Leif Berntman

Cerebral Blood Flow and Oxygen Consumption in the Rat Brain during Extreme Hypercarbia

The effects of hypercapnia (PaCO2 80, 160 and 300 torr) on cerebral metabolic rate for oxygen (CMRO2) and blood flow (CBF) were evaluated in paralyzed, mechanically ventilated rats by use of a 133Xe modification of the Kety-Schmidt inert-gas technique. Hypercapnic rats (PaCO, 80 torr) maintained on N2O, 70 per cent, had a sixfold increase in CBF and a 25 per cent increase in CMRO2, which were not prevented by adrenalectomy or decreases in tissue O2 tensions to near-normal values. Further increases in arterial blood CO2 tensions were associated with decreases in CMRO2 to normal (PaCO2 160 torr) or subnormal values (PaCO2 300 torr). In the last situation there was only a threefold increase in CBF. In rats with PaCO2 about 80 torr that were given propranolol, 2.5 mgċkg-1, during N2O anesthesia, there was only a threefold increase in CBF, while CMRO2 decreased to below normocapnic control values. Rats with PaCO2 80 torr given sedative or anesthetic doses of diazepam (ventilated with O2, 30 per cent, in N2) also had decreased CMRO2 values and had a twofold increase in CBF. It is concluded that hypercapnia activates catecholaminergic neurons in the brain, and that this activation increases oxygen consumption. The increase in flow that occurs with hypercapnia is markedly influenced by activity in catecholaminergic neurons.

Effects of nitrous oxide on human regional cerebral blood flow and isolated pial arteries.

BackgroundResults from previous studies on the effect of nitrous oxide (N2O) on the cerebral circulation are conflicting. Early reports claim N2O to have no effect whereas recent findings demonstrate a cerebral cortical vasodilatation during N2O inhalation, but the regional cerebral blood flow (CBF) in the subcortical structures is unknown. MethodsRegional CBF was measured three-dimensionally with single photon emission computer-aided tomography after injection of xenon 133 in 8 spontaneously breathing men (mean age 29.6 yr) during normocapnia and hypocapnia with and without inhalation of 50% N2O. 8 isolated human pial arterial segments were mounted in organ baths. The segments were contracted with prostaglandin F2α and subjected to 30% oxygen and 5.6% carbon dioxide in nitrogen or N2O. ResultsNormocapnic young men had a global CBF of 55 ± 4 ml · 100 g−1. min−1. Decreasing end-tidal CO2 tension by 1.3 kPa (9.3 mmHg) reduced CBF uniformly, with a decrease in global CBF to 45 ± 2 ml · 100 g−1. min−1 (P < 0.0001). During normocapnia, inhalation of 50% N2O increased mean CBF to 67 ± 7 ml · 100 g−1. min−1 (P < 0.0001). Inhalation of 50% N2O during hypocapnia increased mean CBF to 63 ± 5 ml · 100 g−1. min−1 (P < 0.0001). During N2O inhalation there was no significant difference in mean CBF between normo- and hypocapnia. However, during hypocapnia, but not during normocapnia, N2O inhalation significantly changed the distribution of regional CBF (P < 0.0001). Compared with hypocapnia without N2O, flow increased through the frontal (143%), parietal (140%) and temporal (133%) regions as well as through insula (151%), basal ganglia (145%) and thalamus (133%). In isolated human pial arteries, addition of N2O changed neither basal tension, nor the contraction elicited by prostaglandin F2α. ConclusionsInhalation of 50% N2O increased global CBF mainly by augmenting flow in frontal brain structures. In contrast, changes in carbon dioxide without N2O affected CBF uniformly in the brain. The uneven change in distribution of the CBF when N2O was added during hypocapnia, the reduced carbon dioxide response, and the lack of effect of N2O on isolated human pial arteries suggest that N2O may increase metabolism in selected brain areas.

Effects of hypotensive treatment with α2‐agonist and β1‐antagonist on cerebral haemodynamics in severely head injured patients

Therapy of post‐traumatic brain oedema often includes preservation of high arterial blood pressure to avoid secondary ischaemic injuries to the brain. This practice can be questioned since high arterial blood pressure may aggravate brain oedema through raised hydrostatic capillary pressure, causing fluid filtration across the damaged blood‐brain barrier. This latter view is in agreement with our clinical experience and therefore hypotensive therapy with an α2‐adrenergic agonist (clonidine) and a β1‐adrenergic antagonist (metoprolol) has become part of our treatment protocol for severely head injured patients to decrease the post‐traumatic brain oedema. The present study is an attempt to analyse whether there are any direct local cerebrovascular effects of the hypotensive agents used, which also might influence intracranial pressure. Severely head injured patients were investigated. Heart rate, mean arterial blood pressure, intracranial pressure, cerebral blood flow and arterio‐venous difference in oxygen content were measured before and after a bolus dose of clonidine (six patients) and metoprolol (nine patients).

Restoration of Oxygen Uptake and Blood Flow in the Rat Cerebral Cortex after Halothane Anaesthesia

Halothane decreases both the certal blooi Row (CBF) and the cerebral metabolic rate for oxygen (CMRo2) when given in anaesthetic doses. A recent report (Gjedde & Hindfelt 1975) suggests that when halothane is administered to rats for 1 hour, CBF and CMRo2 are depressed by about 30 and 40%, respectively, for as long as 4 hours after discontinuation of the halothane anaesthesia. In the present study rats were anaesthetized with 1% halothane for 1 hour, and CBF and CMRo2 were measured at the end of a 30 min recovery period, during which 70% N2O was administered. Comparison with animals maintained on 70% N2O throughout the entire 90 min period showed that previous halothane anaesthesia had no effects on CBF or CMRo2.

Influence of “Lytic Cocktail” on Blood Flow and Oxygen Consumption in the Rat Brain

The influence of a sedative dose of “lytic cocktail” (chlorpromazine, promethazine and pethidine) on cerebral blood flow (CBF) and oxygen consumption (CMRo2) was tested in artificially ventilated rats, maintained on either 70% N2 or 70% N2O. When given alone, the lytic cocktail had no significant effect on CBF or CMRo2. However, in the presence of nitrous oxide there was a 25% reduction in blood flow and oxygen consumption.