[Use of indwelling catheters in long term care is still low].
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Biomedical subjects
Publications and source records attributed to B Nyström.
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During neurosurgery the freshly secreted extracellular fluid (ECF) from the choroid plexus was sampled with small pieces of application paper in three patients with intractable epilepsy. The samples were analyzed for free amino acids and for soluble proteins. The results were compared with corresponding data on extracellular fluid from the brain surface obtained with dialysis-perfusion as well as with the cerebrospinal fluid (CSF) acquired by lumbar punction. The dialysis data were calibrated against the paper results. The choroid plexus secretion had a high concentration of transthyretin as well as of an unidentified protein with an isoelectric point of 7.4. The cortical ECF exhibited high concentrations of tau-globulin and gamma-trace protein. Among the amino acids, glutamine had lower concentration in the choroid plexus secretion and higher concentrations in the ECF of the brain compared to the CSF. The amino acid derivative ethanolamine exhibited a similar pattern. This was interpreted to demonstrate that these compounds enter the CSF from the brain tissue. In contrast, alanine, serine, and taurine had a lower concentration in the CSF than in the plexus secretion which suggests that they are removed from the CSF by brain tissue.
As part of a series of experimental investigations of the effects of various pharmacological agents on the outcome of compressive spinal cord trauma in the rat, the time course of the cell changes in the cord at the site of and distal to the compression was studied at the light microscopic level. The degree of compression used with the present model results in a transient paraparesis that recovers almost completely over a period of 3 weeks as judged by the inclined plane technique. The most significant morphological findings were as follows. Initially (1 and 24 h after the impact) there was pronounced swelling and hemorrhage at the compression site, chiefly in the gray matter of the cord. On day 4 there was severe necrosis in the same region, with numerous macrophages and leukocytes. Rats killed after 21 days showed either minor residual signs of necrosis or essentially normal tissue architecture. Surprisingly, necrosis with delayed onset also developed in the dorsal columns, involving the pyramidal tracts. This necrosis was detected in animals killed after 9 and 21 days but not in those observed after 4 days or earlier. The longitudinal tracts of the white matter showed reduced staining in paraffin sections of the compression site. Epon sections revealed splits in the myelin sheaths and enlarged periaxonal spaces as early as 1 h after the impact. The alterations in the longitudinal tracts persisted throughout the 21-day observation period and extended down to L2-L4. There was gradual functional recovery, documented by the inclined plane test. Preinjury values were almost reached on day 21, although the cord still showed some morphological damage. In individual animals, no relation was found between degree of function as tested by inclined plane and extent of morphologic injury. Additional functional and morphological methods obviously are needed in future investigations of the effects of treatments on the outcome of compressive spinal cord injury.
Spinal cord blood flow (SCBF) and motor performance on the inclined plane were measured up to 9 days after a reversible spinal cord compression injury in 49 Sprague-Dawley rats. A load of 35 g on 11 mm2 of the thoracic spinal cord for 5 minutes caused transient paraparesis with a decrease in the capacity angle on the inclined plane from 62 +/- 1 degree (mean +/- SEM) before injury to 33 +/- 1 degree on Day 1, 45 +/- 2 degrees on Day 4, d and 54 +/- 3 degrees on Day 9. SCBF was measured by the [14C]iodoantipyrine method, and in gray matter there was a decrease from 78.4 +/- 2.3 ml/min/100 g of tissue in uninjured animals to 33.7 +/- 1.5 ml/min/100 g of tissue on Day 1 after injury, increasing to 50.1 +/- 2.0 on Day 4 and to 70.5 +/- 2.7 ml/min/100 g of tissue on Day 9. At the corresponding times, the SCBF values in white matter were 14.5 +/- 0.5, 6.7 +/- 0.5, 10.2 +/- 0.6, and 13.4 +/- 0.6 ml/min/100 g of tissue, respectively. The animals in another group were loaded with 25 g for 5 minutes and on Day 1 exhibited a capacity angle of 43 +/- 2 degrees while the SCBF values for gray and white matter were 55.1 +/- 2.0 and 11.1 +/- 0.4 ml/min/100 g of tissue, respectively; thus, the results in this group were similar to the values on Day 4 in the animals loaded with 35 g.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of methylprednisolone (MP) on neurologic recovery and spinal cord blood flow (SCBF) was investigated up to 4 days after a spinal cord compression injury in rats. The injury was produced at midthoracic level by applying a load of 35 g on a 2.2 x 5.0 mm compression plate for 5 min, which resulted in transient paraparesis. MP was given as a bolus dose of 30 mg/kg i.v. 60 min after injury (n = 20) and controls were given saline (n = 10). The motor performance was assessed daily as the capacity angle on the inclined plane and SCBF was measured by 14C-iodoantipyrine autoradiography on Days 1 or 4. On Day 1 the capacity angle was reduced from about 63 degrees preoperatively to 33 +/- 2 degrees (mean +/- SEM) in the control group and to 50 +/- 1 degrees in the group treated with MP (p less than 0.05). Thereafter there was a slight improvement in both groups, but the difference persisted throughout the observation period. On Day 4 both gray and white matter SCBF was better preserved in MP-treated animals than in the control group (59 +/- 4 versus 49 +/- 3 ml/min/100 g tissue for gray matter and 13.6 +/- 0.6 versus 10.7 +/- 0.8 ml/min/100 g tissue for white matter). Posttraumatic treatment with MP, thus, improved both the neurologic recovery during the first 4 days and SCBF as measured on Day 4. It is speculated that the effect of MP is at least partly exerted on the vascular bed.
We assessed wound, air and operative field contamination at 50 total hip operations, performed in a zonal ventilation system. Theatre staff wore either a specially designed polypropylene non-woven coverall or conventional cotton shirt and trousers. The surgeons wore partially impermeable operating gowns. The polypropylene coverall was associated with significantly lower air and wound counts. The coverall was warmer than cotton but judged to be acceptable. The combined use of zonal ventilation and the coverall achieved ultra-clean air conditions.
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The relations between degree of thoracic spinal cord compression causing myelographic block, reversible paraparesis, and extinction of the sensory evoked potential on one hand, and spinal cord blood flow on the other, were investigated. This was done in rats using the blocking weight-technique and 14C-iodoantipyrine autoradiography. A load of 9 g caused myelographic block. Five minutes of compression with that load caused a reduction of spinal cord blood flow to about 25%, but 5 and 60 minutes after the compression spinal cord blood flow was restored to 60% of the pretrauma value. A load of 35 g for 5 minutes caused transient paraparesis. Recovery to about 30% was observed 5 and 60 minutes thereafter. During compression at a load of 55 g, which caused almost total extinction of sensory evoked potential and irreversible paraplegia, spinal cord blood flow under the load ceased. The results indicate that myelographic block occurs at a load which does not cause irreversible paraparesis and that a load which permits sensory evoked potential to be elicited results in potentially salvageable damage.
The role of a calcium-mediated increase in vascular resistance and of vascular damage caused by polymorphonuclear leukocytes (PMNLs) in the development of neurologic deficit and disturbance of spinal cord circulation following spinal cord compression was studied in the rat. Spinal cord injury was induced by 5 min of compression with a load of 35 g on a 2.2 X 5.0 mm compression plate. This caused transient paraparesis. The rats received either the calcium receptor antagonist nimodipine or an anti-rat neutrophil serum (ANS). Nimodipine was infused i.v. for 4 h in an amount of 1.5 micrograms/kg/min starting 60 min after trauma. The number of circulating PMNLs was depleted by intraperitoneal injection of an ANS raised in sheep given 12 h before trauma. This caused a reduction to about 2% of the pre-ANS value. Controls received saline or normal sheep serum. The motor performance was assessed daily on the inclined plane. On day one, the day after injury, the capacity angle had decreased from about 63 degrees preoperatively to close to 32 degrees in the experimental groups. There was then a slow improvement in both the control and experimental groups and on day 4 the capacity angle was close to 43 degrees in all 3 groups. Spinal cord blood flow, as measured with the 14C-iodoantipyrine autoradiography method, was similar in all groups on day 4. As neither the neurologic dysfunction nor the spinal cord blood flow was affected by post-trauma treatment with nimodipine or pretreatment with ANS, the possibility that calcium-mediated vasoconstriction or PMNLs play a role in the development of posttraumatic neurologic disability was not supported by this study.
The ability of thyrotropin releasing hormone (TRH) or naloxone to reduce the motor function deficit and to improve the spinal cord blood flow (SCBF) was investigated in a rat spinal cord compression injury model. Spinal cord injury was induced by compression for 5 min with a load of 35 g on a 2.2 x 5.0 mm sized compression plate causing a transient paraparesis. One group of animals was given TRH, one group naloxone and one group saline alone. Each drug was administered intravenously as a bolus dose of 2 mg/kg 60 min after injury followed by a continuous infusion of 2 mg/kg/h for 4 h. The motor performance was assessed daily on the inclined plane until Day 4, when SCBF was measured with the 14C-iodoantipyrine autoradiographic method. It was found that neither TRH nor naloxone had promoted motor function recovery or affected SCBF 4 days after spinal cord injury.
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Extracellular proteins were collected continuously from the hippocampus of the rabbit by slow perfusion of a protein-permeable thin tubing. After pulse labelling with radioactive amino acids via the tubing a rapid appearance of labelled proteins was seen in the extracellular fluid. The half-life of the proteins in the extracellular space varied between 15 min and 2 h. Protein fractions were separated with gel electrophoresis or HPLC. The extracellular fraction differed distinctly from intracellular proteins with respect to the labelling pattern.
One hundred and one patients, nursed in an intensive care unit for at least 24 h, were monitored for bacterial colonization and infection. The infection rates were similar to those in other reports. Patients were not generally colonized with common environmental strains in the unit. Bacterial dissemination between patients was uncommon. No gentamicin resistant gram negative or Staphylococcus aureus strains were observed, nor methicillin resistant Staphylococcus aureus strains. The hypothesis that these favourable conditions are partly related to the excellent isolation and barrier nursing facilities in the unit cannot be fully substantiated.
Previous reports on early-induced protein-calorie malnutrition (PCM) in rats have indicated alterations in the concentration of free amino acids and of protein synthesis in the brain. Recently it was shown that early-induced protein deprivation (PD) retards the development of thermoregulation. This resulted in a failure to maintain a normal rectal temperature after short exposure to room temperature (+22 degrees C) still at the age of 20-25 days corresponding to changes seen in normal rats at an age of 10-15 days. In the present study, 20-day old PD and normal rats where examined with regard to the effect of exposure to room temperature on brain temperature and on brain free amino acids. The results show a similar reduction in brain and rectal temperature of the PD rats occurring within 30 minutes after exposure to room temperature. The reduction was in the range of 5 degrees C. PD rats kept in room temperature for 5 hours and then allowed to recover at 32.5 degrees C showed a slow increase in brain and rectal temperature but normal temperatures were not reached even after 1 hour. The concentration of free amino acids in the brain was examined in rats kept for 1 hour at room temperature or at 32.5 degrees C. In the PD rats kept at 32.5 degrees C, free aspartate and glutamate were reduced whereas taurine, GABA and glycine were increased as compared to their corresponding control rats. As a result of the reduced brain temperature in PD rats exposed to room temperature there was a reduction in free asparagine.(ABSTRACT TRUNCATED AT 250 WORDS)
In a prospective, randomized, double-blind, placebo-controlled study involving 27 surgical units in six European countries, the effect of preoperative whole-body bathing on two occasions with a detergent containing chlorhexidine (CHX+) on the incidence of wound infection in elective, clean surgery was compared with two bathings with a detergent without chlorhexidine (CHX-). In the CHX+ group 2.62% of 1413 patients and in the CHX- group 2.36% of 1400 patients subsequently became infected. The infection rate in the CHX+ group was 1.11 times that in the CHX- group with 95% confidence limits ranging between 0.69 and 1.82. Consequently, bathing patients twice preoperatively with chlorhexidine-detergent did not reduce the incidence of infection of clean wounds.
A technique for producing graded spinal cord compression injuries in rats is described. A metal plate 2.2 x 5.0 mm in size is applied to the exposed spinal dura and loaded with weights. Neurological function is tested postoperatively on an inclined plane. Reading of the maximal angle of rat performance on this plane was found reproducible on comparison between different observers. Laminectomy per se had a minimal effect on the performance. Compression of 35 g for 5 min caused a pronounced but incomplete injury, with almost total recovery within 14 days and with no difference between animals on artificial respiration and those breathing spontaneously. Animals whose spine was fixed during the compression had a better outcome than those without such fixation.