are explained by hypoventilation and hypercapnia. In contrast, during REM sleep, BBF is substantially in excess of that expected from PaCO2 or brain metabolism. It is postulated that this excess of BBF during REM sleep could reduce the central chemoreceptor pH relative to that present in SWS. The combination of reduction of sensitivity to CO2 and lower tissue PCO2 during REM sleep makes it likely that the output of the central chemoreceptors during this state is less than that during SWS and wakefulness. This may contribute to the low tidal volume and respiratory irregularities of this sleep period.

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Hypoxic arousal in intact and carotid chemodenervated sleeping cats.

To determine whether the carotid chemoreceptors or hyperpnea are required for arousal from sleep by hypoxia, 14 sleep-deprived cats were studied during slow-wave (SWS) and rapid-eye-movement (REM) sleep. Rapid hypoxia was produced by inhalation of 5% O2 in N2 or 6% CO in 40% O2 by intact cats and 5% O2 in N2 after carotid body denervation. Preliminary studies identified a period of SWS unassociated with spontaneous arousals. In 69 studies during SWS unassociated with spontaneous arousals, arterial O2 saturation (SaO2) values at arousal were: 47.1 +/- 1.5% (mean +/- SE) (5% O2, intact); 48.9 +/- 1.4% (6% CO, intact); and 49.9 +/- 2.0% (5% O2, denervated). During SWS associated with spontaneous arousals, SaO2 values at arousal were 71.6 +/- 1.8% (5% O2, intact). Arousal from REM occurred at significantly lower values: 31.7 +/- 3.9% (6% CO, intact) and 43.5 +/- 2.3% (5% O2, intact). During both SWS and REM, inhalation of 5% O2 by intact animals caused a substantial increase in ventilation while 6% CO did not. We conclude that more severe hypoxia is required for arousal from SWS when studies are done in a period unassociated with spontaneous arousals than from SWS associated with spontaneous arousals. Hypoxic arousal does not appear to require activation of the carotid bodies or hyperpnea.

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Blood flow and relative tissue PO2 of brain and muscle: role of carotid chemoreceptors.

The effects of inspiration of low O2 and/or high CO2 gas mixtures on relative tissue PO2 and perfusion of brain and muscle were studied in 60 pentobarbital-anesthetized spontaneously respiring rats. These animals were studied in intact condition, after administration of phenoxybenzamine hydrochloride, 2 mg/kg, or after bilateral denervation of their carotid bodies. In the intact rats, the relative tissue PO2 ratio of biceps brachii to cerebral white matter always decreased after exposure to the above gas mixtures. This indicated a better maintenance of O2 supply to demand in the brain than in muscle. After either carotid denervation or alpha adrenergic blockade, this change in the ratio was no longer significant. Further, cerebral blood flow responses to these gas mixtures were attenuated (avg + 5.3%) compared to previous work in intact rats. It is concluded that the brain is best protected against hypoxia and/or hypercapnia when the carotid chemoreflex is intact.

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Quantitative determination of regional oxygen consumption in the dog heart.

A micro-Fick method has been developed to measure the O2 consumption of different regions of an organ. The method was tested in isolated dog gracilis muscle and consisted of microspectrophotometric determination of arterial and venous O2 saturation in quick frozen tissue to determine O2 extraction and flow measured with 85Sr-labeled microspheres, with O2 consumption calculated from the product. This was compared to electromagnetically measured flow and O2 extraction determined by Van Slyke or CO-oximeter. The accuracy of the new measurement was at worst 8.7% for O2 consumption over the range tested in a single muscle. In the hearts of anesthetized open-chest dogs, right ventricular O2 consumption, 7.1 +/- 0.9 ml O2/min per 100 g, was significantly lower than left, 11.0 +/- 0.4. This gradient was related to a blood flow difference. Right ventricular base had a 51% lower O2 consumption than right ventricular apex. In the left ventricle, subepicardial O2 consumption, 9.5 +/- 0.7, was lower than that of the subenocardium, 12.1 +/- 0.7. This difference was related to a difference in O2 extraction.

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Effect of alpha and beta adrenergic blockade on oxygen transport in rat skeletal muscle and brain.

The effects of phenoxybenzamine HCl and propranolol HCl, 2 mg/kg, on tissue oxygen tension (PO2), perfusion and small vessel blood content of the cerebral cortex and biceps brachii muscle of anesthetized rats were determined. Perfusion and PO2 were measured polarographically and small vessel blood content was measured with 59Fe-siderophilin-labeled blood. Under control conditions PO2, perfusion and small vessel blood content averaged 15.1 mm Hg., 15.6 ml/min/100 g and 0.91 ml/100 g in brain and 15.6 mm Hg, 13.1 ml/min/100 g and 1.63 ml/100 g in muscle. After phenoxybenzamine adminstration, there was a significant increase in muscle perfusion (17.4%) and decrease in cortical PO2 (9.2%). No other factors changed significantly. Propranolol caused no significant changes in any of the above factors. Arteriolar resistance in skeletal muscle decreased after phenoxybenzamine. Small vessel blood content measurements (an estimate of open capillary density) indicate no effects on precapillary sphincters with either agent. Since some changes in metabolism were indicated with these agents, regional oxygen consumption was calculated from this data.

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