| |
May 1999
Volume 63 |
Number 5
|
| |
FAER REPORT
|
| FAER Announces
1999 Award and Fellowship Recipients |
The Board of Directors of FAER is pleased to announce the recipients
of the 1999 Research Fellowships and New Investigator Awards.
The descriptions of the projects have been provided by the investigators.
We thank Abbott Laboratories, Organon, Inc., Smiths Industries
Medical Systems, the Society for Obstetric Anesthesia and Perinatology
and the Society for Pediatric Anesthesia for co-sponsoring these
awards. Without support from corporations and societies, we would
not be able to fund these talented, promising young anesthesiologists.
New Investigator Award Recipients
Ellen M. Lockhart, M.D., Duke University Medical Center,
Durham, North Carolina, Society for Obstetric Anesthesia and Perinatology:
"Progesterone as an Endogenous Neuroprotectant"
The fetus is exposed to very high concentrations of progesterone
in utero. We hypothesize that these high concentrations confer
to the fetal brain enhanced resistance to hypoxia. Exposing
cultured neurons to various neurologic insults such as hypoxia,
hypoglycemia and ischemia, both with and without exposure to
progesterone will test this hypothesis. The degree of cellular
injury will then be assessed. The long-term goal of the study
is to understand the role of naturally occurring hormones such
as allopregnanolone in protecting developing neurons against
such neurologic insults as hypoxia and ischemia. Completion
of this study will yield important new information about how
naturally occurring hormones may act to protect the fetal brain
from injury. These results will be useful in assessing if pharmacologic
manipulation of serum hormone levels has potential as a prenatal
or postnatal intervention during neurologic insults.
Wanda Miller-Hance, M.D., University of California, San
Francisco, California, Society for Pediatric Anesthesia: "Impact
of Intraoperative Transesophageal Echocardiography on Anesthetic
and Surgical Management of Pediatric Patients with Congenital
and Acquired Heart Disease"
Remarkable advances in anesthetic, perfusion and surgical
techniques now allow for correction of major cardiac defects
in children, even in early infancy. Refinements in echocardiography
and the miniaturization of probes that provide for real time
acquisition of information on cardiac structure and hemodynamics
via the transesophageal approach have resulted in increasing
applications of this technology to pediatric patients undergoing
cardiothoracic surgical procedures. The proposed investigation
will prospectively assess the anesthetic and surgical impact
of intraoperative transesophageal echocardiography (TEE) in
neonates, infants and children undergoing surgery for congenital
or acquired heart disease. Potential influences of this technology
on clinical outcomes will be addressed. The study will definitely
establish the incidence of vital new information provided by
intraoperative TEE, identify the cardiac pathology where TEE
is more likely to reveal important residual defects and determine
the true incidence of immediate reoperation for unacceptable
results in pediatric cardiac surgery.
Slobodan M. Todorovic, M.D., Ph.D., Washington University,
St. Louis, Missouri, Abbott Laboratories: "Voltage-gated Ca2+
Channels in Sensory Neurons as Targets for Anesthetic and Analgesic
Agents"
The extent to which voltage-gated Ca2+ channels
may be targets for some anesthetics and analgesics remains incompletely
understood. Recently, the applicant has demonstrated that in
rat sensory neurons N20 blocks selectively T-type
Ca2+ currents in subanesthetic concentrations (IC50
45 percent or 0.3 MAC) while cholinergic agonist carbachol blocks
HVA Ca2+ currents presumably acting at muscarinic
receptors. He proposes to follow up these findings with additional
studies aimed at further clarifying the cellular targets in
sensory neurons for these agents. Specifically: the mechanisms
and functional significance of T-type Ca2+ current
blockade by N20 will be examined and then, pharmacological
characterization and second messengers involved in muscarinic
receptor mediated-modulation of HVA currents will be studied.
Thus, the proposed research will help define the cellular mechanisms
of N20 anesthesia and analgesia and will help the
applicant to develop a new avenue in his research pertaining
to neurotransmitter modulation of voltage-gated Ca2+
channels.
Research Fellowship Recipients:
Paul M. Wischmeyer, M.D., University of Chicago, Chicago,
Illinois, Smiths Industries Medical Systems: "The Effects of Glutamine
on Induction of the Stress Response to Improve Outcome from Sepsis"
My research focuses on the use of nutritional pharmacology,
specifically glutamine, to manipulate the body's response to
stress, injury and illness. I have found that glutamine is a
potent inducer of heat shock protein 72 and that this induction
confers direct cellular protection in vitro. I plan to utilize
my FAER funding to determine if glutamine induces heat shock
protein at the tissue level in a rat model. Using this model,
I hope to determine the ideal dose and route of administration
of glutamine. If these preliminary studies prove successful,
I plan to examine the effects of glutamine on a rat model of
sepsis. If glutamine is effective in enhancing survival against
sepsis, I will examine several other models of in vivo tissue
injury (i.e. hyperoxic lung injury). I hope to use these findings
to enhance the care of the perioperative and critically ill
patient.
Raymond A. Zollo, M.D., University of Rochester Medical
Center, Rochester, New York, Organon Inc.: "The Effect of Antisense
PKG-* Knockdown on Neuropathic Pain"
It is estimated that chronic pain affects more than 50 million
people in the United States, causing partial or total disability
and costing 90 billion dollars annually. A significant proportion
of chronic pain is neuropathic in origin, resulting from nerve
injury. Further, neuropathic pain is notoriously difficult to
treat because its symptoms are remarkably resistant to conventional
analgesics. Recent evidence suggests that the development of
neuropathic pain depends on a plastic reorganization of the
nervous system called central hypersensitization. The involvement
of protein kinase C-gamma (PKC-*) prevent the development of
and/or reverse the neuropathic state. The ultimate goal of this
line of investigation is to demonstrate the feasibility of antisense
oligonucleotide knockdown of PKC-* as a treatment for neuropathic
pain.
return to top
|