Bengt J. Nilsson

Free Fatty Acids in the Rat Brain in Moderate and Severe Hypoxia

Abstract: The effects of mild, moderate, and severe hypoxia on cerebral cortical concentrations of free fatty acids (FFAs) were investigated in artificially ventilated rats under nitrous oxide anaesthesia. No change occurred during either mild (arterial Po2 35–40 mm Hg) or moderate (Po2 25–30 mm Hg) hypoxia. The effects of severe hypoxia (Po2 about 20 mm Hg) combined with hypotension (mean arterial blood pressure 80–85 mm Hg) varied with the EEG pattern and the tissue energy state. Thus, a major increase in total as well as in individual FFAs occurred first when EEG was severely depressed (almost isoelectric) and energy homeostasis disrupted. On a relative basis the greatest change occurred in free arachidonic acid. It is concluded that hypoxia is associated with an increase in the concentrations of FFAs in brain tissue, provided that tissue oxygen deficiency is severe enough to cause tissue energy failure. However, an increase in FFAs does not invariably accompany minor reductions in the adenylate energy charge (EC) of the tissue.

Endogenous substrates utilized by rat brain in severe insulin-induced hypoglycemia

Abstract: Several previous studies have demonstrated that severe hypoglycemia is accompanied by consumption of endogenous brain substrates (glycolytic and citric acid cycle metabolites and free amino acids) and some have shown a loss of structural components as well, notably phospholipids. In the present study, on paralysed and artificially ventilated rats, we measured cerebral oxygen and glucose consumption during 30 min of hypoglycemic coma (defined as hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity) and calculated the non‐glucose oxygen consumption. In an attempt to estimate the missing substrate we measured tissue concentrations of phospholipids and RNA.

Effects of reduced cerebral blood flow upon EEG pattern, cerebral extracellular potassium, and energy metabolism in the rat cortex during bicuculline-induced seizures

Progressive cerebral ischemia was induced by blood pressure (BP) reduction in rats during status epilepticus, and the sequence of cerebral functional (EEG, extracellular K+ activity) and metabolic (levels of high energy phosphates, glucose, glucose-6-phosphate, lactate, pyruvate, alpha-ketoglutarate) changes were determined. Very moderate reductions of BP were accompanied by tissue lactate accumulation and a decrease of the rate of re-uptake of K+ extruded during discharges. These changes were pronounced at BP about 50 mm Hg, when also the energy state showed some deterioration, and the EEG activity changed from one of bursts and suppressions into single spikes. At BP about 30 mm Hg EEG activity was abolished, but not until a slightly lower BP level was there a severe energy depletion and a massive K+ release, indicating generalized membrane depolarization. The results show an increased susceptibility to ischemia during seizures with changes of membrane pump function, and energy metabolism appearing at moderate reductions of BP. Concomitant decrease of seizure activity delayed to some extent the development of massive energy failure and membrane depolarization.

Cerebral metabolic and circulatory changes in the rat during sustained seizures induced bydl-homocysteine

Sustained, generalized seizure activity was induced in anaesthetized (70% N2O), paralyzed and artifically ventilated rats by i.p. DL-homocysteine thiolactone in a dose of 11 mmol/kg. Epileptic discharges in the EEG were accompanied by marked perturbation of tissue metabolites. There was a fall in phosphocreatine concentration to 40% of control but only moderate changes in adenine nucleotides, a marked rise in lactate concentration, and a pronounced increase in the lactate/pyruvate ratio. Excessive amounts of dihydroxyacetone phosphate (and glyceraldehyde phosphate) accumulated, indicating that depletion of NAD+ occurred. There was marked accumulation of ammonia, glutamine and alanine, and reduction in glutamate and aspartate concentrations. Administration of a subconvulsive dose of homocysteine (7.5 mmol/kg) gave rise to changes in ammonia and amino acids, qualitatively similar to those occurring during seizures. It is concluded that although changes in the metabolites of the energy reserve were mainly caused by the induced seizures, those affecting amino acid concentrations were significantly influenced by accumulation of ammonia, secondary to metabolism of injected homocysteine. Cerebral blood flow (CBF) and oxygen utilization (CMRO2) were measured during sustained seizures. CMRO2 rose to 150% of control, with a corresponding increase in CBF.

Hemodynamic changes in brain caused by local infusion of hyperosmolar solutions, in particular relation to blood-brain barrier opening

The intracarotid infusion of hyperosmolar aqueous solutions such as urea is widely used to transiently open the blood-brain barrier in various animal species. In the present study in the rat an attempt was made to analyze the hemodynamic changes caused by the intracarotid infusions with special reference to possible mechanisms underlying the barrier opening. The cerebral blood flow (as reflected by the cerebral venous outflow rate) intracranial pressure, intracarotid pressure and systemic blood pressure were continuously measured during and following the infusions. It was found that intracarotid infusions of hyperosomolar solutions induce cerebral vasodilation and flow increase. Autoregulation is impaired. Probably, a direct vasodilator mechanism is involved but, depending on volume and osmolarity of the solution used, the changes may be heavily influenced by vascular distention due to intracarotid pressure effect, and by systemic pressure changes. These mechanisms are in common with other methods for barrier opening. The local vasomotor and systemic effects of a hyperosmolar solution of urea, capable of opening the barrier, are not normalized until about 6 min after the administration.

Finding the shortest watchman route in a simple polygon

Abstract. We present the first polynomial time algorithm that finds the shortest route in a simple polygon such that all points of the polygon are visible from the route. This route is called the shortest watchman route, and we do not assume any restrictions on the route or on the simple polygon. Our algorithm runs in worst case O(n6) time, but it is adaptive, making it run faster on polygons with a simple structure.

OPTIMUM GUARD COVERS AND m-WATCHMEN ROUTES FOR RESTRICTED POLYGONS

A watchman, in the terminology of art galleries, is a mobile guard. We consider several watchman and guard problems for different classes of polygons. We introduce the notion of vision spans along ...

Sleep apnea syndrome — An alternative treatment to tracheostomy†

Two patients with obstructive sleep apnea syndrome had polygraphic recordings demonstrating upper airway obstruction and sleep with extremely short sleep latency, severely disturbed nightsleep resulting in sleep deprivation, and excessive daytime sleepiness.

Finding the Shortest Watchman Route in a Simple Polygon

We present the first polynomial-time algorithm that finds the shortest route in a simple polygon such that all points of the polygon is visible from some point on the route. This route is sometimes called the shortest watchman route, and it does not allow any restrictions on the route or on the simple polygon. Our algorithm runs in O(n3) time.

Finding shortest paths in the presence of orthogonal obstacles using a combined L 1 and link metric

The problem of computing shortest paths in obstacle environments has received considerable attention recently. We study this problem for a new metric that generalizes the L1 metric and the link metric. In this combined metric, the length of a path is defined as its L1 length plus some non-negative constant C times the number of turns the path makes.