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Biomedical subjects

B Nilsson

Publications and source records attributed to B Nilsson.

At least 685 records · Page 38Linked to original sources
PubMed1977

Taste acuity of the human palate. I. Studies with electrogustometry and taste solutions on young adults.

The purposes of the study were to determine whether or not taste perception was present in the area which would have been covered by the base plate of a full upper denture and, if taste perception was present there, to compare its strength to that of the remainder of the soft palate and of the apex and base of the tongue. The taste acuity of 32 dental students was measured at the apex and base of the tongue and on the hard and soft palate using two methods, an electric current and sweet, salty, sour and bitter test solutions, the latter in order to determine whether or not there exist differences in the perception of the different taste modalities in these areas. No taste perception could be demonstrated on the hard palate except in the region close to the border between the hard and soft palate, where the threshold values were very high compared with those for the soft palate immediately behind this border and for the tongue. The inter-individual range of the threshold values for the soft palate was very large. Further studies on the taste acuity of the human palate and its role in the total perception of taste are indicated.

Adult↗
PubMed1977

Experimental head injury in the rat. Part 1: Mechanics, pathophysiology, and morphology in an impact acceleration trauma model.

Impact acceleration was used to elicit cerebral concussion in the albino rat. The pathophysiological response and morphological damage from the concussion were studied in groups of animals. The animals were grouped according to impact velocity (6-11 m/sec), and the threshold and different degrees of the concussive response were established. The concept of concussion as primarily a neuronal, functional disturbance was confirmed. However, this reaction was readily influenced by respiratory and circulatory changes, and morphological damage. Defined reactions could be elicited in groups of animals according to impact velocity. Thus, the model appeared well standardized for further studies of concussion pathophysiology, expressed in terms of cerebral energy metabolism and blood flow.

Acceleration↗
PubMed1977

Exerimental head injury in the rat. Part 2: Regional brain energy metabolism in concussive trauma.

A standardized model of acceleration concussion in the rat was used for the study of cerebral energy metabolism during the acute concussive reaction. Impact velocities of 7 and 9 m/sec were used, and the cerebral metabolic state was determined 1, 4, and 15 minutes after the impact. A concussive response could be sustained with a normal energy state in the tissue, but with the more intense reaction to a 9 m/sec impact, energy depletion usually occurred. At 1 minute these changes were most pronounced in the brain-stem regions. At 4 minutes the reactions were more varied but a progression usually occurred during this time, while at 15 minutes restitution was indicated. Hypoxia due to neurogenic pulmonary edema aggravated the state. The findings are compatible with a high metabolic rate during concussion, but progressive changes indicate the rapid appearance of complicating factors, including hypoxemia and probably also ischemia.

Adenine Nucleotides↗
PubMed1977

Experimental head injury in the rat. Part 3: Cerebral blood flow and oxygen consumption after concussive impact acceleration.

Cerebral blood flow (CBF) and oxygen consumption (CMRO2) were determined during timmediate posttraumatic period in rats subjected to concussive impact acceleration. According to previous studies an impact of 9 m/sec velocity elicited typical and marked symptoms of experimental concussion and often a prolonged comatose state, accompanied by cerebral metabolic signs of energy failure. During the immediate concussive response there was an increase of the CBF, followed within the next few minutes by a decrease to about one-third of normal flow, and then by a tendency toward normalization of flow 20 to 40 minutes posttrauma. Simultaneous measurements of cerebral oxygen extraction indicated an increase of the CMRO2 during the first minute. During the ischemic phase oxygen extraction increased but the lowest CBF values were only partially compensated for, and normal oxygen availability could not be maintained. The combined data, including cerebrospinal fluid pressure measurements, indicated primary cerebrovascular effects of the concussive trauma. These vasomotor effects may induce critical cerebral ischemia and thus profoundly influence posttraumatic cerebral function, and cause irreversible damage.

Animals↗
PubMed1977

Rate of cerebral energy consumption in concussive head injury in the rat.

The metabolic rate was determined in the rat brain during the immediate concussive response to standardized impact accelerations of 7 and 9 m/sec velocity. In one series, the metabolic state was determined in freeze-clamped cortical and brain-stem tissue 20 seconds after the impact. The metabolic rate was calculated from the rate of energy depletion in the adjacent unclamped tissue during 10 seconds of total ischemia. The freeze-clamping procedure per se was shown to enhance the metabolic rate probably by inducing mechanical excitation. In another series, in situ freezing was used for tissue sampling in the same situation. A 10-second period of heart standstill induced a standardized period of ischemia. During the acute concussive response to impact acceleration at 7 m/sec velocity, there was an increase of the metabolic rate in the brain stem. A more intense concussive impact at 9 m/sec velocity further enhanced this reaction and also involved the cortex. It is concluded that the basis of the immediate concussive response is a mechanically elicited neuronal excitation. This may lead to energy depletion unless the increased metabolic demands are met.

Adenine Nucleotides↗
PubMed1977

[Hypoxia of the central nervous system in rats during acceleration brain injury].

The authors present the results of investigations of the effects of acceleration craniocerebral injury in rats on PaO2 and resulting central nervous system hypoxia. PaO2 fall by 30% of the control value occurred in 25% of rats and in the group of most severe injury this fall amounted to 36% already 1 minute after injury. After 4 minutes this fall rose to 70%. In all animals with injury-induced hypoxia autopsy examination demonstrated on gross inspection acute pulmonary oedema: the weight of the lungs and the lung-body weight index were nearly twice as high as in the animals without oedema. The authors discuss the possible pathological mechanisms of acute neurogenic lung oedema and reach the conclusion that it may be due to excessive, pathological discharge of the sympathetic nervous system. Since the intracranial part of the vascular bed in rats reacts to acceleration trauma with acute spasm, it may be that this factor, together with central nervous system hypoxia caused by neurogenic lung oedema may play a significant role in traumatic secondary central nervous system injury. This risk occurs also in humans with severe brain stem trauma.

Acceleration↗
PubMed1976

Cerebral blood flow and metabolic rate early and late in prolonged epileptic seizures induced in rats by bicuculline.

Cerebral blood flow (CBF) and cerebral metablic rate for oxygen (CMRO2) have been studied during sustained epileptic seizures induced by bicuculline (1-2 mg/kg, i.v.) in paralysed Wistar rats, artificially ventilated with nitrous oxide/oxygen. CBF was determined by venous outflow collection, and by 133Xe desaturation, using sagittal sinus blood (for cerebral cortical flow) or retroglenoid venous blood (for 'whole brain' flow). The procedure employed ensured that arterial oxygenation remained normal and blood glucose concentration was normal or high throughout the seizure. Arterial hypotension was prevented by the infusion of donor blood. CBF increased concurrently with seizure onset, reaching a maximum nine times higher than control value after 15-60 s. This was due to a marked rise in mean arterial pressure (to greater than 180 torr) and a dramatic fall in cerebrovascular resistance to less than 15 per cent of control). Subsequently, with decreasing blood pressure, CBF slowly diminished, being more than four times higher than control at 20 min, and slightly less than three times higher than control at two hours. The different procedures for measuring CBF gave closely similar results. A threefold increase relative to control CMRO2 (7-6 ml/100 g-1/min-1 for 'whole brain,' and 10-2 ml/100 g-1/min-1 for cerebral cortex) was measured after 1-20 min of seizure activity (utilizing either the venous outflow or the 133Xe desaturation procedure for CBF determination). After two hours of seizure activity CMR02 was still more than twice as high as the control. This high metabolic rate during sustained seizure activity will increase the susceptibility of the brain to 'ischaemic' damage during prolonged seizures in man in which an additional metabolic stress may be imposed by cerebral hypoxia, arterial hypotension, hyperpyrexia or hypoglycaemia.

Animals↗
PubMed1976

A method for determining blood flow and oxygen consumption in the rat brain.

Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were measured in rats under nitrous oxide anaesthesia, using a 133Xenon modification of the Kety and Schmidt inert gas technique with sampling of cerebral venous blood from the retroglenoid vein. Extracerebral contamination of the venous blood sampled was studied by comparing the rates at which the activity of 133Xenon decreased in blood and tissues. Contamination was avoided by gentle compression of the contralateral retroglenoid vein during sampling. CBF and CMRo2 of the rat brain were 80+/-2 and 7.6+/-0.2 ml-(100g)-1-min-1, respectively. These values are about 25% lower than those previously obtained for cerebral cortical tissue under similar conditions. Induced hypercapnia (Paco2 about 70 mm Hg) or hypocapnia (Paco2 15-20 mm Hg) gave rise to expected changes in CBF but did not alter CMRo2. The CMRo2 of the rat brain is at least twice that of the human brain. This species difference, which is similar to that previously reported for the oxygen uptake of cerebral tissue in vitro, probably reflects on inverse relationship between brain weight and neuronal packing density.

Animals↗
PubMed1976

Preliminary results from a swedish multicenter trial of a new low dose combined oral contraceptive.

Neovletta, a new combined low estrogen -- low progestogen oral contraceptive was investigated in 226 women over 1921 cycles at three different clinics. This report constitutes a preliminary evaluation of a large scale multicenter study being conducted in Sweden. No pregnancy was reported during the observation period. The length of menstrual cycle was generally 28 days and withdrawal bleeding during the tablet free period was missed in only 0.9 per cent of the cycles. The duration of menstruation was shortened by about one day. The amount of menstrual flow, as registered by the women, showed a reduction during treatment. Spotting and breakthrough bleeding were increased during the first three treatment cycles, whereas from the fourth to 12th cycles the incidence of these bleeding irregularities was not much different from pretreatment values. A total of 46 women (20 per cent) discontinued treatment due to side-effects of which bleeding irregularities constituted the major problem.

Adult↗
PubMed1976

Build-up effects at air cavities measured with thin thermoluminescent dosimeters.

The build-up and build-down situation around air cavities of various size in a polystyrene phantom was evaluated by measurements with LiF-Teflon disks with a thickness of about 1.6 X 10(-2) kg/m2. The measurements demonstrate that when irradiating with two opposed beams the surface dose at the cavity (depth 39 mm) is 74% of the maximum dose for 60 Co, 77% for 6 MV and 87% for 42 MV roentgen radiation.

Air↗