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N Dahlgren

Publications and source records attributed to N Dahlgren.

5 recordsLinked to original sources
PubMed1990

Local cerebral blood flow in spontaneously breathing rats subjected to graded isobaric hypoxia.

Local cerebral blood flow (l-CBF) was measured with an autoradiographic technique in spontaneously breathing rats exposed to air or gas mixtures of O2 and N2, giving inspired oxygen fractions (FiO2) ranging from 0.21 to 0.07. The arterial O2 tension (PaO2) changed from 10.9 +/- 0.3 (FiO2 0.21) to 3.9 kPa (FiO2 0.07) (82 +/- 2 to 29 mmHg). Hypoxia caused hyperventilation, and the arterial CO2 tension (PaCO2) fell from 5.21 +/- 0.05 kPa (FiO2 0.21) to 3.27 kPa (FiO2 0.07) (39.1 +/- 0.4 to 24.5 mmHg). The hyperventilatory response was markedly augmented when changing FiO2 from 0.13 to 0.11, causing a fall in PaCO2 of 0.75 kPa and a shift in arterial pH from 7.45 +/- 0.01 (FiO2 0.13) to 7.54 +/- 0.01 (FiO2 0.11). The l-CBF response to hypoxia was found to be biphasic for all the observed regions. At FiO2 0.13, l-CBF was measured about 75% above control but at FiO2 0.11, only 30% above control. A further reduction in FiO2 to 0.07 caused a marked increase in l-CBF, at least 240% of control; however, the applied CBF technique did not admit quantitation. These results suggest that the mechanisms controlling the cerebrovascular response to hypoxia and changes in arterial CO2 tensions are different. The results also indicate that hyperventilation might be harmful to the patient suffering from acute hypoxia.

Animals↗
PubMed1979

Local versus regional cerebral blood flow in the rat at high (hypoxia) and low (phenobarbital anesthesia) flow rates.

Local cerebral blood flow (CBF) was measured in rats, using an autoradiographic technique with 14C-iodoantipyrine as diffusible tracer, in situations with low, normal and high flow rates (phenobarbital anesthesia, analgesia with 75% N2O, and hypoxia, respectively). A comparison of the results with previous data obtained in conscious rats (Sakurada et al. 1978) demonstrates that 75% N2O moderately reduces local CBF in some, but not all, cortical and subcortical areas, that phenobarbital anesthesia reduces local CBF to between 30 and 65% of (conscious) control, and that pronounced hypoxia (arterial P02 about 25 mmHg) increases local CBF 3- to 4-fold. A comparison of the values obtained for cortical structures with those previously measured with a technique based on the Fick principle shows that the autoradiographic technique gives similar values at low and normal flow rates but that it moderately underestimates CBF at high flow rates, probably due to diffusion limitation.

Anesthesia, General↗
PubMed1979

Increase in local cerebral blood flow induced by circulating adrenaline: involvement of blood-brain barrier dysfunction.

The influence of intravenous infusion of adrenaline (8 micrograms.kg-1.min-1) upon local cerebral blood flow (CBF) in paralyzed and artifically ventilated rats was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. At this dose, adrenaline invariably increased local CBF even though blood pressure was close to normal at the time of the CBF measurement. In average, local CBF increased to 400% of control. In 6 of 9 animals the increase in flow was inhomogenous with randomingly distributed areas of very high flow rates. Experiments with i.v. administration of Evans blue prior to infusion of adrenaline showed that areas of Evans blue extravasation appeared in 3 of 4 animals. Although areas of extravasation often corresponded to areas of high flow rates the former were much more circumscribed. Furthermore, very high flow rates were found in areas showing no sign of blood-brain barrier dysfunction. It is concluded that the increase in CBF was at least partly due to a pressure-mediated passage of adrenaline across the blood-brain barrier but that such a passage can occur in the absence of macroscopically visible extravasation of protein.

Animals↗
PubMed1978

Influence of intravenously administered catecholamines on cerebral oxygen consumption and blood flow in the rat.

In order to study effects of catecholamines on cerebral oxygen consumption (CMRo2) and blood flow (CBF), rats maintained on 75% N2O and 25% O2 were infused i.v. with noradrenaline (2, 5, or 8 microgram.kg-1.min-1) or adrenaline (2 or 8 microgram.kg-1.min-1) for 10 min before CBF and CMRo2 were measured. In about 50% of animals infused with 2--8 microgram.kg-1.min-1 of noradrenaline, CMRo2 (and CBF) rose. However, there was no dose-dependent response, and CMRo2 did not exceed 150% of control. The effects of noradrenaline in a dose of 5 microgram.kg-1.min-1 on CMRo2 and CBF were blocked by propranolol (2.5 mg.kg-1). In animals infused with adrenaline (8 microgram.kg-1.min-1) CMRo2 was doubled and, in many, CBF rose 4- to 6-fold. It is concluded that, when given in sufficient amounts, catecholamines have pronounced effects on cerebral metabolism and blood flow, the effects of adrenaline on CMRo2 and CBF resembling those observed in status epilepticus.

Animals↗