Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Changes in ICBF, morphology and related parameters by fluid percussion injury (1996)
    Springer
    Acta neurochirurgica 138 (1996), S. 90-98 
    Details
    ISSN: 0942-0940
    Keywords: Cerebral blood flow ; fluid percussion injury ; pathophysiological responses ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an original midline fluid percussion injury device. Following different grades of trauma, lCBF was measured continuously in the right parietal cortex through a burr hole using laser Doppler flowmeter, and physiological parameters were monitored. Pathological changes also were evaluated microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pathophysiological response occurred after percussion pulses of less than 1.33 atmospheres (atm). In animals subjected to pulses of greater than 4.30 atm, lCBF increased synchronously with blood pressure, and then both parameters decreased continuously until death. In animals subjected to pulses of 1.53 to 2.33 atm, trauma produced a transient increase in 1CBF with no synchronous rise in blood pressure. In animals subjected to pulses of 2.70 to 3.87 atm, lCBF increased synchronously with blood pressure immediately following the injury, but had decreased markedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The transient increase in lCBF occurred within 5 seconds following percussion pulses of greater than 1.53 atm and appeared to be independent of the rise in systemic blood pressure. Apnoea occurred in animals subjected to pulses of greater than 1.53 atm, and the duration of apnoea and mortality rate correlated with the magnitude of the applied injury. A power decrease in the electroencephalogram post-injury and a delay in its recovery, both depended on the magnitude of the injury with few regional differences in the beta-2 band power. The distribution and extent of blood-brain barrier disruption and small haemorrhages also correlated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma. The four patterns of lCBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01411731
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Postprandial Response of Jejunal Slow Waves and Mediation via Cholinergic Mechanism (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 1506-1511 
    Details
    ISSN: 1573-2568
    Keywords: INTESTINAL MOTILITY ; SLOW WAVE ; JEJUNUM ; ATROPINE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The postprandial characteristics of jejunalmyoelectrical activity and its mediation via cholinergicnerves were investigated in this study. Four pairs ofbipolar electrodes were implanted on the serosa of the proximal jejunum of nine female hounddogs (14-22 kg). In the control session, the recordingof jejunal myoelectrical activity was made for 30 min inthe fasting state and for 90 min after a solid meal (0.45 kg, 838 kcal). The study sessionfollowed the same protocol except that a bolus of 0.25mg/kg atropine was injected intravenously 30 min afterthe meal. Computerized spectral analysis was performed to calculate the frequency, power, andpercentage of 17-22 cycles/min (cpm) slow waves. Aspecial artificial neural network program was applied tocompute the spike bursts superimposed on slow waves. All data were expressed as mean ± SE. Thepostprandial frequency of the jejunal slow waves wassignificantly increased from 18.42 ± 0.28 cpm inthe fasting state to 18.95 ± 0.22, 19.28 ±0.23, and 19.28 ± 0.22 cpm during the first, second, andthird 30-min periods after the meal (all P 〈 0.03 incomparison with the fasting state). The percentage ofthe slow waves superimposed with spike bursts was increased from 19.33 ± 3.90% at fastingstate to 35.16 ± 2.76%, 32.87 ± 4.06%, and34.88 ± 3.51% during the first, second, and third30-min periods after the meal (all P 〈 0.03 incomparison with fasting state). Atropine abolished thepostprandial increases in the frequency of slow wavesand the number of spike bursts. No significantpostprandial changes in the power and the percentage of17-22 cpm slow waves were observed. In conclusion,the postprandial response of the jejunal slow wavesafter a solid meal presents as an increase of thefrequency of slow waves and the number of the spikebursts which can be abolished by atropine, and thepostprandial response of the jejunal slow waves is aneural reflex dominantly mediated via vagal cholinergicnerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026638221467
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...