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PubMed1977

The effect of mild hyperventilation on red cell sodium.

Control subjects voluntarily overbreathed to produce end-tidal PCO2 levels similar to those found in patients suffering from neurotic or endogenous non-retarded depression. Red cell sodium content was found to decrease during overbreathing in all the subjects. The changes were similar to those usually reported for depressed patients. The results imply that red cell sodium levels are in part dependent on respiratory behaviour. They suggest a need for considerable caution in interpreting red cell sodium values from psychiatric patients.

Adult↗
PubMed1986

Regional cerebral blood flow and cerebral metabolic rate of oxygen during hyperventilation in the newborn dog.

Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured during normocarbia and during both moderate and severe hypocarbia. Eighteen newborn mongrel dogs, 1 to 7 days of age, were given pancuronium and ventilated with 70% N2O and 30% O2. The respirator was adjusted to achieve a PaCO2 of 15 torr, all subsequent changes to 25 and 40 torr were made by adjusting the inspired concentration of CO2. The sequence of PaCO2 levels was randomized. CBF was measured by microsphere technique and CMRO2 calculated as arterial-sagittal sinus O2 content difference times hemispheric blood flow. All measurements were made after 30 min at each PaCO2. Total CBF was reduced at a PaCO2 of 25 torr (p less than 0.001), further reduction in PaCO2 to 15 torr resulted in a significant decrease in total CBF (p less than 0.01) compared to 25 torr CO2. All regional cerebral blood flows were reduced at a PaCO2 of 25 torr (p less than 0.001), and most regional CBFs had further significant decreases in flow at a PaCO2 of 15 torr. CMRO2 was 1.28 +/- 0.47 ml/100 g/min at a PaCO2 of 40 torr and fell to 1.09 +/- 0.34 (p less than 0.05) and to 1.04 +/- 0.28 (p less than 0.025) ml/100 g/min at PaCO2 values of 25 and 15 torr, respectively. Cardiac output was calculated to be 169 +/- 71 ml/kg/min at a PaCO2 of 40 torr and fell to 135 +/- 27 (p less than 0.025) and to 127 +/- 36 (p less than 0.005) ml/kg/min at PaCO2 values of 25 and 15 torr, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Hyperventilation restores autoregulation of cerebral blood flow in postictal piglets.

Autoregulation of cerebral blood flow is impaired in the postictal state. This loss of autoregulation may in part be mediated by a rise in perivascular hydrogen ion and carbon dioxide concentration. We hypothesized that hypocarbia with a concomitant reduction in perivascular hydrogen ion and carbon dioxide concentration would restore autoregulation during the postictal state. We studied autoregulation of cerebral blood flow in 13 ventilated, awake 3- to 4-d-old piglets during the postictal state under normocarbic and hypocarbic conditions. During the postictal state, cerebral blood flow was pressure-passive in normocarbic piglets, whereas the relationship between cerebral blood flow and cerebral perfusion pressure was described by a polynomial curve in hypocarbic piglets. Because hypocarbia restores cerebral blood flow autoregulation in postictal newborn piglets, we speculate that the perivascular hydrogen ion and carbon dioxide concentration contribute significantly to the state of cerebral autoregulation in the postictal subject.

Animals↗