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Reference 31-40

Reference 31-40
Prof. Sven Kurbel MD, PhD - personal web pages
Dept. of Physiology, Osijek Medical Faculty
J. Huttlera 4, 31000 Osijek, Croatia
e-mail: sven@jware.hr

 

 


31 Inertia of endocrine systems due to hormone binding to circulatory proteins.
Kurbel S, Zucić D, Kurbel B, Gulam D, Gmajnić R, Krajina Z.
Med Hypotheses. 2003 Mar;60(3):430-8.


Osijek Medical Faculty, University of JJ Strossmayer, Croatia.
sven.kurbel@public.srce.hr
It is often presumed that the main role of hormone binding to albumins and
binding proteins (BPs) is to reduce oscillating levels of free hormone
molecules and to transport steroid hormones. This paper is an attempt to
define possible consequences of hormone molecules binding to carrier
proteins in circulation.Binding to albumins and BPs prevents exact and
quick control of hormone actions. Hormones without significant protein
binding govern vital and fast acting regulatory mechanisms (blood glucose
or calcium) in which any added inertia might be dangerous. In the
presented model, the added inertia for a partially bound hormone (H) is
defined as: H(bound)/H(free). Values, calculated from the reported data,
range from 0.4 for GH to more than 2000 for T(4). In comparison to
albumins, high-affinity BPs make more stable reserve that would cover
periods of low or no hormone secretion. At the same time, hormone
molecules are taken away from the blood level control and thus might be
considered sequestrated.For hormones without protein binding, the
well-perfused areas of the body, or the areas with increased capillary
permeability, would be more exposed, making an uneven distribution among
target tissues. For the hormone that binds blood proteins, places of
secretion and tissue perfusion become unimportant, since the hormone is
being liberated anywhere in the circulation (i.e., for strongly bound
IGFs, IGF binding proteins do not just stabilize proinsulin actions of
IGF-1, but also make all parts of body to be under the same exposure to
liberated IGFs, an important feature to promote a symmetrical bone
growth).Estrogens are known to stimulate liver secretion of different BPs.
A possible explanation is that in the follicular phase there is a small
initial mass of granulosa cells, and it takes time to saturate free
estrogen carriers, before the normal free hormone level can be reached and
FSH secretion inhibited. Less inert peptide inhibin might suppress FSH
before free estrogens reach the required level. Without inhibin
suppression, an increased FSH level with an increased number of growing
follicles can be expected. Estrogens increased production of BPs augments
inertia of the estrogen loop and possibly modulates the FSH/estrogen
negative feedback.
Publication Types:
Research Support, Non-U.S. Gov't
MeSH Terms:
Albumins/metabolism
Animals
Endocrine System/pathology/*physiology
Estrogens/metabolism
Growth Hormone/metabolism
Hormones/*metabolism
Humans
Models, Theoretical
Protein Binding
Substances:
0 (Albumins)
0 (Estrogens)
0 (Hormones)
9002-72-6 (Growth Hormone)
Publication Status: ppublish
PMID: 12581625 [PubMed - indexed for MEDLINE]
From PubMed



32 The osmotic gradient in kidney medulla: a retold story.
Kurbel S, Dodig K, Radić R.
Adv Physiol Educ. 2002 Dec;26(1-4):278-81.


Department of Physiology, Osijek Medical Faculty, 31000 Osijek, Croatia.
sven.kurbel@public.srce.hr
This article is an attempt to simplify lecturing about the osmotic
gradient in the kidney medulla. In the model presented, the kidneys are
described as a limited space with a positive interstitial hydrostatic
pressure. Traffic of water, sodium, and urea is described in levels (or
horizons) of different osmolarity, governed by osmotic forces and positive
interstitial pressure. In this way, actions of the countercurrent
multiplier in nephron tubules and of the countercurrent exchanger in vasa
recta are integrated in each horizon. We hope that this approach can help
students to better accept conventional presentations in their textbooks.
Publication Types:
Research Support, Non-U.S. Gov't
MeSH Terms:
Humans
Kidney Medulla/*metabolism
Osmosis
Physiology/*education
*Teaching
Publication Status: ppublish
PMID: 12443999 [PubMed - indexed for MEDLINE]
From PubMed
Free at producer site



33 Amoxycillin, clarithromycin and either sucralfate or pantoprazole for eradication of Helicobacter pylori in duodenal ulcer (a randomized
controlled trial).
Vcev A, Vceva A, Kurbel S, Takac B, Stimac D, Ivandić A, Ostojić R, Barbir
A, Hovat D, Mihaljević S.
Wien Klin Wochenschr. 2001 Dec 17;113(23-24):939-41.


Internal Clinic, Clinical Hospital Osijek. btakac@gmx.net
BACKGROUND: Sucralfate enhances the anti-Helicobacter pylori activity of
antimicrobials and has an inhibitory effect on H. pylori. AIM: To evaluate
the efficacy and safety of one-week sucralfate-based eradication therapy
for H. pylori infection in patients with duodenal ulcers, compared with
treatment based on pantoprazole, in a randomized controlled multicenter
study. METHODS: One hundred and twenty patients with active duodenal
ulcers and H. pylori infection were treated with amoxycillin 1 g b.d. plus
clarithromycin 500 mg b.d. for the first 7 days. Patients were randomly
assigned to receive either sucralfate 1 g t.d.s. for 4 weeks (SAC group; n
= 60) or pantoprazole (PAC group; n = 60) 40 mg b.d. for the first 7 days
and 40 mg o.d. for the next 3 weeks. The patient's H. pylori status was
determined by a urease test and histological investigation before the
treatment, and again 4 weeks after cessation of all medication. RESULTS:
One hundred and eleven patients completed the study. H. pylori infection
was eradicated in 76.4% (42/55) of patients in the SAC group (ITT
analysis: 70%, 95% CI: 58-80%) vs. 85.7% (48/56) of patients in the PAC
group (ITT analysis: 80%, 95% CI: 70-89) (N.S.). All ulcers had healed.
There were no significant differences between the two regimens regarding
the occurrence of adverse effects. CONCLUSION: Our study shows that
one-week triple therapy with amoxycillin, clarithromycin and either
pantoprazole or sucralfate are effective regimens to cure H. pylori
infection in patients with duodenal ulcer.
Publication Types:
Clinical Trial
Comparative Study
Randomized Controlled Trial
MeSH Terms:
2-Pyridinylmethylsulfinylbenzimidazoles
Adult
Aged
Amoxicillin/*administration & dosage/adverse effects
Benzimidazoles/*administration & dosage/adverse effects
Clarithromycin/*administration & dosage/adverse effects
Drug Therapy, Combination
Duodenal Ulcer/diagnosis/*drug therapy
Duodenoscopy
Female
Follow-Up Studies
Helicobacter Infections/diagnosis/*drug therapy
Helicobacter pylori/*drug effects
Humans
Male
Middle Aged
Omeprazole/analogs & derivatives
Sucralfate/*administration & dosage/adverse effects
Sulfoxides/*administration & dosage/adverse effects
Substances:
0 (2-Pyridinylmethylsulfinylbenzimidazoles)
0 (Benzimidazoles)
0 (Sulfoxides)
102625-70-7 (pantoprazole)
26787-78-0 (Amoxicillin)
54182-58-0 (Sucralfate)
73590-58-6 (Omeprazole)
81103-11-9 (Clarithromycin)
Publication Status: ppublish
PMID: 11802510 [PubMed - indexed for MEDLINE]
From PubMed



34 Model of interstitial pressure as a result of cyclical changes in the
capillary wall fluid transport.
Kurbel S, Kurbel B, Belovari T, Marić S, Steiner R, Bozíć D.
Med Hypotheses. 2001 Aug;57(2):161-6.


Osijek Medical Faculty, University JJ Strossmayer, 31000 Osijek, Croatia.
sven.kurbel@public.srce.hr
Reported interstitial pressures range from -8 to +6 mm Hg in different
tissues and from <-20 mm Hg in burned tissue or more than +30 mm Hg in
tumors. We have tried to link interstitial pressure to the here proposed
cyclical changes in the fluid transport across the capillary wall.In the
presented model interstitial pressure is considered as an average of
pressures in numerous pericapillary spaces. A single pericapillary
pressure is a dynamic difference between the net outward (hydraulic
pressure+interstitial colloid osmotic pressure) and inward (plasma colloid
oncotic pressure) forces. Hence, dominating net outward forces would
result in a positive pericapillary interstitial pressure, while stronger
inward forces would produce negative pressures in the pericapillary space.
All interruptions of blood flow leave some blood in capillaries with a
normal oncotic pressure and no hydrostatic pressure that might act as a
strong absorber of interstitial fluid until the blood flow is
reestablished.Model assumptions for the systemic circulation capillaries
include (a) precapillary sphincters can almost entirely stop the capillary
flow, (b) only a minority of sphincters are normally open in the tissue,
and (c) hydrostatic pressures in unperfused capillaries are similar to the
pressures at their venous ends.The key proposal is that capillaries with
closed precapillary sphincters along their entire length have low
hydrostatic pressure of 10 to 15 mm Hg. This pressure cannot force
filtration, so these capillaries reabsorb interstitial fluid from the
pericapillary space along their entire length. In the open capillaries,
hydrostatic pressure filtrates fluid to the pericapillary space along most
of their length. Fluid enters, moves some 20 or 30 micrometers away and
back to be reabsorbed at the same point. Closed periods are periods of
intense fluid reabsorption, while the short open periods refill the space
with fresh fluid. It can be calculated that subcutaneous tissue
interstitial pressure values might develop if the closed periods are 1.14
to 2.66 times longer than the open periods. Positive interstitial
pressures observed in some organs might develop if open periods are longer
than the closed periods.High interstitial colloid pressure in lungs makes
both perfused and unperfused capillaries absorptive, resulting in more
negative values of lung interstitial pressure. The same model is used to
explain interstitial pressure values in tumors, burned tissue and
intestinal villi.
Copyright 2001 Harcourt Publishers Ltd.

MeSH Terms:
*Blood Pressure
Capillaries/*physiology
Endothelium, Vascular
*Models, Biological
Publication Status: ppublish
PMID: 11461165 [PubMed - indexed for MEDLINE]
From PubMed



35 A model of the gastric gland ejection cycle: low ejection fractions
require reduction of the glandular dead space.
Kurbel S, Kurbel B, Dmitrović B, Vcev A.
J Theor Biol. 2001 Jun 7;210(3):337-43.


Osijek Medical Faculty, University JJ Strossmayer, Osijek, Croatia.
sven.kurbel@public.srce.hr
This paper was inspired by the reported results of authors from Uppsala
and Lund that gastric glands in rats rhythmically contract 3-7 cycles per
minute and develop luminal pressures more than 10 mmHg. To ensure that
pepsinogen is not retained in the acid-rich section of the gland, ejection
fractions would need to be more than 50% of the gland volume. We have
tried to calculate the ejection fraction of such contractions. Dimensions
of human gastric glands were measured on the fresh frozen samples of
macroscopically and histologically normal gastric mucosa. In total, 18
specimens (from nine persons) were measured under the microscope. The
density of glands was 135 +/- 11 (mean +/- S.D.) glands per mm( 2) of
gastric mucosa. A typical gastric gland is a tubular structure 1.2 +/-
0.22 mm long and 0.03-0.05 mm wide. We have used 1 mm for length and 0.03
mm for the gland diameter to calculate that each gland approximates a
volume of 707 pl, suggesting that the total glandular volume for 15
million glands reaches 10.6 ml. Further calculations based on one to five
contractions per minute on an average and on the total volume of gastric
glands of 10 ml showed that only ejection fractions less than 10% deliver
daily volumes less than 3 l. The presented model of the gastric gland
activity is based on the idea that the low ejection fractions require a
reduction of the glandular dead space. The reduced luminal pressure during
the gland relaxation might cause backflux of hydrophobic viscoelastic
mucus through the gland aperture. Repeated glandular contractions and
relaxations would move the mucus all the way to the gland bottom, filling
the gland cavity below the neck with an axial semisolid mucous cylinder.
This filling would reduce the gland dead space. During contractions, the
gland would eject mainly the peripheral, the more liquid part of its
content. The decreasing luminal pressure in the relaxing gland would pull
the outlet mucus inside, protecting gland apertures from the gastric
juice.
Copyright 2001 Academic Press.

MeSH Terms:
Bicarbonates/*metabolism
Gastric Mucosa/anatomy & histology/*secretion
Humans
Hydrogen-Ion Concentration
Ion Transport
Models, Biological
Mucus/*secretion
Substances:
0 (Bicarbonates)
Publication Status: ppublish
PMID: 11397134 [PubMed - indexed for MEDLINE]
From PubMed



36 A model of hydraulic interactions in liver parenchyma as forces behind
the intrahepatic bile flow.
Kurbel S, Kurbel B, Dmitrovic B, Wagner J.
Med Hypotheses. 2001 May;56(5):599-603.


Physiology, Osijek Medical Faculty, University JJ Strossmayer, Osijek,
Croatia. sven.kurbel@public.srce.hr
The small diameters of bile canaliculi and interlobular bile ducts make it
hard to attribute the bile flow solely to the process of secretion. In the
model liver within its capsule is considered a limited space in which
volume expansions of one part are possible only through the shrinking of
other parts. The liver capsule allows only very slow volume changes. The
rate of blood flow through the sinusoides is governed by the
Poisseuill-Hagen law. The model is based on a concept of circulatory liver
units. A unit would contain a group of acini sharing the same conditions
of arterial flow. We can imagine them as an acinar group behind the last
pressure reducer on one arterial branch. Acini from neighboring units
compose liver lobules and drain through the same central venule. One
lobule can contain acini from several neighboring circulatory units. The
perfusion cycle in one unit begins with a transient tide in the arterial
flow, governed by local mediators. Corresponding acini expand, grabbing
the space by compressing their neighbors in the same lobules. Vascular
resistance is reduced in dilated and increased in compressed acini. Portal
blood flows through the dilated acini, bypassing the compressed neighbors.
The cycle ends when the portal tide slowly diminishes and acinar volume is
back on the interphase value until the new perfusion cycle is started in
another circulatory unit. Each cycle probably takes minutes to complete.
Increased pressures both in dilated and in compressed acini force the bile
to move from acinar canalicules. Both up and down changes in acinar volume
might force the acinar biliary flow. In cases of arterial
vasoconstriction, increased activity of vasoactive substances would keep
most of the circulatory units in the interphase and increased liver
resistance can be expected. Liver fibrosis makes all acini to be of fixed
volume and result in increased resistance. Because of that, low pressure
portal flow would be more compromised, as reported. In livers without
arterial blood flow, although some slow changes in the portal flows can be
expected, acinar volume changes should be reduced. In acute liver injury,
enlarged hepatocytes would diminish sinusoidal diameter and increase
acinar resistance. In liver tumors, areas of neovascularization with
reduced resistance would divert the arterial flow from the normal tissue,
while in the compressed perifocal areas, increased vascular resistance
should diminish mainly the portal flow.
Copyright 2001 Harcourt Publishers Ltd.

MeSH Terms:
Bile/*secretion
Bile Ducts, Intrahepatic/*physiology/secretion
Blood
Liver/*physiology
Publication Status: ppublish
PMID: 11388774 [PubMed - indexed for MEDLINE]
From PubMed



37 Intracranial infection after missile brain wound: 15 war cases.
Hećimović I, Dmitrović B, Kurbel S, Blagus G, Vranes J, Rukovanjski M.
Zentralbl Neurochir. 2000;61(2):95-102.


Division of Neurosurgery, University Hospital Osijek, Osijek University
Medicine School.
OBJECTIVES: The present study describes 15 cases of intracranial
infections developed in a group of in patients with missile brain wound
(MBW), during the war in Croatia in the region of East Slavonia. METHOD:
The retrospective study included 88 MBW casualties. There were 11 females
and 77 males aged 2-80 years. The projectile penetration of the cranial
dura was confirmed and the presence of intracranially retained foreign
bodies was evaluated with computerized tomography (CT) in all the
patients. The wounded were treated according to the modern recommendations
of neurotrauma care. However, we extracted only accessible bone/metallic
fragments during intracranial debridement. All intracranial infections
were documented by cultures, CT, surgery or autopsy. The mean follow-up
period of wounded with intracranial infections was 2.4 years (range, 10
days to 7 years). RESULTS: Intracranial infection developed in 14 patients
(17%) as "early intracranial infections". Among 14/15 cases, infection
developed within the first 8 weeks, and in 1 case 5 months after wounding.
We recorded 4 cases of isolated bacterial meningitis, whereas in 9 cases
brain abscess had developed. In 6 cases brain abscess was associated with
concomitant meningitis and epidural empyema. Local cerebritis developed in
one case, as well as subdural empyema with the concomitant meningitis in
one case. There were 8 deaths in total of 15 cases. Glasgow Outcome Score
3 was observed in 2 and good outcome in 5/15 cases. The infectious
organisms were isolated in 8 cases. Gram-positive bacteria were found in
12 different specimens. Gram-negative bacteria were found in 9 specimens.
The most frequently isolated organism was Staphylococcus aureus.
beta-hemolytic streptococcal and clostridial infections were not observed.
Among the 15 patients with intracranial infection, just one did not have
intracranially retained bone and/or metallic fragments. However, among the
73 head injuries without intracranial infections only 10 did not have
retained fragments. CSF fistula and/or dehiscence developed in 13/15
patients with intracranial infection. In 67/73 wounded without
intracranial infections, wound complications were not registered.
CONCLUSIONS: The liberal use of post-contrast CT of the brain within the
first 2 months after injury, especially if performed early in the clinical
course, can lead to a prompt diagnosis of most of "early intracranial
infections". The surgical procedures in order to prevent wound CSF
fistula/dehiscence development are absolutely necessary. The immediate
scalp and dural wound repair in case of wound complications are absolutely
indicated and if needed, the procedures can be repeated. However, it seems
that retained fragments are not responsible for an increased rate of
intracranial infection.
MeSH Terms:
Adolescent
Adult
Brain Abscess/*etiology/physiopathology
Brain Diseases/*microbiology
Brain Injuries/*complications
Croatia
Female
Fever
*Foreign Bodies
Glasgow Coma Scale
Gram-Negative Bacterial Infections/etiology
Gram-Positive Bacterial Infections/etiology
Humans
Male
Middle Aged
Retrospective Studies
*War
Wound Infection/*diagnosis/physiopathology
Wounds, Gunshot/*complications/physiopathology
Publication Status: ppublish
PMID: 10986758 [PubMed - indexed for MEDLINE]
From PubMed



38 Cancer incidences in the digestive tube: is cobalamin a small intestine
cytoprotector?
Kurbel S, Kovacic D, Radic R, Drenjancevic I, Glavina K, Ivandic A.
Med Hypotheses. 2000 Mar;54(3):412-6.


Physiology, University 'JJ Strossmayer', Osijek Medical Faculty, Osijek,
Croatia. sven.kurbel@public.srce.hr
Malignancies are common in the digestive tube, although with unequal
distribution among segments. The aim of this paper was to compare
available interpretations of the low cancer incidence in the small bowel
and high in the large bowel. Supposed mechanisms include relatively small
bacterial population, large secretion of liquid and rapid transit in the
small bowel. Small bowel mucosa is the main absorptive part of the
digestive tube with absorption rates for various nutrients so high that
they can even be considered as clearances from the intestinal content.
Consequently, these nutrients are not present in the large bowel. An
alternative explanation is that an absorbable protective substance from
the intraluminal content, might protect the mucosa from malignant
transformations. It can be speculated that if there are any cytoprotective
substances in the digested food their effect would be expressed mostly in
the absorptive small intestine, leaving the large bowel mucosa
unprotected. Vitamin B12 might be a possible candidate for this role.
Cobalamin molecules are initially bound to haptocorrin (Hc) in the
stomach, but in the small intestine B12 is transferred to intrinsic factor
(IF) after the action of pancreatic trypsin on Hc. Cobalamin-IF complexes
are absorbed in the terminal ileum leaving only a small fraction of B12 to
enter the large bowel. We have tried to summarize available data regarding
cancer incidences in digestive tube, segmental length and transit times of
tube content. Cancer density is calculated as incidence per length and
transit speed as length per transit time. Cancer incidences for seven
intestinal segments were considered low if they were below one case per
100 000 inhabitants annually, while the low cancer density meant less than
six cases per 100 000 inhabitants per metre. For instance, transverse
colon was considered as a high cancer incidence place (2.15 cases), with
low cancer density (4.3 cases/m). Transit speed more than 0.3 metre/hour
was associated with low cancer incidences (accuracy 0.85) and low cancer
density segments (accuracy 1.00). Cobalamin availability showed similar
distribution, available in low incidence segments and unavailable in high
incidence segments. Experimental studies are needed to quantify B12
availability in the large bowel and to determine whether small amounts of
B12-IF or, perhaps, B12-haptocorrin complexes are absorbed by the small
bowel mucosa. Without that, no cytoprotective effects of B12 in the
digestive tube can be expected.
Copyright 2000 Harcourt Publishers Ltd.

MeSH Terms:
Anticarcinogenic Agents/*pharmacology
Digestive System Neoplasms/*epidemiology/*prevention & control
Humans
Incidence
Intestine, Small/*pathology
Vitamin B 12/*pharmacology
Substances:
0 (Anticarcinogenic Agents)
68-19-9 (Vitamin B 12)
Publication Status: ppublish
PMID: 10783476 [PubMed - indexed for MEDLINE]
From PubMed



39 Histochemical changes in the rectal mucosa of diabetic patients with
and without diarrhea or constipation.
Ivandić A, Prpic-Krizevac I, Dmitrović B, Vcev A, Kurbel S, Peljhan V, Bacun T.
Wien Klin Wochenschr. 2000 Jan 14;112(1):21-6.


Department of Internal Medicine, Osijek University Hospital, Croatia.
Sixty-four diabetic patients, 35 with diarrhea, 15 with constipation and
14 without stool problems, and forty healthy subjects, were subjected to
rectosigmoidoscopy. During rectosigmoidoscopy, rectal biopsy specimens for
histological and histochemical analysis were obtained. Histological
findings of nonspecific colitis in 25 out of 64 diabetic patients were
uniformly distributed among the three groups (p = 0.959). However, the
finding was slightly more common in diabetic patients than in controls
(eight out of 40 control subjects, p = 0.043). A positive PAS reaction was
observed in 30 out of 64 diabetic patients and was also uniformly
distributed among the three groups (p = 0.508), but was significantly more
common among diabetic patients than controls (three out of 40, p < 0.001).
A positive reaction to cholesterol was found in 46 out of 64 diabetic
patients, also uniformly distributed among the three groups (p = 0.773).
It was significantly more common in diabetic patients than in controls
(nine out of 40, p < 0.001). Reactions of the rectal mucosa histological
specimens to glycogen and triglycerides were negative, both in diabetic
patients and in controls. In conclusion, it appears that stool problems
among our diabetic patients were not related to the positivity of PAS or
to the positive cholesterol reaction in the rectal mucosa histological
specimens. Since positive findings of both reactions were more common in
specimens taken from diabetic patients than in controls, positive
reactions might be related to metabolic disturbances in diabetic patients.
MeSH Terms:
Adult
Aged
Biopsy
Cholesterol/metabolism
Colitis/pathology
Constipation/pathology
Diabetes Mellitus, Type 1/*pathology
Diabetes Mellitus, Type 2/*pathology
Diarrhea/pathology
Female
Humans
Intestinal Mucosa/*pathology
Male
Middle Aged
Rectum/*pathology
Sigmoidoscopy
Substances:
57-88-5 (Cholesterol)
Publication Status: ppublish
PMID: 10689736 [PubMed - indexed for MEDLINE]
From PubMed



40 Minoxidil and male-pattern alopecia: a potential role for a local
regulator of sebum secretion with vasoconstrictive effects?
Kurbel S, Kurbel B, Zanić-Matanić D.
Med Hypotheses. 1999 Nov;53(5):402-6.


Department of Physiology, Osijek Clinical Hospital, Croatia.
sven.kurbel@public.srce.hr
Regulation of the hair cycle takes place at the pilo-sebaceous unit with
the sebaceous gland as a sex hormone-dependent part. Although minoxidil
stimulates proliferation of follicular cells and activation of
prostaglandin endoperoxide synthase-1, it was suggested that other
mechanisms, such as an increase in the local blood flow, might mediate the
drug effect on hair growth. If that is the case, it is possible that
minoxidil counteracts some vasoconstrictive mediator of male-pattern
alopecia. This hypothetical vasoconstrictive mediator X would have to meet
some criteria: (I) vasoconstriction both in the general circulation and in
the hair-growing skin; (II) local vasoconstrictive activity in the hair
growing skin should be related to the circulating testosterone level;
(III) only an increase in the local mediator X activity causes
male-pattern alopecia, since hypertensive patients are not balder than
expected. The sebaceous gland is a possible place of the mediator X
secretion since it is a sex-hormone-dependent part of the pilo-sebaceous
unit. ET-1 might be a suitable candidate for the mediator X, since male
hormones raise ET-1 plasma levels and female hormones lower them. The
speculation presented here is that ET-1, beside vasoconstriction in the
general circulation, might also regulate the sebum secretion, by
triggering contractions of the myoepithelial cells. This hypothetical
mechanism would normally remain confined to the sebaceous gland. During
puberty, sex hormones stimulate growth of sebaceous glands in both sexes.
In women hypertrophied sebaceous glands under estrogen control would not
increase its ET-1 content, while in men, testosterone would increase ET-1
secretion that might affect the neighboring arterioles. Induced
vasoconstriction might reduce the hair growth and promote hair loss. If
ET-1 plays the described role, then an ET-1 antagonist, i.e. bosentane,
should also have some hair-growing properties.
MeSH Terms:
Alopecia/blood/*drug therapy
Endothelin-1/pharmacology
Estrogens/blood
Humans
Male
Minoxidil/pharmacology/*therapeutic use
Models, Theoretical
Sebum/*secretion
Testosterone/blood
Vasoconstriction/drug effects
Vasodilator Agents/pharmacology/*therapeutic use
Substances:
0 (Endothelin-1)
0 (Estrogens)
0 (Vasodilator Agents)
38304-91-5 (Minoxidil)
58-22-0 (Testosterone)
Publication Status: ppublish
PMID: 10616041 [PubMed - indexed for MEDLINE]
From PubMed