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Biomedical subjects

C P Bianchi

Publications and source records attributed to C P Bianchi.

At least 19 recordsLinked to original sources
PubMed2006

Uterine estrogen receptor alpha and progesterone receptor during the follicular and luteal phase in llamas.

Estrogen receptor-alpha (ERalpha) and progesterone receptor (PR) were characterized in different endometrial cell types as luminal and glandular epithelium and stroma during the follicular (FP) and the luteal phase (LP) in llamas. Animals were examined daily by transrectal ultrasonography for the determination of the presence of an ovulatory follicle and ovulation was immediately induced by a GnRH injection (Day 0). Endometrial samples were obtained by transcervical biopsies from the left uterine horn on Day 0 (FP) and 9 days after the GnRH injection (Day 9, LP). Blood samples were collected on these days for estradiol 17beta and progesterone determination by RIA. An immunohistochemical technique was used to visualize ERalpha and PR immunostaining which was then analyzed by two independent observers. Total positive area and average staining for ERalpha were affected by the phase of the ovarian activity: in the three cell types there was more positive area and intense staining during the FP than during the LP. Similar findings were observed for PR, more positive stained areas were found during the FP than during the LP in the epithelia. In addition, the three cell types had more intense staining during the FP than during the LP. An effect of the cell type for ERalpha and PR was observed; epithelia (luminal and glandular) had more positive stained areas and greater intensity than stromal cells. In conclusion, the results of the present study suggest that in llamas, like in other ruminants, estradiol has a stimulatory effect while progesterone downregulates the ERalpha and PR and that the receptor is cell type specific.

Animals↗
PubMed1997

Conformation state of the ryanodine receptor and functional effects of ryanodine on skeletal muscle.

The ryanodine receptor (RyR) and the dihydropyridine (DHP) receptor (L-channels) comprise the main elements of the functional feet of the triadic element in skeletal muscle. These two main elements have conformational states that are regulated by the membrane potential and the consequent electrical field. The pharmacological action of ryanodine on skeletal muscle depends upon the physiological functional state of the RyR. At a resting potential of -90 m V, ryanodine at very low concentrations, 10(-11) M, causes the RyR to have a low conductance state which allows calcium to leak from the terminal cisternae of the sarcoplasmic reticulum and to be recycled with ATP utilization, leading to a marked increase in oxygen consumption and aerobic metabolism. At concentrations greater than 10(-6) M, ryanodine can cause a slowly developing contracture of resting muscle, inhibit the muscle twitch when the RyR complex is formed during stimulation, and, if formed before stimulation, accelerate the development of contracture. Biochemical studies have revealed that the RyR has four binding sites in which the conductance state depends upon the number of sites occupied by ryanodine. Our present understanding of the RyR-operated calcium channel is the result of an interdisciplinary approach in which each discipline (anatomy, physiology, biophysics, and biochemistry) contributes to our knowledge of the pharmacological action of ryanodine.

Animals↗
PubMed1996

Cisplatinum enhancement of myocardial Mg2+ transport.

Cisplatinum in a concentration (4.3 x 10(-6) M) corresponding to the therapeutic plasma concentration for cancer patients was found to cause a marked enhancement of magnesium efflux and uptake in perfused frog myocardium. The magnesium content of the perfused frog ventricle is increased from 6.66 +/- 0.34 mumol/g wet wgt to 8.03 +/- 0.38 mu mol/g wet wgt. Cisplatinum had a negative inotropic action reducing contractile force to 46 +/- 8% of initial force after 40 min of perfusion. The corresponding control contractile force was reduced to 74 +/- 7%. Removal of calcium and magnesium from the perfusion solution containing 0.5 mM EDTA for 10 minutes caused contractile force to be reduced to 0 after 6 beats at 24 min-1. After ten minutes of perfusion with EDTA, 1.87 mu mol/g wet wgt of magnesium was lost from control ventricles. Cisplatinum increased the loss to 4.08 +/- 0.34 mu mol/g wet wgt. The magnesium lost during EDTA perfusion was completely recovered after 5 minutes of perfusion in Ringer or Tyrode solution by both control and cisplatinum treated frog ventricles. The contractile force also recovered to the level prior to perfusion with EDTA Ringer. The rate of Mg2+ efflux in EDTA Ringer is largest during the first 3 minutes and was 0.170 +/- 0.051 p mol cm-2 sec-1 for controls and 0.798 p mol cm-2 sec-1 for the cisplatinum treated ventricles. During the last 7 min of perfusion in EDTA Ringer the Mg2+ efflux was reduced to 0.057 +/- 0.005 p mol cm-2 sec-1 for control ventricles and 0.170 p mol cm-2 sec-1 for the cisplatinum treated ventricles. Cisplatinum increased both magnesium efflux and influx and influx in the frog myocardium, increased magnesium content to a higher level and reduced contractile force. The effect of cisplatinum on magnesium transport is attributed to an increase in the charged form of cisplatinum that accumulates inside the cell where chloride content is low and the chloride of cisplatinum is displaced to form a positively charged cisplatinum.

Animals↗
PubMed1994

Myocardial magnesium transport: effect of gramicidin S and epinephrine.

Initial magnesium transport in low magnesium Ringer in the frog myocardium consists of at least two systems, a fast system with high capacity with a time constant of 30 seconds and a slow transport system that operates with a time constant of 165 seconds. Both transport systems appear to be electroneutral and can operate either against an electrochemical gradient or with an electrochemical gradient. The fast transport system can transport Mg2+ in an outward direction at 1.84 p mol cm-2 sec-1; the slow system causes Mg2+ to be transported outward at 0.05 p mol cm-2 sec-1. Gramicidin S (5 microM) decreases the slow outward transport system to 0.01 p mol cm-2 sec-1 and at concentrations greater than 1 microM inhibits not only slow magnesium outflux in low calcium Ringer but also inhibits magnesium influx during recovery of Mg2+ in Ringer. Gramicidin S at 5 microM decreases Mg2+ influx from .04 p mol cm-2 sec-1 to 0.01 p mol cm2 sec-1 indicating that influx and efflux may take place on the same transport system. In the presence of 10 mM Mg2+ Gramicidin S increases magnesium content. Epinephrine increases magnesium efflux and overcomes the inhibition of Mg2+ efflux by Gramicidin S.

Animals↗
PubMed1993

Calcium dependent magnesium uptake in myocardium.

The frog myocardium maintains magnesium content at a steady state level when stimulated at 0.4Hz while being perfused with Ringer's solution containing 1 x 10(-3) M Ca2+ and 5 x 10(-7) M magnesium. When calcium is removed 43% of tissue magnesium is lost within 30 seconds or 12 beats. Restoration of calcium to the perfusion solution causes reaccumulation of magnesium from a solution containing 5 x 10(-7) M magnesium. The reaccumulation of magnesium indicates a highly selective transport system for magnesium which is dependent upon the presence of calcium. Calcium appears to reduce the leak of magnesium from the myocardium and enhances the transport of magnesium into the myocardial cell. Intracellular magnesium is a necessary cofactor for hundreds of enzymes, and is essential for protein synthesis and as an extracellular divalent cation helps to stabilize excitable membranes in conjunction with calcium. The concentration of ionized magnesium in the sarcoplasm of myocardial muscle has an average value of 1.45 mM +/- 1.37 (standard deviation), N = 19) with a range of 0.5 to 3.6 mM (1). The heart with its numerous mitochondria and high enzymatic activity is vulnerable to myocardial damage due to magnesium loss. The isolated frog ventricle conserves intracellular magnesium when perfused with Ringer's solution containing no added magnesium and maintains function for hours. The ability to conserve magnesium suggests a low permeability of the sarcolemma to magnesium and an extremely efficient inward transport system. Removal of calcium as well as magnesium from the perfusion solution causes a rapid loss of tension in the electrically driven frog ventricle (0.4) Hz.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

The readers' NIH.

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Education, Graduate↗
PubMed1992

Stimulation-enhanced 3-O-methylglucose efflux from the frog sartorius: kinetics and properties of the system.

The characteristics of the process by which contraction enhances glucose transport in the frog sartorius were studied. Electrical stimulation increased the permeability of muscles to 3-O-methylglucose (3-O-MeGlc), a nonmetabolizable glucose analogue, increasing efflux as well as uptake. Enhanced efflux was due to an increase in Vmax of the efflux process. A lactacidosis had no effect on basal 3-O-MeGlc efflux, and replacement of media Na+ with Li+ did not affect stimulation-induced uptake. Also, basal and stimulated uptake was not affected by 1 microM 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator. Lastly, N-carbobenzoxy-glycyl-L-phenylalaninamide, which inhibits insulin-enhanced, but not basal, glucose uptake in adipocytes, inhibited both basal and stimulated 3-O-MeGlc fluxes in the frog sartorius. From these findings, we conclude: (1) contraction and exercise enhance glucose transport in muscle by increasing the number of transporters in the plasma membrane, or their turnover, by an unknown process; and (2) basal glucose transport of muscle, unlike that of adipocytes, can not be distinguished from stimulated transport on the basis of its insensitivity to N-carbobenzoxyglycyl-L-phenylalaninamide.

3-O-Methylglucose↗
PubMed1992

The George B. Koelle symposium on the cholinergic synapse.

The George B. Koelle Symposium on the Cholinergic Synapse described the early development of the importance of ACh as a transmitter at both cholinergic synapses of the CNS, ganglion and neuromuscular junction. While a great deal is known about the function of cholinergic transmission at the neuromuscular junction, the integrated role of cholinergic, nicotinic and muscarinic receptors in the overall process of CNS functions, i.e., behavior, motor control, abstract thinking, memory and speech remains as a challenge for future investigation. The architecture of the cholinergic synapse appears to be a dynamic process involving ARIA, Agrin and the various forms of ACh esterase. The regulation of gene expression and site directed localization of postsynaptic cholinergic receptor proteins during the life cycle involves the dynamic interactions of these agents with the postsynaptic membrane and postsynaptic gene express. The last two papers at the symposium dealt with the chemistry of the nicotinic receptor regulated channel involved in ACh binding and the consequent cationic channel conductional changes.

Acetylcholine↗
PubMed1992

Trace metal (Cu and Zn) adaptation of organ systems of the American eel, Anguilla rostrata, to external concentrations of cadmium.

1. The impact of external cadmium on the concentrations of cadmium (Cd), copper (Cu) and zinc (Zn) in seven tissues of the American eel, Anguilla rostrata was investigated. Even after a week in freshwater with undetectable levels of Cd, the tissues of eels caught in fresh and/or brackish waters of the United States east coast contained Cd in kidney, liver, gut, and brain. 2. When the eels were exposed up to 16 weeks to low and high sublethal concentrations of Cd (75 and 150 micrograms/l, respectively), the highest tissue concentrations of Cd were found after two weeks of exposure. The accumulation was dose-related in all tissues studied except for the kidney. After 8 weeks of Cd exposure, the tissue levels of Cd were markedly reduced, and they were in a similarly low range after 16 weeks. At this time, the highest Cd concentrations were found in the gills and kidney. 3. After two weeks of Cd exposure, there was a drop of the tissue concentrations of Cu in liver and heart, and of Zn in gut and liver. The low concentrations of the two metals in other organs did not allow an evaluation of the Cd impact. After 16 weeks, the Cu concentrations in all tissues, with the exception of the liver, were similar to, or even higher than control levels. At the same time, Zn concentrations exceeded the control levels in heart and kidney of eels exposed to 75 and 150 micrograms Cd/l, respectively. 4. It is clear that some tissues of the eel are able to maintain or restore normal levels of Cu and Zn, up to 16 weeks, despite concomitant Cd accumulation.

Adaptation, Physiological↗
PubMed1990

Bimodal operation of the ryanodine-sensitive transducer calcium channel.

Ryanodine binds to the transducer calcium channel complex that links depolarization of the transverse tubule to calcium release from the terminal cisternae during excitation-contraction coupling of skeletal muscle. Ryanodine exerts a bimodal action on the transducer calcium channel complex depending upon membrane potential and concentration. When the transmembrane potential is at resting level (-90 mV inside cell vs outside), low concentrations of ryanodine 10(-10) M to 10(-8) M favor calcium influx from outside which in turn causes calcium release from the terminal cisternae via calcium operated calcium channels. The leak from the terminal cisternae is insufficient to cause contraction but does cause a large increase in aerobic energy utilization by the Ca-ATPase of the sarcoplasmic reticulum. When the transmembrane potential is made more positive (-40 mV) the transducer channel is opened to the terminal cisternae of sarcoplasmic reticulum and is maintained in an open state by ryanodine allowing calcium efflux from the terminal cisternae to the sarcoplasm. At higher concentrations of ryanodine the transducer-calcium channel becomes open to the terminal cisternae and its store of ionized calcium leaks from the terminal cisternae in sufficient quantities to cause a contracture. The ryanodine-sensitive calcium transducer calcium channel operates in a bimodal manner. At low concentrations less than 10(-4) M the ryanodine-sensitive transducer calcium channel is open to the lumen of the T-tubule and allows calcium to flow in and trigger further calcium release. At higher concentrations the ryanodine-sensitive transducer channel opens to allow a calcium efflux from the terminal cisternae in sufficient quantities to cause contracture.

Animals↗
PubMed1987

Reversible inhibition of acetylcholine contracture of molluscan smooth muscle by heavy metals: correlation to Ca++ and metal content.

The present study examined the effects of three heavy metals on the acetylcholine (ACh) contracture and Ca++ kinetics of the anterior byssus retractor muscle of Mytilus edulis. An isolated tissue bioassay using anterior byssus retractor muscle was prepared according to standard procedures and the isometric tension produced in response to ACh was measured. Ten millimolar Ni++, Co++ or Cd++ reduced the maximum contracture response to ACh in zero-Ca medium in a time-dependent manner. The inhibition was reversed upon restoration of medium containing 10 mM Ca++. The loss (and re-establishment) of contracture response to ACh corresponded to the influx (and efflux) of the heavy metal ions opposite to the direction of Ca++ flow. These results are consistent with the concept that the loss of the ACh contracture response is attributable to the displacement of tissue Ca++ from release sites by heavy metals.

Acetylcholine↗
PubMed1986

Antagonism of receptor-activated biological effects mediated by second messenger pathways.

It is generally held that many biologically active compounds produce their effects through a sequence of events that are initiated when the substances combine with selective receptors located on the cell surface membrane. Activation of these receptors produces a stimulus that is somehow transmitted intracellularly. The transduction between the stimulus and the response is now known to be mediated, in many systems, by an intracellular intermediary or second messenger. A model describing the relation of agonist concentration, receptor occupation, and biological response in such a system is herein extended to include antagonist binding at two target sites the cell-surface receptor and the receptor for the second messenger. It is demonstrated that the shift of an agonist's dose-response curve is characteristic of the site of antagonism and that analysis of this shift can reveal the existence of a second messenger pathway or, if this is known, the site of action of the antagonist.

Binding, Competitive↗
PubMed1986

Capillary fiber ratio and electrolyte content of compensatory hypertrophied rat soleus.

Capillary-to-fiber ratio and the content (mu moles/g muscle) of Na, K, Mg, Ca and Zn was measured in compensatory hypertrophied (CH) soleus muscles of adult Sprague-Dawley rats. The soleus hypertrophy was induced by unilateral tenotomy of the gastrocnemius and the plantaris muscles. Seven days after synergistic tenotomy the compensatory hypertrophied Soleus muscles showed no difference in the capillary-fiber ratio, Sr-extractable calcium ([Ca]Ext.) or the total content of Na, K, Mg and Zn. However, compared to the contralateral control side, the CH muscles showed an increase in the wet muscle weight (31.6%, P less than 0.01) and a significant decline (57.1%, P less than 0.05) in the residual calcium ([Ca]Res.) and 43.2% (P less than 0.05) decrease in the total calcium ([Ca]Total) content. It is concluded that during compensatory hypertrophy of skeletal muscles, the residual Ca reserves are significantly depleted, which may lead to a lower isometric tension generation in the muscle.

Animals↗
PubMed1984

Effect of diazepam on calcium translocation during physiological muscle fatigue.

Stimulation of frog sartorius muscle at 1 Hz leads to an initial positive staircase during the first 120 twitches and is followed by a negative staircase. There is a net calcium influx into two distinct compartments within the muscle during the positive staircase. The two compartments are separated by measuring the calcium extracted from muscles soaked in strontium-Ringer for 15 min and the calcium remaining in the muscle. A net gain of extractable Ca++ (0.32 mumol/g wet wt.) and residual Ca++ (0.18 mumol/g) is observed during positive staircase. A loss in residual Ca++, a gain in extractable Ca++ and a net loss of Ca++ (0.09 mumol/g) to the bathing medium occur during the period preceding physiological muscle fatigue (60 to 120 twitches). Diazepam (EC50, 5.6 X 10(-6) M) causes a marked reduction in the latent period and increases the rate constant 2.6 times the control value for physiological muscle fatigue. A net loss of 0.31 mumol/g of Ca++ to the bathing medium occurs during the interval between 60 and 120 twitches. Diazepam increases net Ca++ efflux 3.5-fold during this interval when compared to control muscles. Diazepam does not affect the Ca++ gained during the positive staircase but accelerates the loss of calcium from the residual and the extractable compartments during the initial phase of physiological muscle fatigue. Physiological muscle fatigue is attributed to an accumulation of calcium in the transverse tubular network and an uncoupling of the muscle action potential from contraction.

Animals↗