Mailing List Archive Mailing List Archive
>Do you have any good biochem/cell biology references you find useful
>over and over again? Any level is fine, I'll pick up what extra
>knowledge I need between the lines and from auxiliary sources. I'm
>simply looking for more info to explain what physics & physiology
>don't explain about DCI, AGE, et al..
>
>Anything come to mind (or hand? :)
Start with these...
Ward CA, McCullough D, Yee D, Stanga D, Fraser WD (1990) Complement=20
activation involvement in decompression sickness of rabbits. Undersea=20
Biomedical Research 17:51-66
A hypothesis has been proposed that claims much of the phenomena of=20
decompression sickness (DCS) are mediated by the complement system of blood=
=20
plasma. This "complement hypothesis" can be used to explain the variation in=
=20
susceptibility of individuals to DCS, including the phenomena of=20
acclimatization and de-acclimatization. In this study, certain predictions=
=20
of the complement hypothesis were examined by exposing rabbits to a=20
particular pressure profile; some were observed to have symptoms of DCS and=
=20
some showed none. Those that were observed to have symptoms were also found=
=20
to have native complement systems that were activated by air bubbles, and=20
those that did not show symptoms of DCS when exposed to the same pressure=20
profile had native complement systems that were not activated by air=20
bubbles. Rabbits that had shown symptoms of DCS the first 2 times that they=
=20
were exposed to the pressure profile could be acclimatized to the pressure=
=20
profile by pharmacologically decomplementing them in vivo. After being=20
decomplemented, they showed no symptoms of DCS when they were exposed to the=
=20
same pressure profile for a third time. When the decomplemented rabbits were=
=20
allowed to remain inactive for a period of time that was sufficient to allow=
=20
their complement systems to return to normal, after having been=20
decomplemented, and were then subjected to the pressure profile for the=20
fourth time, they were each again observed to have symptoms of DCS, i.e.,=20
they became de-acclimatized when their complement systems had returned to=20
their native sensitivity. These results provide further experimental support=
=20
for the complement hypothesis.
Ward CA, Koheil A, McCullough D, Johnson WR, Fraser WD (1986) Activation of=
=20
complement at plasma-air or serum-air interface of rabbits. Journal of=20
Applied Physiology 60:1651-1658
The possibility of the air-plasma interface giving rise to compliment=20
activation is investigated. After incubationof the plasma of a group of=20
rabbits with zymosan and measurment of the degree of autologous=20
polymorponuclear leukocyte aggregation that follows the injection of a=20
sample of the incubated plasma into a leukocyte suspension it is found that=
=20
the rabbits can be divided into two groups, sensitive and insensitive=20
depending on the degree of leukocyte aggregation. For the sensitive group it=
=20
is found that both the plasma-air interface and the serum-air interface give=
=20
rise to significant leukocyte aggregation. If the animal is decomplimented=
=20
before the plasma is incubated in the presence of of the air interface there=
=20
is no longer any significant leukocyte aggregation. It would appear that=20
the compliment system is activated by the presence of an air interface in=20
plasma but that fibrinogen does not play a pivotal role in the process.
Ward CA, McCulloch D, Fraser WD (1987) Relation between compliment=20
activation and susceptibility to decompression sickness. Journal of Applied=
=20
Physiology 62:1160-1166
The consequences of compliment activation and the symptoms of decompression=
=20
sickness are similar. Consequently, the relation between the sensitivity of=
=20
individual to compliment activation by air bubbles and their susceptibility=
=20
to decompression sickness has been examined. Plasma samples from 34=20
individuals were incubated with air bubbles and the concentration of the=20
fluid phase metabolites of compliment activation C3a, C4a and C5a were=20
measured by radioimmunoassay. It was found that both the anaphylatoxins C3a=
=20
and C5a were produced by the presence of air bubbles but that the=20
anaphylatoxin C4a was not. These findings indicate that air bubbles=20
activate the compliment system by the alternate pathway. One group of=20
individuals was found to be particularly sensitive to compliment activation=
=20
by this pathway. They produced 3.3 time more C3a and 5 times more C5a in=20
their plasma samples incubated with air bubbles as did the other group. =20
Sixteen individuals were subjected to a series of decompression profiles=20
severe enough to produce air bubbles in their circulation which could be=20
detected by ultrasonic Doppler monitoring. The group of individuals=20
identified as more sensitive to compliment activation by the alternate=20
pathway was also found to be more susceptible to decompression sickness.
Helps SC, Gorman DF (1991) Air embolism of the brain in rabbits pretreated=
=20
with mechlorethamine. Stroke 22:351-354
Infusion of 400 microliters air into the left internal carotid artery of=20
five anesthetized rabbits caused transient pial arteriole air embolism, an=
=20
immediate 41.9 =B1 0.8% dilatation of the embolized vessels, suppression of=
=20
the cortical somatosensory evoked response to 29.4 =B1 2.7% of baseline, and=
a=20
progressive decline in ipsilateral cerebral blood flow (measured by hydrogen=
=20
clearance) to 46 =B1 4.1% of baseline after 2 hours. These values were=20
significantly different from those at baseline and from the responses of 10=
=20
control rabbits given equivalent intracarotid saline infusions. Twelve other=
=20
rabbits were made leukopenic by treatment with 1.5 mg/kg i.v.=20
mechlorethamine 72 hours prior to study. Mean =B1 SEM leukocyte count=20
decreased from 6,320 =B1 73/mm3 to 1,890 =B1 66/mm3 without any change in=
the=20
leukocyte differential or erythrocyte and platelet counts. Intracarotid=20
infusion of saline into seven of the leukopenic rabbits caused no changes.=
=20
In the other five leukopenic rabbits, infusion of 400 microliters air caused=
=20
air embolism but did not produce the anticipated declines in cerebral blood=
=20
flow or the cortical somatosensory evoked response, both of which remained=
=20
indistinguishable from baseline values and responses in the seven=20
saline-treated leukopenic controls. Similarly, air-embolized arterioles=20
showed nonsignificant dilatation in leukopenic rabbits. Our data suggest=20
that the decreases in both cerebral blood flow and brain function seen after=
=20
air embolism require the presence of leukocytes.
/Rat
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
shelps@ac*.ma*.ad*.ed*.au* Stephen Helps
Anaesthesia & Intensive Care
University of Adelaide
ADELAIDE, 5005, South Australia
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
If everything seems to be going well, you've probably overlooked something=
=20
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Navigate by Author:
[Previous]
[Next]
[Author Search Index]
Navigate by Subject:
[Previous]
[Next]
[Subject Search Index]
[Send Reply] [Send Message with New Topic]
[Search Selection] [Mailing List Home] [Home]