Lactate metabolism and hypocarbic hyperventilation. An experimental study in piglets.

Hyperventilation has been reported to increase blood lactate levels. Uncertainty exists as to whether high lactate levels are caused by increased peripheral release or decreased hepatic uptake. Seven piglets were investigated during controlled normoventilation and 13 piglets during controlled hyperventilation. Blood was drawn from catheters in the femoral artery and vein and in the hepatic vein. Blood flow was measured in the femoral artery by an electromagnetic flow meter and in the splanchnic area by indocyanine green extraction. In addition, repeated muscle biopsies from the hind limb and back muscles were taken. The mean PaCo2 was 5.4 in the normoventilated and 3.5 kPa in the hyperventilated group. The average hind limb oxygen uptake was the same in both groups. The arterial blood lactate concentration was significantly higher (P = 0.03) in the hyperventilated group (2.6 mmol.l-1) as compared to the normoventilated group (1.5 mmol.l-1). However, the release of lactate from the hind limb, and the muscular content of lactate were the same in both groups. Similar and unchanged skeletal muscle contents of glucose-6-phosphate, fructose-1,6-diphosphate, alpha-glycerophosphate, pyruvate, citrate and ATP were recorded in both groups. The splanchnic region did not take up or release lactate at normal PaCO2, but released lactate after 120 minutes of hyperventilation. The results indicate that the increased concentration of lactate during hypocarbic hyperventilation was not caused by an increased peripheral release from the skeletal muscles of the pig but could be caused by an altered splanchnic turn-over of lactate.

Central and regional blood flow during hyperventilation. An experimental study in the pig.

Mechanical hyperventilation not only reduces brain oedema after neurotrauma but also affects the central and systemic circulation. We have, in pigs, measured blood flow in the pulmonary artery, the portal vein and in the femoral artery, as well as estimated the splanchnic blood flow and studied the relative perfusion using the microsphere technique in normo- and hypocarbia during intermittent positive pressure ventilation. A normoventilated control group did not change in cardiac output, portal vein blood flow, splanchnic blood flow and femoral arterial blood flow. Hyperventilation was performed to a PCO2 of 3.0 +/- 0.1 kPa. We found that in pigs ventilated with high tidal volume skeletal muscle blood flow did not change during the first 60 min of hyperventilation but gradually decreased thereafter. Blood flow to the cerebellum decreased soon after the induction of hyperventilation, whereas the cerebral blood flow did not decrease until the second hour of hyperventilation. Cardiac output, splanchnic perfusion and portal vein blood flow all decreased. Myocardial perfusion and arterial blood flow to spleen and kidney decreased while pancreatic and liver arterial blood flows were unaffected. It is concluded that mechanical hyperventilation with low frequency and large tidal volumes reduces the flow to most tissues, where the relative decrease according to microsphere measurements is most pronounced in skeletal muscles, heart muscle and cerebellum. However, the changes in cardiac output and splanchnic blood flow were not observed when hyperventilation was induced by increased frequency, keeping the tidal volume constant.