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September 1998
Volume 62 |
Number 9
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FAER REPORT
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| Component Society
Support: 'Encouraging and Impressive' |
Through its grant programs, the Foundation for Anesthesia Education
and Research (FAER) inspires, perfects and perpetuates the spirit
of inquiry within the specialty. This search for discovery must
be nurtured and will be provided for through the FAER endowment.
The goal is for the endowment to support FAER programs in the
21st century. We appeal to you, as our colleagues, to join us
in achieving this ambitious undertaking.
Growth of the endowment comes from three sources: contributions
from the ASA, individual anesthesiologists and ASA component societies.
The endowment is approaching $8 million and FAER currently funds
nearly $1 million of awards annually. We are grateful to the ASA
and all the funding sources and will focus on the ASA component
societies in this report.
The increasing commitment to FAER by the ASA component
societies is encouraging and impressive. The recent level of growth
in contributions demonstrates a widening sense of responsibility
and resolution to maintain the specialty. We seem to have learned
that to succeed as a specialty, we must set aside resources to
afford sustained development even in difficult times.
Widespread participation by all component societies is
the logical target. Last year, we received contributions from
31 of 49 societies (63 percent), the highest level of participation
yet. FAER has awarded 262 grants since 1987, across 30 states
(including Washington, DC). Consequently, if this is a valid assumption,
component societies with no residency programs should support
FAER.
Throughout the past 10 years, component societies have
contributed about $350,000. Currently the annual average component
society contribution is around $2 per active member with a range
from $.53 per member on the low end to gifts of $10 - $20 (IA,
TN, MN) at the high end. One of our colleagues has suggested anesthesiologists
contribute $1 to research for each anesthetic administered. While
this is highly improbable, it does not seem unreasonable to suggest
component societies consider annual gifts of $5 - $10 per active
member. This level of giving would yield about $175,000 a year.
For 1998 we are working toward a 10-percent increase in component
society giving.
If we can join together, we can create a growing epicenter
of training in research that will ultimately improve the care
of our patients.
Grant Applications
FAER accepted 31 grant applications for its July 31 deadline:
| Program |
1997 |
1998 |
| Clinical Research Starter Grant |
14 |
8 |
| Research Starter Grant |
10 |
16 |
| Anesthesiology Research Fellowship |
1 |
3 |
| Education Research Grant |
2 |
4 |
FAER Announces 1998 New Investigator Award Recipients
The Board of Directors of the Foundation for Anesthesia Education
and Research (FAER) is pleased to announce the recipients of the
1998 New Investigator Awards. The ASA Committee on Research reviewed
19 applications and identified many projects worthy of funding.
FAER was able to fund nine of these projects thanks to the generous
contributions of FAER's corporate and society sponsors. The descriptions
of the remaining four projects are outlined below:
Thomas S. McDowell, M.D., Ph.D., FAER/American Society of
Regional Anesthesia New Investigator, University of Wisconsin,
Madison Medical School, Madison, Wisconsin: "Mechanisms of Analgesia
in Primary Nociceptive Neurons"
Opioids produce analgesia in part by inhibiting
the transmission of painful stimuli at the first synapse in
the nociceptive pathway, between the primary sensory neuron
and the secondary neuron in the dorsal horn of the spinal cord.
Neurotransmitter release from primary nociceptive neurons may
be reduced by opioids through inhibition of voltage-activated
calcium channels, facilitation of potassium channels, or both.
The overall goal of my research is to identify the cellular
mechanisms responsible for opioid-induced reductions in transmitter
release from primary nociceptive neurons. Neurons will be identified
as nociceptive by their sensitivity to pain-producing agents
such as capsaicin. The effects of opioids on specific types
of calcium and potassium currents in nociceptive neurons will
be assessed using the patch clamp technique. The results of
these studies will further our understanding of presynaptic
control mechanisms, and may present options for the development
of new methods to treat acute and chronic pain.
Timothy E. Morey, M.D., FAER/Zeneca Pharmaceuticals, Inc.,
New Investigator, University of Florida, Gainesville, Florida:
"Modulation of triggered activity by intravenous anesthetics in
rabbit isolated ventricular myocytes: Mechanisms and clinical
implications"
Early after depolarizations (EADs) are oscillations
in the cardiac membrane potential and cause most episodes of
torsades de pointes-type tachyarrhythmias. A variety of therapies
(e.g., quinidine) and deranged physiological conditions (e.g.,
hypokalemia) promote formation of EADs. Interventions that further
prolong ventricular repolarization in this setting (i.e., acquired
long QT syndrome) significantly increase the likelihood of developing
EADs. Intravenous anesthetics may differentially modulate the
genesis of EADs. Using current-and voltage-clamp techniques
in isolated ventricular myocytes, the objective of this study
is to determine if and how thiopental, methohexital, and propofol
affect the genesis of EADs caused by certain drugs (i.e., quinidine,
isoproterenol, and cocaine). The results of this study will
provide new information on the modulatory role of intravenous
anesthetics on the genesis of EADs and propagation of torsades
de pointes, and lead to more rationale anesthetic selection
in patients predisposed to developing these dysrhythmias (e.g.,
cocaine intoxication, antiarrhythmic drug therapy).
Mark A. Schumacher, M.D., Ph.D., FAER/Smiths Industries Medical
Systems New Investigator, University of California, San Francisco,
San Francisco, California: "The Role of Capsaicin Receptors in
Nociception"
Painful sensations originate from the activation
of peripheral nociceptive neurons in response to stimuli associated
with tissue injury. We have recently characterized a cDNA clone
encoding a 'capsaicin receptor' (Nature 389:816-824, 1997) which
probably represents a pain transducing element in the peripheral
nervous system. The capsaicin receptor is an ion channel which
is activated not only by the hot chili pepper extract, capsaicin,
but is also activated by noxious heat. My proposal examines
what role the capsaicin receptor or related subtypes play in
the detection and maintenance of thermal or mechanically induced
nociception and how it is modulated under peripheral inflammation
or nerve injury. Since capsaicin and its analogs are used as
topical analgesics to treat pain, characterization of capsaicin
receptors and identification of the factors that regulate their
number and activity should provide important insight into new
strategies designed to selectively block the sensation of pain
in the periphery.
Brian K. Tsang, M.D., FAER/Glaxo Wellcome New Investigator,
University of Mississippi Medical Center, Jackson, Mississippi:
"Spinal Opioid Receptor and the Corresponding mRNA Regulation
upon the Development of Tolerance to Intrathecal Opioids"
Recently, intrathecal (IT) opioids have gained
wider acceptance to treat patients with nonmalignant sources
of pain. The problem of analgesic tolerance is magnified by
the long duration of the therapy in these patients as most of
them are expected to require IT opioids for years or even decades.
With our established model of analgesic tolerance to IT opioids
in rats, we will examine the spinal cord tissue slices for the
change of different opioid receptor densities, as well as the
receptor agonist-and antagonist-affinity by quantitative autoradiography
that yields location-specific data with excellent anatomical
resolution. Further, we will assess the changes of the opioid
mRNA expression by in-situ hybridization with cDNA to provide
additional evidence for the corresponding receptor regulation.
This understanding should pave the way for further delineating
the mechanisms underlining analgesic tolerance and, possibly,
for devising rational, novel approaches to counter its undesirable
side effects.
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