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D Wilhelm

Publications and source records attributed to D Wilhelm.

At least 19 recordsLinked to original sources
PubMed1992

Studies on the formation of dipalmitoyl species of phosphatidylcholine and phosphatidylethanolamine in pulmonary type II cells.

Endogenous content of and incorporation of labelled glycerol into alkenylacyl-, alkylacyl- and diacyl-glycerol, -glycerol-3-phosphocholine and -glycero-3-phosphoethanolamine of pulmonary type II cells were measured. On prolonged incubation of type II cells with labelled glycerol, the proportion of label incorporated into the diacyl subclass of these glycerolipids increased and the proportion of label incorporated into the ether lipids declined. Endogenous phosphatidylcholine (PtdCho) of type II cells contained 38.4% of the dipalmitoyl species, but endogenous phosphatidylethanolamine (PtdEtn) only 2.5%. In contrast, similar proportions of labelled glycerol were incorporated into dipalmitoyl-PtdCho and -PtdEtn after short-time incubation but, with prolonged incubation time the proportion of labelled dipalmitoyl-PtdCho increased from 11.3 to 18.8%, whereas that of dipalmitoyl-PtdEtn did not change significantly. Type II cell membranes were found to exhibit cofactor-independent and CoA-mediated transacylations of [1-14C]palmitoyl-lyso-PtdCho and -lyso-PtdEtn. The distribution of label among the palmitic acid-containing species of PtdCho and PtdEtn formed by both transacylation activities was determined. Cofactor-independent and CoA-mediated transacylation showed a strong selectivity for palmitate and arachidonate and a strong discrimination against oleate. The amount (nmol) of dipalmitoyl-PtdEtn formed by both transacylation activities after short-time incubation (2 min) decreased with prolonged incubation time (60 min). In contrast, the nmol of dipalmitoyl-PtdCho formed by cofactor-independent transacylation remains nearly the same after short-time and longer incubation. The nmol of dipalmitoyl-PtdCho formed by CoA-mediated transacylation increased strongly in the same time interval. Beside synthesis de novo via the CDP-choline pathway and reacylation of lyso-PtdCho with palmitoyl-CoA, the CoA-mediated transacylation of lyso-PtdCho may be an effective pathway for the formation of dipalmitoyl-PtdCho in pulmonary type II cells.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1992

The effect of some alpha-adrenoceptor antagonists on spontaneous myogenic activity in the rat portal vein and the putative involvement of ATP-sensitive K+ channels.

In the present study we showed that the alpha-adrenoceptor antagonists phentolamine, yohimbine, prazosin, corynanthine and idazoxan, when cumulatively applied in high concentrations (1-100 mumol/l), can increase spontaneous myogenic activity in the rat portal vein. 5-Methyl-urapidil and rauwolscine were ineffective in this respect. Pretreatment with phenoxybenzamine in a concentration of 1 mumol/l (20 min), which results in alkylation of all functional alpha-adrenoceptors in the rat portal vein, was unable to antagonize the increase in spontaneous myogenic activity elicited by phentolamine. Antazoline (1-100 mumol/l), a H1 antagonist and 2-substituted imidazoline which is devoid of alpha-adrenoceptor blocking properties, exhibited similar effects on spontaneous myogenic activity as its structurally closely related analogue phentolamine. Since phentolamine is reported to interact with ATP-sensitive K+ channels we investigated the role of K+ channels in more detail. The K+ channel openers cromakalim and diazoxide elicited a decrease in spontaneous myogenic activity. Glibenclamide (0.3-3 mumol/l), a selective blocker of ATP-sensitive K+ channels in cardiac and pancreatic tissues, and phentolamine (1-10 mumol/l) shifted the concentration-response curves of cromakalim and diazoxide concentration dependently to the right. Yohimbine showed only a modest effect in the highest concentration (100 mumol/l) applied. E-4031 (0.01-0.3 mumol/l), a sotalol derivative and one of the most selective blockers of the delayed rectifier current (Ik) in cardiac tissue, was a potent contractile agent when added to the rat portal vein in the same way as the alpha-adrenoceptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Effects of R 56865 and phenytoin on mechanical, biochemical, and morphologic changes during ouabain intoxication in isolated perfused rabbit heart.

The Na+/Ca2+ overload inhibitor R 56865 (N-[1-[4-(4-fluorophenoxy)-butyl]-4-piperidinyl)-N-methyl-2- benzothiazolamine) has been reported to prevent or attenuate ischemia- as well as ouabain-induced cellular sodium and calcium load. We investigated the potency of this compound in preventing mechanical, biochemical, and ultrastructural consequences of ouabain (OUA) intoxication in isolated rabbit heart. The protective effect of the digitalis antidote phenytoin (PHT) on the consequences of ouabain intoxication was examined for comparison. In isolated perfused rabbit heart, OUA (0.4 microM) caused an increase in left ventricular end-diastolic pressure (LVEDP) that was accompanied by depletion of high-energy phosphates (80% less than in control), accumulation of tissue lactate (12-fold) and damage of contractile elements and mitochondria. Accumulation of lactate was associated with a decrease in oxygen consumption by the isolated perfused heart. R 56865 (1.0 microM) and phenytoin (60 microM) prevented increase in LVEDP, breakdown of the energy-rich phosphates creatine phosphate (CrP) and ATP, accumulation of lactate, and morphologic changes induced by OUA. The above-mentioned toxic effects of OUA are interpreted as consequences of mitochondrial failure finally leading to breakdown of the oxidative phosphorylation. Thus, we conclude that the protective action of both compounds, R56865 and PHT, may be attributed to prevention or attenuation of mitochondrial failure due to OUA-induced disturbance of ion homeostasis.

Adenosine Triphosphate↗
PubMed1992

Alpha 1-adrenoceptor-mediated Ca(2+)-entry from the extracellular fluid and Ca(2+)-release from intracellular stores: no role for alpha 1A,B-adrenoceptor subtypes in the pithed rat.

1. In the present study, we tested the hypothesis that in the pithed rat preparation two subtypes of the alpha 1-adrenoceptor are linked to two different signal transduction mechanisms, both of which contribute to vasoconstriction, one facilitating Ca(2+)-entry from the extracellular fluid (alpha 1A) and one promoting the release of Ca2+ from intracellular sources (alpha 1B). 2. The selective alpha 1A-adrenoceptor antagonist, 5-methyl-urapidil, and the selective alpha 1B-adrenoceptor antagonist, chloroethylclonidine, were unable to discriminate between alpha 1-adrenoceptor-mediated pressor responses, which relied on an entry of extracellular Ca2+ sensitive to nifedipine and an intracellular release of Ca2+ insensitive to nifedipine, respectively. 3. Chloroethylclonidine, 12.5 and 25 mg kg-1 i.v., were equieffective, and had only minor effects on alpha 1-adrenoceptor-mediated increases in diastolic blood pressure. This could be associated with a small decrease in the receptor-reserve of the pithed rat preparation due to irreversible receptor blockade by this antagonist. These data indicate that chloroethylclonidine-sensitive alpha 1-adrenoceptors constitute only a minor fraction of the total alpha 1-adrenoceptor population on rat arterial resistance vessels. 4. Chloroethylclonidine behaved as a partial agonist eliciting a small increase in baseline diastolic blood pressure which could be inhibited by Ca(2+)-entry blockade with nifedipine. 5. Chloroethylclonidine potentiated the pressor responses elicited by the alpha 2-adrenoceptor agonists UK-14,304 and azepexole (B-HT 933). 6. No evidence was found in the pithed rat that alpha 1-adrenoceptor-mediated Ca(2+)-entry from the extracellular fluid and Ca(2+)-release from intracellular stores are mediated by alpha 1A and alpha 1B-adrenoceptors, respectively.

Adrenergic alpha-Antagonists↗
PubMed1992

In vitro pharmacology of R 80122, a novel phosphodiesterase inhibitor.

The cardiac in vitro effects of R 80122, a novel phosphodiesterase (PDE) inhibitor, were investigated and compared with those of the reference compound milrinone and of the calcium-sensitizer adibendan. In guinea pig left atria, both milrinone and R 80122 increased contractile force; 10 microM milrinone was equieffective to 1 microM R 80122. The rate of spontaneously beating atria was not altered by R 80122 in the concentration range of 0.01-0.3 microM. Higher concentrations (1-10 microM) led to a statistically insignificant increase of 20%. Milrinone's effect on frequency was more pronounced and amounted to 21% at 10 microM and to 40% at 100 microM. Adibendan increased heart rate (HR) by 10% at a concentration of only 0.03 microM. This effect was not enhanced any further by increasing the concentration. In papillary muscle, the positive inotropic effects of both milrinone and R 80122 were inhibited by carbachol, indicating involvement of cyclic AMP. Further indications for a cyclic AMP-dependent action were obtained by induction of slow action potentials and synergism with isoprenaline. In electrophysiologic measurements, milrinone reduced action potential duration (APD) in a high concentration whereas R 80122 had no effect. Action potential changes elicited by a toxic concentration of ouabain were reduced by R 80122. Relaxation of rat aortic rings contracted by KCl and relaxation of guinea pig aortic rings contracted by norepinephrine (NE) was comparable for both milrinone and R 80122. R 80122 also caused relaxation of canine coronary arteries constricted with prostaglandin F2 alpha (PGF2 alpha) both with and without endothelium. NE-induced contractions in canine gastrosplenic arteries were not affected by R 80122. Cardiac contractility that had been impaired to various degrees by pentobarbital or by aging was restored to control values by both milrinone and R 80122. R 80122 enhanced cardiac contractility at lower concentrations than milrinone with no concomitant increase in frequency or shortening of the action potential, which may be advantageous for treatment of heart failure.

Action Potentials↗
PubMed1992

Expression of the fragile-X in the "premutated"/"non-imprinted" state.

Data about the expression of the fragile site at Xq27.3 from 74 daughters of normal transmitting males (NTMs) were collected from 7 different genetic centers. The majority (85.1%) of these obligate female carriers did not show any cytogenetic expression of fra-X. The remaining 14.9% of these females had frequencies below 3%. In cases with a frequency below 3% of fra-X, a "premutated"/"non imprinted" state of a female carrier should be considered. The results of this collaborative study are in accordance with data from DNA studies taking the premutation model into account.

Female↗
PubMed1991

Differences between full and partial alpha-adrenoceptor agonists in eliciting phasic and tonic types of responses in the longitudinal smooth muscle of the rat portal vein.

The aim of the present investigation was to study, taking into account both quantitative and qualitative differences, the influence of full and partial alpha-adrenoceptor agonists on spontaneous myogenic activity in the rat portal vein. We found that the alpha-adrenoceptor agonists cirazoline, adrenaline, noradrenaline, phenylephrine, St 587, Sgd 101/75, B-HT 920 and UK-14,304 could increase the amplitude of the phasic myogenic contractions in the rat portal vein with apparent differences in EC50 and Emax values. In addition to an increase in phasic myogenic activity, the alpha-adrenoceptor agonists cirazoline, adrenaline, noradrenaline, and phenylephrine were also able (in higher concentrations) to increase the basal tone of the rat portal vein preparation, again with apparent differences in EC50 and Emax values. Changing the extracellular Ca2+ concentration from 0.9 mmol/l to 2.5 mmol/l had no influence on the phasic character and the concentration range in which St 587 and UK-14,304 increased spontaneous myogenic activity, although changes in amplitude and frequency of the spontaneous myogenic contractions were less pronounced at a higher extracellular Ca2+ concentration (2.5 mmol/l). By the use of Schild analysis with the competitive alpha-adrenoceptor antagonists prazosin (pA2 = 8.74) and 5-methyl-urapidil (pA2 = 8.37), it was established that the contractile responses to St 587 were mediated by the same alpha 1-adrenoceptor subtype as the phasic and tonic type of contraction elicited by phenylephrine as described in a previous study. The concentration-response curve of UK-14,304 was significantly shifted to the right by low concentrations of prazosin (3 nmol/l-30 nmol/l), indicating stimulation of alpha 1-adrenoceptors by UK-14,304 in the rat portal vein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1991

The role of alpha 1-adrenoceptor subtypes in the phasic and tonic responses to phenylephrine in the longitudinal smooth muscle of the rat portal vein.

The purpose of this investigation was to determine whether alpha 1-adrenoceptor subtypes (co)exist in the rat portal vein and, if so, whether they could be functionally associated with the phasic and tonic types of contraction as a response to alpha 1-adrenoceptor stimulation by phenylephrine. A low Ca2+ concentration (0.9 mmol/l) in the Tyrode solution enabled us to quantify changes both in the phasic myogenic activity and in the basal tone of the rat portal vein preparation very precisely. We used both competitive and non-competitive alpha-adrenoceptor antagonists which have been employed successfully by other investigators to discriminate between alpha 1-adrenoceptor subtypes in vascular and other tissues. Schild analysis showed that the competitive alpha-adrenoceptor antagonists prazosin, phentolamine, yohimbine, corynanthine, idazoxan, rauwolscine and 5-methyl-urapidil could not distinguish between the phasic and tonic responses to phenylephrine and/or different alpha 1-adrenoceptor subtypes in the rat portal vein. However, when we compared our pA2 values with those found to be representative indicators according to subclassifications based on the use of selective antagonists in different tissues, the alpha 1-adrenoceptors in the rat portal vein appeared to belong to the alpha 1L- or alpha 1a-subtype. This subclassification was not in accordance with the data obtained with the irreversible alpha-adrenoceptor antagonist chloroethylclonidine. However, the validity of this alkylating agent as a tool for receptor classification was restricted, at least in the rat portal vein, by its effects on receptor reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1991

Differential effect of R 56865 on ouabain binding to isolated sarcolemma and intact atrial tissue of guinea-pig.

1. R 56865 (N-[1-[4-(4-fluorophenoxy)-butyl]-4-piperidinyl]-N-methyl- 2-benzothiazolamine) is a compound known to antagonize cardiac glycoside intoxication. Therefore, the effect of the compound on ouabain binding to intact cardiac tissue as well as cardiac membrane preparations was investigated. 2. The binding of ouabain to highly purified sarcolemmal membranes was not influenced by R 56865 1 x 10(-6) mol l-1 (ouabain: KD = 1.3 x 10(-7) mol l-1, Bmax = 160 pmol mg-1; ouabain + R 56865: KD = 1.4 x 10(-7) mol l-1, Bmax = 168 pmol mg-1). 3. In contrast to the results in purified membranes, the binding of ouabain (10(-8) mol l-1 to 5 x 10(-7) mol l-1) to intact atria was significantly reduced. 4. Ouabain, 5 x 10(-7) mol l-1, led to a transient positive inotropic effect of about 220% followed by a developing negative inotropic effect after 3 h. R 56865, 10(-7) mol l-1, led to a maximal positive inotropic effect of about 290% also followed by a delayed decline of contractile force. A tenfold higher concentration of R 56865 led to sustained positive inotropic effect of about 250% in the same time interval. 5. The different effects of R 56865 on ouabain binding in subcellular preparations and intact tissue do not support the view that R 56865 interferes directly with the action of ouabain on Na/K-ATPase. An indirect effect, which may be mediated by a lowered intracellular sodium load is discussed.

Animals↗
PubMed1991

Characterization of the interaction of R 56865 with cardiac Na- and L-type Ca channels.

1. In isolated cardiac muscle, submicromolar concentrations of R 56865 (N-[1-[4-(4-fluorophenoxy)-butyl]-4-piperidinyl]-N-methyl-2- benzothiazolamine) have been shown to attenuate the toxicity of cardiac glycosides. 2. We studied the influence of R 56865 on calcium and sodium currents in single isolated ventricular cardiomyocytes. The effect of R 56865 on action potential and contractile force in the presence of increased sodium load was also tested by exposing papillary muscles to veratridine or Anemonia sulcata toxin ATX II. 3. The calcium current was not affected by R 56865 as assessed in slow action potentials of papillary muscles and current measurements in ventricular cardiomyocytes. 4. In papillary muscles, R 56865 (1 mumol l-1) abolished veratridine-induced aftercontractions and afterdepolarizations without affecting the profound prolongation of the action potential. When pretreated with R 56865, the occurrence of afterdepolarizations was prevented and the decline of the resting membrane potential was attenuated. 5. Pretreatment with R 56865 (1 mumol l-1) did not counteract the ATX II-induced prolongation of the action potential. 6. The sodium current (Nao 30 mmol l-1) was concentration-dependently decreased by R 56865 (0.1-10 mumol l-1). The blocking effect was more pronounced at less negative holding potentials. 7. Our results demonstrate that the protective effect of R 56865 against veratridine-induced electrical and mechanical oscillations is not due to a direct effect on the calcium current. A potential-dependent inhibition of the sodium current may contribute. Additional sites of action, like interference with intracellular calcium release and inhibition of potassium currents, remain to be investigated.

Action Potentials↗
PubMed1991

Evaluation of vulvar irritancy potential of a menstrual pad containing sodium bicarbonate in short-term application.

The effect on the skin of menstrual pads containing sodium bicarbonate as a fragrance substitute and of sodium bicarbonate alone was studied in 50 healthy women. Skin changes were monitored by transepidermal water loss, capacitance, laser Doppler flowmetry, skin surface pH and visual scoring. No clinical signs developed after the volunteers had been patched with the menstrual pads for 24 hours. No subclinical vulvar skin irritant reactions were observed with bioengineering methods. The menstrual pads containing sodium bicarbonate as a deodorant did not significantly affect the vulva in short-term use.

Bandages↗
PubMed1991

Standardized trauma (tape stripping) in human vulvar and forearm skin. Effects on transepidermal water loss, capacitance and pH.

Mechanical trauma to genital skin may favor the transmission of sexually transmitted diseases. To study differences between vulvar and forearm skin in epidermal repair after standardized trauma, transepidermal water loss, capacitance and pH of forearm and vulvar skin in 10 healthy premenopausal women were monitored for 7 days after a standardized trauma induced by tape stripping to glistening. Vulvar and forearm skin showed similar responses immediately after tape stripping: a sudden increase in transepidermal water loss and capacitance. Forearm skin, however, reacted more intensely than vulvar skin; forearm skin readings remained significantly higher than normal values for 2 days after tape stripping, whereas vulvar skin readings were not significantly different from normal. Thus, vulvar skin did not respond as extensively as forearm skin, presumably because it is a less complete barrier against excess body water loss. On the other hand, vulvar skin seemed to recover faster from skin damage than forearm skin, probably because of its higher epidermal cell turnover.

Adult↗
PubMed1991

Effect of low-concentration sodium lauryl sulfate on human vulvar and forearm skin. Age-related differences.

The reactivity of forearm and vulvar skin to low-concentration sodium lauryl sulfate (SLS) was studied in 20 healthy women, 10 before and 10 after menopause. SLS at concentrations of 0.1%, 0.5% and 1.0% was applied to the forearm and labium majus for 24 hours. Skin changes were monitored with transepidermal water loss (TEWL), capacitance (CAP) (as an indicator of stratum corneum hydration) and visual scoring (VS). In forearm skin, irritant dermatitis developed in most subjects, as indicated by a VS and TEWL increase, with the reaction in premenopausal women significantly more intense than in postmenopausal women. In vulvar skin, however, irritant reactions were not observed. CAP increased significantly in the forearm of premenopausal but not postmenopausal women, whereas it decreased significantly in postmenopausal vulvar skin. Thus, vulvar skin was less reactive to SLS at low concentrations than was forearm skin. However, SLS did affect vulvar skin stratum corneum hydration. The irritant response in the forearm decreased with age for all parameters studied, whereas in vulvar skin age-related differences in irritant reaction were limited to stratum corneum hydration.

Adult↗
PubMed1990

Effects of R56865 on membrane currents in isolated ventricular cardiomyocytes of the guinea-pig.

In isolated heart muscle, the compound R56865 (N-[1-[4-(4-fluorophenoxy)butyl]-4-piperidinyl]-N-methyl-2- benzothiazolamine) has been shown to protect against intoxication by cardiac glycosides. We studied the influence of R56865 on various membrane currents in single isolated ventricular cardiomyocytes of the guinea-pig. The sodium current, INa, was investigated at reduced extracellular Na+ (30 mM) in the presence of Cd2+ to block the calcium current, ICa, and with Cs+ substituted for K+ to reduce the K+ currents, IK. Under these conditions, R56865 concentration dependently decreased the peak INa with a half-maximum effect at about 1 microM. The steady state inactivation and normalized conductance of INa were not significantly different from the control. In 'normal' Tyrode solution, R56865 (10 microM) did not markedly reduce ICa, and did not affect the quasi steady state IK, which was taken as an index of K+ conductance. We conclude that R56865 possesses Na+ channel-blocking properties, whereas ICa and membrane K+ conductance were not influenced.

Animals↗
PubMed1990

An approach to differentiate between noradrenaline-elicited contractile processes in the rat isolated aorta.

The aim of the present study was to assess the different processes contributing to the contraction induced by noradrenaline (NA, 1 mumol/l) in the rat isolated aorta. Pretreatment with maximally effective concentrations of nifedipine or cromakalim reduced the NA-induced contraction to 80 +/- 3.5% or 63 +/- 2.0%, respectively, without alteration of the shape of the response. After pretreatment with Mn2+, NA caused a transient phasic contraction followed by a sustained tonic component, comparable to the response obtained in "Ca2(+)-free" medium. Ryanodine--in the presence of extracellular Ca2(+)-caused a slight increase in resting tension, but did not modify the NA-induced contraction. In "Ca2(+)-free" medium the contraction elicited by NA consisted of a transient phasic and a sustained tonic component. The amplitude of the phasic contraction decreased exponentially with the time of exposure to "Ca2(+)-free" medium. The phasic component was identified as elicited by Ca2+ released from the sarcoplasmic reticulum (SR) by means of ryanodine. If Ca2+ depleted tissues (80 min in "Ca2(+)-free" solution) were exposed to Ca2+ in the presence of Mn2+ or cromakalim, the NA-induced phasic response was inhibited, suggesting that Mn2+ and cromakalim blocked the refilling of the store. It can be concluded that activation of alpha 1-adrenoceptors in the rat aorta by NA elicits Ca2(+)-entry processes which have a different sensitivity to nifedipine, cromakalim and Mn2+. The Ca2+ released from SR contributes about 20% to the overall contractile response. Our data suggest that the depleted SR can be refilled from the extracellular space via a direct cromakalim- and Mn2(+)-sensitive pathway.

Animals↗
PubMed1990

Sodium lauryl sulfate-induced irritant contact dermatitis in vulvar and forearm skin of premenopausal and postmenopausal women.

Reactivity of the skin of the forearm and labia majora to three concentrations (2%, 3%, 5%) of sodium lauryl sulfate was studied in 20 healthy women, 10 premenopausal and 10 postmenopausal. Patches with the irritant were applied on day 0 for 24 hours. Skin changes were monitored by visual scoring and by the measurement of transepidermal water loss and capacitance as indicators of stratum corneum hydration on days 2, 3, 7, and 10. In forearm skin, irritant dermatitis developed in the majority of subjects as indicated by visual scoring and increase of transepidermal water loss. These changes were not significantly dependent on the concentration of sodium lauryl sulfate. In labia majora skin, irritant dermatitis developed in 50% of the women as determined by visual scoring; however, because of the pigmentation, visual scoring readings were less reliable in labia majora skin. Transepidermal water loss did not increase, but a significant and immediate decrease in capacitance was noted in labia majora skin. In forearm skin, postmenopausal women reacted less frequently and more slowly to sodium lauryl sulfate than premenopausal women whereas no age-related differences were observed in reaction of the vulvar skin. It is concluded that labia majora skin is not more reactive to sodium lauryl sulfate than forearm skin and that capacitance is more sensitive than transepidermal water loss in monitoring vulvar irritant dermatitis. Age-related differences in irritant reaction are apparent in the forearm, but not the vulva.

Adult↗
PubMed1990

Mechanical properties of human forearm and vulvar skin.

Using a newly developed suction device, the mechanical properties of forearm and vulvar skin were studied in 22 healthy women, 12 before and 10 after the menopause. The ratio between viscous deformation (Uv) and elastic deformation (Ue) and the biological elasticity, i.e. the ratio between immediate recovery (Ur) and total deformation (Uf), were both significantly lower in vulvar than in forearm skin. Ur/Uf decreased significantly with load in vulvar, but not in forearm skin, whereas Uv/Ue was not load-dependent in either site. Uv/Ue remained constant with age in both test sites, whereas Ur/Uf was significantly lower in post-menopausal women in both forearm and vulvar skin. In vulvar, but not in forearm skin, Uv/Ue was significantly correlated with body height which may be an indicator of mechanical connective tissue properties. Viscous deformation plays a lesser role and biological elasticity is decreased in vulvar compared to forearm skin. Despite differences in mechanical parameters at both sites, age-related changes seem to be similar.

Adult↗