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Biomedical subjects

E Eriksson

Publications and source records attributed to E Eriksson.

At least 343 records · Page 19Linked to original sources
PubMed1981

Isokinetic thigh muscle strength after ligament reconstruction in the knee joint: results from a 5-10 year follow-up after reconstructions of the anterior cruciate ligament in the knee joint.

We evaluated the thigh muscle strength using an isokinetic dynamometer in 80 patients 5 to 10 years following anterior cruciate ligament reconstruction. Patients with good results also had good muscle function, both of their flexor and their extensor muscles. Patients with poor results demonstrated reduced muscle strength in both their hamstrings and their quadriceps. Patients with fair functional results demonstrated reduced strength of their extensor muscles compared to their normal leg. However, strength in their operated leg's flexor muscles was unchanged compared to their normal leg. This may be due to the fact that strong hamstring muscles can compensate for some instability of the anterior cruciate ligament.

Adolescent↗
PubMed1981

Fiber type area and metabolic potential of the thigh muscle in man after knee surgery and immobilization.

The muscle atrophy of the quadriceps muscle was investigated in patients after knee operations and immobilization in a long leg plaster cast. Muscle biopsies were taken before operation and after 5 weeks immobilization. The activity of oxidative (SDH) and glycolytic (PFK) enzymes was determined. The fiber area of the different fiber types were measured and enzyme activities in single characterized fibers were analyzed. A selective type 1 atrophy was found with a reduced cross-cut area of the type 1 fiber, and a reduced oxidative enzyme activity occurred in the slow-twitch type 1 fibers. The effect of the muscle tension in the immobilized leg and the inhibiting role of the postoperative pain is discussed.

Adult↗
PubMed1981

Effect of electrical stimulation on human skeletal muscle.

The acute and adaptive effects of electrical stimulation of the quadriceps muscle were investigated in healthy male volunteers. The acute effects, i.e., depletion of phosphagen and glycogen stores and formation of lactate as well as decreases in certain enzyme activities, were similar to those found earlier for intense muscular exercise. Intermittent electrical stimulation for 4 to 5 weeks did not cause any significant changes in enzyme activities, muscle fiber characteristics, or mitochondrial properties. A 4-week period of electrical stimulation resulted in improvements of muscle strength comparable to the results of a corresponding program of voluntary training. However, the effects of electrical stimulation appeared more "position-specific" and less "speed-specific" than those of voluntary training with slow isokinetic contractions.

Adult↗
PubMed1981

Time course of muscle metabolic changes during tourniquet ischemia in man.

Muscle biopsies form the vastus lateralis muscle of the thigh were obtained from 11 patients before and at 15-min intervals following tourniquet application and 15 min after tourniquet release. The total circulatory occlusion time varied from 60 to 120 min. The concentrations of lactate, creatine phosphate and adenosine triphosphate were determined, and the muscle temperature was recorded. During the ischemic period, the lactate concentration increased from 1.9 mmol x kg-1 wet wt to 14.9 mmol x kg-1 wet wt after 90 min of ischemia. During the last 30 min of ischemia, no further increase in lactate concentration was observed. The creatine phosphate concentration decreased from 20.4 to 5.2 mmol x kg-1 wt wt after 120 min of ischemia. The temperature fell rapidly during the first 15 min from 35.9 degrees to 33.5 degrees and was then constant until 95 min when a further small decrease was observed. The adenosine triphosphate concentration did not change significantly during the ischemic period.

Adenosine Triphosphate↗
PubMed1981

Evidence for a growth hormone releasing factor mediating alpha-adrenergic influence on growth hormone secretion in the rat.

The effects of adrenergic receptor agonists on GH secretion were studied in adult, male rats pretreated with reserpine and somatostatin antiserum. Frequent blood samples were obtained from intra-aortic cannulae. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg i.p.) caused a complete suppression of the normal, pulsatile secretion of GH in all animals. Administration of somatostatin antiserum resulted in rapid elevations of plasma GH in reserpine-pretreated rats with peak levels at 30 min. GH levels then fell but remained slightly elevated for the duration of the sampling period (8 h). Apomorphine (0.5 mg/kg i.p.) had no effect on plasma GH levels, whereas clonidine (0.5 mg/kg i.p.) induced release of GH in both antiserum treated and control rats. The results indicate that the alpha-adrenergic influence on the secretion of GH is mediated not by inhibition of somatostatin release but rather by effects on the release of a GHRF.

Animals↗
PubMed1981

Importance of norepinephrine alpha 2-receptor activation for morphine-induced rat growth hormone secretion.

The normal pulsatile secretion of rat growth hormone (rGH) requires intact function in monoaminergic neurons. The importance of norepinephrine (NE) for the secretion is well documented, while the roles of dopamine (DA) and 5-hydroxytryptamine (5-HT) are still a matter of controversy. Morphine, as well as endogenous opioid peptides, are known to stimulate the secretion of GH. Whether the opiate-induced GH release is dependent on monoamines was investigated in the present study. Administration of morphine (10 mg/kg) resulted within 30 min in elevations of plasma rGH exceeding 40 ng/ml. This effect was almost completely antagonized by reserpine (10 mg/kg), given 5 h before morphine and partially antagonized by reserpine (2 mg/kg) administered 25 h before morphine. Administration of tetrabenazine (75 mg/kg) protects monoamine granules from irreversible destruction and counteracted the morphine antagonistic effects of reserpine (2 mg/dg) on rGH secretion indicating that the latter effect is due to blockade of monoaminergic neurotransmission. Pretreatment with either haloperidol (1 mg/kg), p-chlorophenylalanine (PCPA) (300 mg/kg x III) or phenoxybenzamine (10 mg/kg) did not reduce the effect of morphine on rGH release whereas yohimbine (3 mg/kg) effectively prevented it. In reserpine-pretreated animals administration of clonidine (0.5 mg/kg) potentiated the GH releasing effect of morphine. These results indicate that morphine-induced GH release is dependent on activation of postsynaptic NE receptors of the alpha 2-subtype.

Animals↗
PubMed1980

Histamine-mediated delayed permeability response after scald burn inhibited by cimetidine or cold-water treatment.

Scald injury to one ear of the hairless mouse induced significant (P < .05) delayed edema formation in remote, uninjured skin. This remote edema formation was completely inhibited by immediate cold-water treatment of the scalded ear. Cold-water treatment significantly reduced histamine loss from the scalded ear, and the edema-inhibiting effect of the treatment could be mimicked by treating the animal prior to injury with the H2-histamine receptor antagonist cimetidine or a drug that causes histamine depletion. These observations suggest (i) that a histamine-mediated, delayed permeability response occurs after thermal injury that causes remote edema formation and (ii) that one mechanism of remote edema inhibition by cold-water treatment is the prevention of histamine release from thermally injured tissues.

Animals↗
PubMed1980

Ultradian rhythm in rat hypothalamic dopamine levels.

Rats housed under identical conditions were sacrificed with 15-min intervals between 9.30 a.m. and 2.15 p.m. for determinations of DA and NA concentrations in whole hypothalami. The NA levels showed no obvious fluctuation with time, whereas the DAS levels showed an apparent periodicity with a cycle length of approximately 2 hours and with peaks around 11.30 a.m. and 1.45 p.m. A possible relation between this DA rhythm and the secretion of pituitary hormones is discussed.

Animals↗
PubMed1980

In vivo microcirculation of a scald burn and the progression of postburn dermal ischemia.

The homozygous hairless mouse ear provides a reproducible model for the study of the microcirculatory changes of the burn wound during and following a scald burn injury. This model has allowed us to correlate the dynamic changes of the microcirculation to progressive zones of injury, which show an approximate tenfold increase in the area of complete capillary occlusion during the first 48 hours after injury. Platelet thromboembolism appears to be the major factor causing this progression of postburn dermal ischemia. Edema (increased skin water content) was greatest in the burned ear at 6 hours after the burn (20 percent greater than control values); edema of the unburned, contralateral ear was significant at 2 hours after the burn (9 percent greater than control values).

Animals↗