Message Number: SG15721 | New FHL Archives Search

From: Sukie Crandall
Date: 2005-10-17 16:45:03 UTC
Subject: [ferrethealth] Re: Melatonin Implant
To: ferrethealth@smartgroups.com

Here is a sample of the sort of thing I am finding:

START QUOTE
Cesk Fysiol. 2004;53(1):29-33.
Related Articles, Links

[Melatonin and the heart]

[Article in Slovak]

Vazan R, Beder I, Styk J.

Fyziologicky ustav, Lekarska fakulta Univerzity Komenskeho,
Bratislava. rastislav.vazan@fmed.uniba.sk

Evidence gathered during the last years shows that the pineal hormone
melatonin participates in the regulation of the heart. Melatoninergic
receptors were found in the heart and vessels and also in the higher
centers involved in the regulation of cardiovascular system.
Melatonin protects the heart against ischaemia-reperfusion injury and
also against cardiotoxic effects of adriamycin and alloxan. Lack of
melatonin was repeatedly reported in patients with coronary heart
disease. Intake of this hormone leads to decrease of blood pressure
in normotensive and hypertensive subjects, while pinealectomy induces
hypertension. In addition melatonin can probably influence the levels
of intracellular calcium in cardiomyocytes. The aim of this review is
to summarize available evidence about effects of melatonin on the
heart. Mechanisms involved in these effects are also suggested.
END QUOTE

and another:

START QUOTE
Physiol Res. 2005 Jan 10; [Epub ahead of print]
Related Articles, Links

Protective effects of melatonin on myocardial ischemiareperfusion
induced infarct size and oxidative changes.

Sahna E, Parlakpinar H, Turkoz Y, Acet A 6.

Department of Pharmacology, Faculty of Medicine, Firat University,
Elazig, Turkey. esahna@firat.edu.tr.

Free radicals, calcium overloading and loss of membrane phospholipids
play an important role in the devolopment of ischemia/reperfusion (I/
R) injury. Melatonin is a well-known antioxidant and free radical
scave nger. Melatonin may also reduce the intracellular calcium
overloading and inhibit lipid peroxidation. This study was designed
to investigate the effects of melatonin on the I/R- induced cardiac
infarct size in an in vivo rat model. We also investigated the
glutathione (GSH) levels, an antioxidant which levels are influenced
by oxidative stress and malondialdehyde (MDA) levels, an index of
lipid peroxidation. To produce cardiac damage, the left main coronary
artery was occluded for 30 min, followed by 120 min reperfusion, in
anesthetized rats. Melatonin (10 mg/kg) or vehicle was given 10 min
before ischemia via jugular vein. Infarct size, expressed as the
percentage of the risk zone, was found significantly higher in I/R
group than in the melatonin-treated I/R group. MDA levels were
significantly higher but GSH levels were lower in the I/R group than
the control group. Melatonin significantly reduced the MDA values and
increased the GSH levels. These results suggest that oxidative stres
contributes myocardial I/R injury and melatonin administration exerts
limiting effect on infarct size. In addition the results indicated
that melatonin improves the antioxidant capacity of the heart, as
well as attenuates a degree of lipid peroxidation after I/R.
END QUOTE

Another:

START QUOTE
J Appl Toxicol. 2004 Nov-Dec;24(6):505-12.
Related Articles, Links


Protective role of melatonin in ochratoxin a toxicity in rat heart
and lung.

Okutan H, Aydin G, Ozcelik N.

Suleyman Demirel University, School of Medicine, Department of
Cardiovascular Surgery, Isparta, Turkey. okutanh@yahoo.com

Ochratoxin A (OTA) is a mycotoxin produced by different fungi. The
most pronounced adverse effect of OTA is hepatonephrotoxicity.
Melatonin (MEL) has an antioxidant effect and has free-radical
scavenger properties. The effects of OTA on heart and lung tissue and
possible ameliorating effects of MEL were investigated in rats.
Twenty-four rats were allocated to three groups (each with eight
rats): control; OTA-treated group (OTA dose 289 microg kg(-1) per
day); and OTA + MEL-treated group (MEL dose 10 mg kg(-1) per day).
After 30 days of treatment, the histopathological changes in the
heart and lung of all groups were examined. Compared with the control
rats, myocardial tissue of rats treated with OTA showed extensive
cytoplasmic vacuole formation, necrosis of the myocytes, dissolution
of the nucleus, clumped fibres, fibrillolysis, swollen myocardial
fibres, small haemorrhagic areas and hyperaemic vessels (P <0.05). In
addition, lungs of rats treated with OTA showed alveolar congestion,
alveolar cell hyperplasia, prominent alveolar septal vessels,
variable intensity loss of alveolar architecture, intraparenchymal
inflammatory infiltration, intraparenchymal hyperaemic vessels,
respiratory epithelial proliferation, perivascular and peribronchial
inflammation, pneumonic infiltration, distorted appearance of lung
parenchyma and emphysematous areas (P <0.05). In comparison with the
OTA groups, the ameliorating effects of MEL in the lung damage
parameters were on alveolar cell hyperplasia, prominent alveolar
septal vessels, variable intensity loss of alveolar architecture,
intraparenchymal inflammatory infiltration, perivascular inflammatory
inflammation, distorted appearance of lung parenchyma and focal
emphysematous areas in lung (P <0.05). Melatonin also significantly
reduced myocardial damage in most of the parameters: extensive
cytoplasmic vacuole formation, necrosis of the myocytes, clumped
fibres, fibrillolysis, small haemorrhagic areas and hypaeremic
vessels in heart (P <0.05). On the other hand, MEL did not lower the
degree of damage in lung and heart to the level of the control rats,
except for the parameters of the interstitial oedema and small
haemorrhagic areas only in myocardial tissue. Histopathological
findings showed that OTA induced damage in heart and lung and MEL
treatment significantly reduced the degree of damage.
END QUOTE

BUT THERE ARE 141 STUDIES ON HEART HEART AND MELATONIN IN FERRETS in
Pubmed. So far, I am just finding GOOD things it can do for the
heart. I have already searched some other health sites.

After searching widely I still find NO indication in any of the
species I have so far looked into that melatonin can cause any heart
problems, and what you describe are cardiac symptoms -- with the
enlarged heart requiring existing cardiomyopathy over a space of
time. In fact, not only did I NOT find any studies so far indicating
that melatonin is hard for the heart, but i found multiple types of
heart problems for which it looks to be beneficial in studies:
including reducing toxicity of some meds (including doxirubicin),
reducing high blood pressure, evening out serious arrhythmias, etc.
I wish we had known about this when Meltdown had her ventricular
bigemini, and esp. when she began throwing clots (thromboses).

Lupron is another matter. In humans it is best avoided when cardiac
disease is present and has been linked with superventricular
tachycardia, heart attack, etc. when care is not taken on that
regard. Could it do so in ferrets? I honestly don't know, but
hearts generalize pretty well, so I think that for now one when we
have one who needs a Lupron Depot and the ferret is older or has
suggestive symptoms I will have the heart tested beforehand to be
safest, just as we do pre-surgically on such ferrets. It is not that
I have problems with Lupron itself; it is a GREAT drug, but like any
med there are just some medical conditions with which it may not be a
good thing to use.

I think that it is important here to remember that dilated hearts are
from cardiomyopathy that has been present enough to cause that muscular
effect over time, and that the symptoms at death and in necropsy
which you gave are consistent with a cardiovascular cause, and also
that right now the cause is not firmly
established so it is way too early to draw conclusions based on
temporal factors.

Plus, in the same time frame you lost one from rampant pneumonia, and
that while rampant pneumonia would show up in a plain old necropsy, a
lesser infection that could be too much combined with heart disease
would
not. Remember that the word on necropsies is that the vast majority of
the causes of death in mammals that are not obvious with a necropsy need
timely pathology done to find out what actually truly occurred. There
is a figure -- I think in the Ferret Mailing List Archives
<http://listserv.cuny.edu/archives/ferret-search.html>
but perhaps in the Ferret Health List Archives -- on that. There are a
huge number of things that just can not be told without pathology done.
Without pathology all that exists is a monetary settlement unless there
are other such cases in which the pathology has been done (I have not
heard of any) and monetary settlements can happen for a range of
reasons.

There IS a known case of a very small sized female who appeared to
possibly have trouble with the melatonin implant dose, but that is not
firmly known as the cause, especially since larger doses per weight had
been seen in other ferrets. She was part of a study and she became very
(very) lethargic for an extended period, then rebounded. The cause
remains unknown, but it is possible that she was particularly sensitive
to the tiring effects of melatonin due to some individual factor, or
her size, or both. On the other hand, she may simply have been
fighting an infection; not all are overt.

What has happened on the pathology front? Did the preps to get that
done
happen rapidly enough? The window is a short one. Remember that if the
tissue isn't in formalin within 48 hours then nothing at all can be
learned from it, and with some aspects of the digestive system like the
gall bladder and intestine that needs to be done by the vet within hours
of death. See:
http://ferrethealth.org/archive/browse.php?msg=YG10682
http://ferrethealth.org/archive/browse.php?msg=YG647
etc.

It is possible that the stress of the large bore may have been factor
given the signs of preexisting heart disease discussed on the FHL,
especially is combined with the limitations of a lung infection that
simply wasn't overt enough to be spotted on a simple necropsy, though
the latter two together could have been enough, or *maybe* a ferret who
is already dealing with either or both of those problems is not a good
candidate for something that can further deepen sleep. (Note that is a
*maybe*.)

Remember that she had already been on oral melatonin, and that the body
itself produces melatonin in response to darkness.

(Melatonin serves MANY functions in the body.)

The only way to KNOW what happened here would be through timely
pathology
before tissue degradation. The enlarged heart alone says that this was
already a compromised ferret with cardiomyopathy.

-- Sukie (not a vet)
Ferret Health List co-moderator
http://www.smartgroups.com/groups/ferrethealth
FHL Archives fan
http://ferrethealth.org/archive/
replacing
http://fhl.sonic-weasel.org
International Ferret Congress advisor
http://www.ferretcongress.org




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