Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound
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Pentobarbital-anesthetized greyhounds were passively hyperventilated using intermittent positive-pressure breathing (IPPV) and the effects of raised airway pressure, accompanied by hypocapnia and then by normocapnia, on liver blood flow and oxygen consumption were studied. Electromagnetic flowmeters were used to measure hepatic arterial, portal venous, and splenic venous blood flow. Studies were carried out at three levels of raised airway pressure, both at normocapnia and hypocapnia. It was found that hypocapnic hyperventilation produced a decrease in portal venous and hepatic arterial blood flow. Normocapnic hyperventilation resulted in a restoration of portal venous blood flow but with a further decrease in hepatic arterial blood flow. A decrease in oxygen consumption with hypocapnia, returning to control values with normocapnia, was seen. It is suggested that the reduction in liver blood flow and oxygen consumption seen with passive hyperventilation is chiefly an effect of hypocapnia and is largely reversed by restoration of normocapnia.Keywords:
Normocapnia
Hypocapnia
Arterial blood
Venous blood
Normocapnia
Hypocapnia
Nitrous oxide
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Arterial blood
Venous blood
pCO2
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Hypocapnia
Normocapnia
Arterial blood
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The effect of hypocapnia on autoregulation of cerebral blood flow (CBF) and the lower limit of autoregulation (LLA) was determined in dogs anesthetized with nitrous oxide (66%) and halothane (0.2%, end-expired concentration). CBF and cerebral vascular resistance (CVR) were determined during both normocapnia and hypocapnia (PaCO2 21-22 mmHg) at control cerebral perfusion pressure (CPP) and after reducing CPP (by hemorrhage) to 80%, 60%, 50%, and 40% of control. At control CPP hypocapnia decreased CBF from 75 +/- 5 to 48 +/- 3 ml.100 g-1.min-1 (mean +/- SEM, P less than 0.05). During both normocapnia and hypocapnia CVR decreased and CBF did not change as CPP was reduced to 60% of control. When CPP was reduced to 50% or 40% of control, CVR remained decreased and CBF fell sharply. The LLA during hypocapnia, 61 +/- 2% of control CPP, was not different than that during normocapnia, 59 +/- 3% of control CPP. Below the LLA the CBF-CPP slopes differed from zero but did not differ between hypocapnia and normocapnia. Hypocapnia does not produce a substantial shift of the LLA, and over the range of CPP values studied here, autoregulatory cerebral vasodilation only partially abolishes hypocapnia-induced cerebral vasoconstriction. The results suggest that when cerebral autoregulation is intact and in the absence of cerebrovascular disease, hypocapnia does not reduce global CBF to a level that is likely to produce ischemia and remains a useful therapeutic treatment so long as CPP remains above the LLA.
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Hypocapnia
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Hyperventilation syndrome
Hypocapnia
Normocapnia
Stroop effect
Polygraph
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Changes in partial pressure of carbon dioxide (PaCO2) are associated with a decrease in cerebral blood flow (CBF) during hypocapnia and an increase in CBF during hypercapnia. However, the effects of changes in PaCO2 on cerebral arterial compliance (Ca) are unknown.We assessed the changes in Ca in 20 normal subjects using monitoring of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV). Cerebral arterial blood volume (CaBV) was extracted from CBFV. Ca was defined as the ratio between the pulse amplitudes of CaBV (AMPCaBV ) and ABP (AMPABP). All parameters were recorded during normo-, hyper-, and hypocapnia.During hypocapnia, Ca was significantly lower than during normocapnia (.10±.04 vs. .17±.06; P<.001) secondary to a decrease in AMPCaBV (1.3±.4 vs. 1.9±.5; P<.001) and a concomitant increase in AMPABP (13.8±3.4 vs. 11.6±1.7 mmHg; P<.001). During hypercapnia, there was no change in Ca compared with normocapnia. Ca was inversely correlated with the cerebrovascular resistance during hypo- (R2=0.86; P<.001), and hypercapnia (R2=0.61; P<.001).Using a new mathematical model, we have described a reduction of Ca during hypocapnia. Further studies are needed to determine whether Ca may be an independent predictor of outcome in pathological conditions.
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Hyperventilation may reverse increases in cerebral blood flow velocity caused by inhalation of nitrous oxide (N2O). This study sought to determine whether inhalation of 50% nitrous oxide after the induction of hyperventilation increases cerebral blood flow velocity as measured by transcranial Doppler ultrasonography. Seven volunteers breathed air/O2 through a modified Circle system at normocapnia followed by air/O2 with hyperventilation, and then N2O/O2 with hyperventilation. Expired gas concentrations were measured in the expiratory limb of the circuit distal to a one-way valve. Hyperventilation reduced end-tidal carbon dioxide from 38 ± 1mmHg to 26 ± 1mmHg. Hypocapnia was maintained during inhalation of N2O (EtCO2=28 ± 1mmHg). Mean cerebral blood flow velocity decreased 34% with hyperventilation (38 ± 4 cm/second versus 59 ± 9 cm/second, p < 0.05) and returned to baseline with the addition of nitrous oxide (58 ± 7 cm/second), despite persistent hypocapnia. The addition of nitrous oxide to the inspired gas mixture after induction of hypocapnia reversed reductions in cerebral blood flow velocity associated with hyperventilation. Potential benefits of induced hypocapnia in patients with intracranial pathology may be offset by the administration of N2O.
Hypocapnia
Normocapnia
Nitrous oxide
Transcranial Doppler
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The purpose of this study is to investigate the effects of hyperventilation upon spinal dorsal horn neuronal single-unit activities under nitrous oxide anesthesia.Eight decerebrated spinal cats with laminectomy were maintained with oxygen and pancuronium bromide. Following the control period of normocapnia, 50% nitrous oxide was administered for 30 minutes after a hypocapnia period of 20-25 mmHg for 20 minutes. The recoveries of activities followed with normocapnia and pure oxygen administration. The changes of spontaneous and evoked activities by the pinching were investigated every 5 minutes after control study.Inhalation of 50% nitrous oxide suppressed the WDR neuronal activities and with hyperventilation the suppressions significantly increased.These results were compatible with clinical reports on the effectiveness of hyperventilation as a maintenance method under N2O anesthesia.
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Nitrous oxide
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Pulmonary O2 uptake (V(O₂p)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate-leg knee-extension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P(ET, CO₂)) ~40 mmHg], i.e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; P(ET, CO₂) ~20 mmHg), i.e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; P(ET, CO₂) ~40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (~5%). The V(O₂p) was measured breath by breath using mass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 V(O₂p) kinetics (τV(O₂p)) was different (P < 0.05) amongst all three conditions (CON, 19 ± 7 s; HYPO, 43 ± 17 s; and NORMO, 30 ± 8 s), while LBF kinetics (τLBF) was slower (P < 0.05) in HYPO (31 ± 9 s) compared with both CON (19 ± 3 s) and NORMO (20 ± 6 s). Similar to previous findings, HYPO was associated with slower V(O₂p) and LBF kinetics compared with CON. In the present study, preventing the fall in end-tidal P(CO₂) (NORMO) restored LBF kinetics, but not V(O₂p) kinetics, which remained 'slowed' relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower V(O₂p) kinetics observed during HYPO.
Hypocapnia
Normocapnia
Respiratory alkalosis
Alkalosis
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Hypocapnia
Normocapnia
Capnography
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