Defence strategies against hypoxia and hypothermia.
Author: P.W. Hochachka Subjects: Biochemistry - Hypothermia -
Physiological aspects Metabolism - Research Hypoxia
Electronic Collection: A4100454 RN: A4100454
Though some degree of hypoxia and hypothermia can be sustained by all
animals, both conditions ultimately are incompatible with survival of
most mammalian tissues. Some ectothermic animals, however, are capable of surviving for long periods without O.sub.2, and some mammals (notably
hibernators) can tolerate--in fact, can take advantage of --hypothermia. When we investigated the means by which these abilities
are achieved at the cellular level, we found that the most serious
perturbations of hypoxia and of hypothermia arise from an imbalance
between (i) the extent of depression of adenosine triphosphate (ATP)
synthesis rates and (ii) the depression of processes requiring
membrane-based ATP. When metabolic and membrane functions are
decoupled, the cells (tissues or organisms) necessarily
become sensitive to hypoxia, to hypothermia, or to both conditions.
When, however, the two rate processes are matched despite O.sub.2
limitations or low temperature, then an impressive tolerance to
hypoxia, to ypothermia, or to both conditions is achievable. The
situation of simultaneous resistance to lack of O.sub.2 and to low
temperature arises because some of the fundamental mechanisms used by
hypoxia-tolerant animals to protect tissues and organs against hypoxia
are the same as, or at least remarkably similar to,those used by cold-
tolerant organisms such as hibernators to sustain prolonged hypothermia.
In this article, similarities and differences in
mechanisms of adaptation to hypoxia and hypothermia are analyzed, with
emphasis on opportunities, wherever possible, for novel intervention
strategies.
How Animals Survive Oxygen Lack: contd.
Source: The Biological Bulletin, June 2001 v200 i3 p247.
Title: Structure of Sequence Conservation of a Putative Hypoxia Response Element in the Lactate Dehydrogenase-B Gene
Author: BERNARD B. REES, JOHN A. L. BOWMAN and PATRICIA M. SCHULTE
Subjects: Killifishes -Hypoxia - Gene expression - Aquatic biology -
Aquatic ecology - Research Electronic Collection: A78400891 RN:
A78400891 Full Text COPYRIGHT 2001 Marine Biological Laboratory
Many aquatic habitats are characterized by periodic or sustained
episodes of low oxygen concentration, or hypoxia, and organisms that
survive in these habitats do so by utilizing a suite of behavioral, physiological and biochemical adjustments to low oxygen [1-3]. n the killifish Fundulus heteroclitus, one response to prolonged exposure to hypoxia is an increase in the activity of lactate dehydrogenase-B (LDH-B), the terminal enzyme of anaerobic glycolysis, in liver tissue [4]. An increase in glycolytic enzyme activity also occurs in mammalian cells during hypoxia, a
process due, in part, to increased rates of gene transcription mediated
by the hypoxia-inducible transcription factor, HIF-1 [5].
Source: The Lancet, Sept 15, 2001 v358 i9285 p897.
Title: S-nitrosothiols--lots of deep breaths required
Author: James Butcher Subjects: Nitric oxide -Hypoxia -Ventilation-perfusion ratio - Physiological aspects
Magazine Coll: 108D3510 Electronic Coll: A78432385 RN: A78432385
The reflex respiratory response to hypoxia--increased ventilation--may
not be due to just low blood oxygen concentrations after all. Rather, a
group of molecules called the S-nitrosothiols (SNOs), which are
released from haemoglobin in deoxygenated blood, directly affect the
respiratory centres in the brainstem to cause an increase in
ventilation, investigators report this week (Nature 2001; 413: 171-74).
S-nitrosothiols are molecules that ferry the nitric oxide (NO) group
around the body, by transferring NO to a cysteine thiol or sulphydryl
group (S-nitrosylation). "S-nitrosylation is akin to phosphorylation--a
post-translational modification of protein that can control the
protein's function", explains Stuart Lipton (Burnham Institute, La
Jolla, CA, USA), the author of an accompanying commentary (Nature
2001;413: 118-21).
Previous work has shown that SNOs have a role in matching ventilation
to perfusion in the lungs, and in controlling the supply of oxygenated
blood to the tissues. The new study adds one more skill to their
repertoire--they appear to also control respiration centrally. The US
researchers, led by Benjamin Gaston (University of Virginia,
Charlottesville, VA, USA) and David Gozal (University of Louisville,
KY, USA), showed this by injecting tiny quantities (0.1[micro]L) of
nitrosothiols into the nucleus tractus solitarius (NTS) of freely
moving conscious rats, and measuring the resultant changes in
ventilation. The NTS, located in the dorsal medulla, is the site of
termination of a wide variety of visceral afferents, including those
from the peripheral chemoreceptors. The nitrosothiols caused a reflex
increase in ventilation following injection into the NTS, a response
that looked qualitatively similar to that elicited when the rats were
placed in an environment containing 10% oxygen. In addition, injection
of plasma from deoxygenated, but not from oxygenated, blood into the
NTS produced a similar ventilatory effect to both SNOs injection and
hypoxia. The precise mechanism of action, however, remains undetermined
at present. Several neurotransmitter receptors are S-nitrosylated to
regulate their activity, most notably the N-methyl-D-aspartate (NMDA)
receptor that responds to the excitatory transmitter glutamate.
But a multitude of other targets are also possible, including neurons
outside the brainstem, such as the carotid body, which project to the NTS.
"To date it has been assumed that hypoxia-induced augmentations resulted
from 'classical neurophysiological' pathways with afferents from the
carotid bodies causing release of excitatory neurotransmitters",
comments Walter St John (Dartmouth Medical School, Lebanon, NH, USA).
"While such pathways without doubt exist, this new study demonstrates
that the release of SNOs may also be a potent and important mechanism
for augmentations of ventilation." Lipton thinks that this avenue of
research holds great promise: "In the future, it may be possible to
specifically inhibit or augment the effects of specific SNOs on targets
in the brain and elsewhere to affect not only respiration, but also cell
survival after hypoxic or other insults." Indeed, Lipton is working on
"targeted delivery of the NO group to the brain in areas that need control
to avert damage under pathological states".
[Source needed]
Nitric Oxide Found To Control Oxygen Delivery To Tissues; Findings
Could Lead To Therapies For Diseases Of Heart, Lung, Blood. Hemoglobin
as biosensor, nitric oxide as dilator
We have found that when red blood cells are exposed to abnormally low
oxygen for long periods, they become depleted of an essential
substance that they normally release to relax blood vessels in the
lung," McMahon continued. "But not only do blood cells, which of
course perfuse the lung, cause lung problems, we've also found that
inhalation of a new drug designed to correct the blood defect can
reverse this condition."
Stamler's group reported in 1996 that hemoglobin in red blood cells
acts as a finely tuned biosensor, adjusting blood flow to provide
exactly the optimum amount of oxygen to tissues and organs. The blood
cell adjusts blood flow by changing shape and releasing a nitric
oxide-like molecule called s-nitrosothiol (SNO), which the cell
carries through the bloodstream along with oxygen.
When oxygen levels are high, hemoglobin scavenges excess oxygen and
NO, constricting blood vessels and reducing blood flow. When oxygen
levels drop, the NO is released to relax blood vessels and improve
blood flow. The Duke team now finds that with prolonged oxygen
shortage, or hypoxia, blood cells become depleted of SNOs, therefore
losing their ability to relax blood vessels.
http://www.nytimes.com/2006/12/26/science/26obse.html
Gray seals, it seems, have a problem. They can’t dive and digest simultaneously. [Protein digestion consumes oxygen]
A study by Carol E. Sparling and colleagues at the University of St. Andrews in Scotland suggests that seals delay digesting their food for many hours after foraging dives. Seals and other marine mammals that dive for food encounter prey only intermittently, and they are underwater when they do so. So they don’t have much opportunity for a leisurely meal — they have to wolf down the food when they can.
But diving and digesting are both energy-intensive activities. So it makes sense that the animals might not always do both at once. The St. Andrews researchers used an experimental setup in which they could present seals with underwater prey at set intervals, and could measure the seals’ metabolic rate at the surface. They found that the metabolic rate was up to seven times higher than baseline during extended surface periods when the seals were motionless. These periods were most often at night, and frequently many hours after the end of feeding dives.
The researchers, whose study is published in Biology Letters, also found that the rate of oxygen consumption during these periods correlated well with the amount of food that the seals had eaten. The researchers say they do not know what happens to the food between when it is eaten and when it is digested. But they say that an interesting avenue of future study would be to see if the seal has some way to delay the release of digestive enzymes and prevent peristalsis, the muscle action that moves food through the digestive tract.
[See also seal shiver study]
Well, I do not think it is important - we all know what it is. I am just trying to tell you that the computer you use has fonts that are either outdated or poorly designed, and that they are worth of updating. If you have problems with this character, there may be many others that do not display correctly (Unicode fonts contain several thousands of characters)
