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Biomedical subjects

F J Hans

Publications and source records attributed to F J Hans.

28 records · Page 2Linked to original sources

Nosocomial infections in a neurosurgery intensive care unit.

In order to identify overall and site-specific nosocomial infection (NI) rates in patients receiving neurosurgical intensive care therapy, a prospective study was started in February 1997 in the eight-bed neurosurgical ICU of the University Hospital of Freiburg, Germany. Case records were reviewed twice a week, all microbiology reports were reviewed and ward staff was consulted. NI were defined according to the CDC-criteria and were categorised into specific infection sites. Within 20 months, 545 patients with a total of 5,117 patient days were investigated (mean length of stay: 9.4 days). 113 NI were identified in 90 patients (72 pts. with one, 13 with two and 5 with three infections, respectively). A moderate to high overall incidence (20.7/100 pts.) and a moderate incidence density (22.1/1,000 patient days) of NI in the neurosurgical ICU could be documented; these figures are well within the range of published data. Site specific incidence rates and incidence densities were: 1 bloodstream infection per 100 patients (0.9 central line-associated BSIs per 1,000 central line-days), 9 pneumonias per 100 patients (15.1 ventilator-associated pneumonias per 1,000 ventilator-days), 7.3 urinary tract infections per 100 patients (8.5 urinary catheter-associated UTIs per 1,000 urinary catheter-days). Additionally, 1.1 cases of meningitis, 0.7 brain abscesses/ventriculitis, and 1.7 other infections (surgical site infection, bronchitis, catheter related local infection, diarrhoea) were documented per 100 patients, respectively. 14.6% of isolated pathogens were E. coli, 10.2% enterococci, 9.6% S. aureus, 6.4% CNS, 6.4% Klebsiella spp., 5% Enterobacter spp. and 5% Pseudomonas spp. In 11 cases of NI no pathogen could be isolated.

Adolescent↗

Nicotine raises the influx of permeable solutes across the rat blood-brain barrier with little or no capillary recruitment.

Nicotine (1.75 mg/kg s.c.) was administered to rats to raise local CBF (lCBF) in various parts of the brain, test the capillary recruitment hypothesis, and determine the effects of this increase in lCBF on local solute uptake by brain. lCBF as well as the local influx rate constants (K1) and permeability-surface area (PS) products of [14C]antipyrine and [14C]-3-O-methyl-D-glucose (3OMG) were estimated by quantitative autoradiography in 44 brain areas. For this testing, the finding of significantly increased PS products supports the capillary recruitment hypothesis. In 17 of 44 areas, nicotine treatment increased lCBF by 30-150%, K1 of antipyrine by 7-40%, K1 of 3OMG by 5-27%, PS product of antipyrine by 0.20% (mean 7%), and PS product of 3OMG by 0-23% (mean 8%). Nicotine had no effect on blood flow or influx in the remaining 27 areas. The increases in lCBF and K1 of antipyrine were significant, whereas those in K1 of 3OMG and in PS for both antipyrine and 3OMG were not statistically significant. The lack of significant changes in PS products implies that in brain areas where nicotine increased blood flow: (a) essentially no additional capillaries were recruited and (b) blood flow within brain capillary beds rises by elevating linear velocity. The K1 results indicate that the flow increase generated by nicotine will greatly raise the influx and washout rates of highly permeable materials, modestly elevate those of moderately permeable substances, and negligibly change those of solutes with extraction fractions of < 0.2, thereby preserving the barrier function of the blood-brain barrier.

3-O-Methylglucose↗

Slightly altered permeability-surface area products imply some cerebral capillary recruitment during hypercapnia.

To test the capillary recruitment hypothesis in brain, cerebral blood flow was raised markedly in rats by exposure to 8% CO2 (hypercapnia), and capillary permeability-surface area (PS) products were measured. Local cerebral blood flow (LCBF), volume of radiolabeled blood in parenchymal microvessels (also referred to as the blood space or Vb), plus the local capillary influx rate constants (K1) and PS products of [14C]antipyrine and 3-O-[14C]methyl-D-glucose (3OMG) were estimated in 44 brain areas. Hypercapnia raised PaO2 to 140 mm Hg, elevated LCBF by two- to threefold through out the brain, and increased Vb from 5 to 33% (mean = 22%) in 42 of 44 brain areas; hypercapnia did not, however, alter microvessel hematocrit. With hypercapnia, the influx of antipyrine was increased by 40-65% in all brain areas, and the PS products of antipyrine were elevated from 0-35% (mean = 17%). The PS products of antipyrine plus the parenchymal blood spaces suggest modest (< 30%) capillary recruitment in most brain areas as well as some microvessel dilation, mainly in forebrain gray matter and white matter areas. In contrast, hypercapnia did not appreciably alter K1 nor PS of 3OMG; it slightly but not significantly raised the blood levels of glucose. In view of the blood space and antipyrine evidence for modest capillary recruitment and vasodilation, the lack of change in PS of 3OMG implies that glucose transporter activity was lowered by hypercapnia, an effect similar to that reported for high-dose pentobarbital. Finally, the microvessel hematocrit and 3OMG data suggest that cerebral capillary permeability (P) was not increased by hypercapnia. Overall, hypercapnia seems to increase LCBF mainly by raising the velocity of blood flow; capillary recruitment and dilation appear to play relatively minor roles in this flow increase.

3-O-Methylglucose↗

Simultaneous measurement of bidirectional capillary permeability, vascular volume, extracellular space, and rCBF in experimental gliomas and surrounding edema.

Measurements of bidirectional capillary permeability in the ASV tumor model revealed a heterogeneous distribution of transport rates for the small water-soluble molecules which are believed to be the driving force in perifocal edema formation. Mean K1 values were 8.1 +/- 5.5 microliters/g/min in whole tumor and 18.89 +/- 12.3 microliters/g/min in highly permeable areas. Tumor blood flow ranged between normal white matter and cortex, whereas the plasma vascular space in the tumors was increased as compared to the normal brain. The size of the extracellular space was depending on the regional capillary permeability, underlining the vasogenic nature of peritumoral edema which was capable of being studied using in vivo methods.

Animals↗

Virtually unaltered permeability-surface area products imply little capillary recruitment in brain with hypoxia.

OBJECTIVE: To test the capillary recruitment hypothesis for the brain with control and hypoxic rats. METHODS: Local cerebral blood flow (LCBF) was sharply raised by respiring 10% O2 (hypoxia). LCBF as well as local influx rate constants (K1) and permeability-surface area (PS) products of 14C-antipyrine and 14C-3-O-methyl-D-glucose (30MG) were estimated for capillary systems in 44 brain areas. RESULTS: With this testing, an increase in PS product would be suggestive of capillary recruitment. In all brain areas, LCBF was increased by 30-90% by hypoxia. Hypoxia modestly raised the influx of antipyrine in brain but did not appreciably alter its PS products. With hypoxia, K1's and PS products of 30MG were significantly lowered (5-25%) throughout the brain, and the blood levels of glucose were sizeably raised. The latter increase would diminish the transfer of 30MG across the blood-brain barrier by the hexose transporter because of increased glucose competition. By applying a glucose-concentration correction to the data, the apparent PS product of 30MC for the hypoxic group became equal to that for the controls, which agrees with the antipyrine PS product results. CONCLUSIONS: Hypoxia, thus, leads to virtually no increase in PS products and no capillary recruitment in brain, and elevates LCBF mainly, perhaps exclusively, by raising the velocity of flow through already perfused capillaries.

3-O-Methylglucose↗

Impact of stereotactic interstitial radiation on brain capillary physiology.

rCBF, capillary permeability and vascular volume have been measured during the time course of interstitial stereotactic radiosurgery in normal and tumour-bearing dog brain. For rCBF measurement the stable Xenon-CT-technique with a modified Kety-Schmidt equation has been used, and for measurement of blood-to-brain transport of meglumine iothalamate the two-compartment CT-method as developed by Groothuis, which also reflects vascular volume. Anaplastic gliomas had been induced by intracerebral injection of avian sarcoma virus. Radiation sources have been 192-iridium and 198-gold. Both of the isotopes caused spherical blood-brain-barrier lesions with a more than 10-fold blood-to-brain transport increase. These effects occurred earlier and more pronounced with 192-iridium, but much longer lasting with 198-gold. Interstitial radiosurgery of the tumours led to a further increase of capillary permeability. Blood flow was significantly lowered not only within radionecrosis but also in the adjacent brain areas.

Anaplasia↗

Hypercapnia slightly raises blood volume and sizably elevates flow velocity in brain microvessels.

The increase in local cerebral blood flow (LCBF) caused by hypercapnia may be mainly accomplished by raising the velocity of plasma and/or red blood cell (RBC) flow through the microvessels and not by perfusing more capillaries. This suggestion was tested in awake rats exposed to 8% CO2 and in control rats. LCBF was measured by the 14C-labeled iodoantipyrine method. The volume of blood in small parenchymal microvessels was estimated from the distribution spaces of 125I-labeled serum albumin (RISA) and 55Fe-labeled RBCs. Hypercapnia elevated LCBF 2.0- to 3.5-fold in the 40 brain areas studied, marginally raised the RBC spaces, and significantly increased the RISA and whole blood distribution spaces (approximately 25 and 19%, respectively). These changes in microvessel distribution volumes could be the result of perfusing a slightly larger fraction of capillaries (recruitment), increasing microvessel diameter somewhat, or both. With hypercapnia, the mean transit times fell to approximately 45% of control, which indicated that LCBF was mainly increased by raising the velocity of RBC and plasma flow through already perfused microvessels. Overall, few, if any, capillaries or other microvessels were recruited by hypercapnia.

Animals↗

Nicotine increases microvascular blood flow and flow velocity in three groups of brain areas.

To examine the mechanism of local cerebral blood flow (LCBF) elevation, nicotine (1.75 mg/kg sc) was administered to rats, and LCBF plus the distribution spaces of radiolabeled albumin (RISA) and red blood cells (RBC) in parenchymal microvessels were measured throughout the brain. Microvascular blood spaces and transit times were calculated from the data. From 1.5 to 3 min after nicotine administration, LCBF was raised by 40-150% in 16 of the brain areas and unaltered in the remaining 28 areas. The affected structures included parts of the visual-auditory, sensorimotor-cortical, and interpeduncular systems. RBC spaces were not changed by nicotine treatment. RISA and blood spaces were increased slightly but not significantly in some of the LCBF-affected areas but nowhere else. Nicotine seemingly elevates LCBF in the affected areas mainly by increasing linear velocity of flow through the microvascular beds. In agreement with this, mean transit time, which is inversely related to velocity, was decreased from 0.3-0.5 to approximately 0.2 s in the microvascular systems of the nicotine-affected areas.

Animals↗

Smaller local brain volumes and cerebral atrophy in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) have enlarged cerebral ventricles from 8 weeks of age onward and smaller brains than age-matched, normotensive Wistar-Kyoto (WKY) rats (controls). At 6-7 months of age local cerebral glucose utilization is apparently lower in many brain areas of SHR relative to WKY rats. These observations led to the hypothesis that there are morphological differences between these two strains of rats in many, if not all, brain areas. This hypothesis was tested in 6-7-month-old SHR and WKY rats by quantitating 1) the volumes of the ventricular system, whole brain, six gray matter structures, and two white matter areas; 2) the thickness of two regions of the cerebral cortex; and 3) the frequency of neuronal nuclei (neuronal frequency) in nine brain areas. Ventricular volume was twofold greater in SHR than in control rats. The volumes of the entire brain and all six gray matter structures plus the thickness of the two cortical regions were 11-25% less in SHR. Neuronal frequency was, however, similar in the two rat strains. The latter finding coupled with the smaller regional tissue volumes indicates appreciably fewer neurons per brain structure in young adult SHR than in controls. These results indicate significant cerebral structural differences between young adult SHR and WKY rats and suggest that structure as well as metabolism are abnormal in the SHR brain.

Animals↗

[Determination of cerebral blood flow using an 81Rb/81mKr generator system].

A method is being developed which not only measures cerebral blood flow as a static quantity but also its changes with time. For that purpose a semiconductor device ascertains the proportion of intracerebral 81 Rb and 81mKr activities. By opening the hemato-encephalic barrier in animal experiments a sufficient concentration of intracerebral 81 Rb could be attained and the modified blood circulation after step-wise ligature of all brain arteries brought into relation to the corresponding Rb/Kr quotient. Over the range from undisturbed to completely interrupted cerebral blood flow this quotient varied up to 25% of its initial value.

Animals↗