SEARCH · PubMed Health

Results for “variable methylation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,567 records · Page 87Linked to original sources

PubMed1975

Ontogenesis of monoamine oxidase and catechol-O-methyl transferase in various tissues of domestic swine.

Activities of monoamine oxidase (MAO) and catechol-o-methyl transferase (COMT) in liver, kidney, heart, spleen, hindbrain, and adrenal glands were compared in adult dogs, cats, guinea-pigs, rabbits, rats, sheep, and 150-day-old swine. Swine had the highest COMT activity and dogs or cats, the lowest in most tissues. MAO was more tissue and species variable. The ontogenesis of MAO or COMT was evaluated in the same six tissues of swine from 10 days before birth through 150 days of age. COMT and MAO generally increased in swine kidney and liver with age, but the developmental patterns were more variable in other tissues. COMT increased in heart, spleen, and adrenals through 14 days of age, decreased in spleen and adrenals to 150 days, but remained elevated in heart. Brain MAO activities were near or above 150-day-old levels at birth and changed little with age. Cardiac MAO fell from birth to 70 days of age, while splenic and adrenal activities increased with age. MAO substrate specificity to tyramine, benzylamine, and serotinin along with selective inhibition by harmine, pargyline, and clorgyline were used as indices of multiple enzymic forms. Type B MAO may dominate in all swine tussues except spleen, although the biochemical characteristics of this enzyme form do not seem to fit all of the patterns described for other species. Thermal stability of MAO in swine resembles that in the guinea-pig.

Age Factors↗

PubMed1987

Experimental neovascularization in vivo: the early changes in a stable adult vasculature responding to angiogenic stimulation by a syngeneic neoplasm.

To examine the vascular changes that lead to the development of new vessel sprouts from differentiated vessels the early response of an uninjured, stable, adult vascular bed to the presence of neoplastic tissue has been studied. Small grafts of a squamous cell carcinoma were implanted above the cremaster muscle of host rats syngeneic with the rat in which the neoplasm arose. The vascular response was examined by light microscopy of whole cremaster preparations after intravenous injection of colloidal carbon to label leaky vessels, and by scanning electron microscopy of methyl methacrylate injection casts. Three to five days after implantation there was a dramatic increase in the number of visible blood vessels of the microcirculation adjacent to the graft as a result of altered blood flow through the existing microvasculature. Capillaries and post-capillary venules became widely distended, tortuous and variably permeable to the introduced colloidal marker. Capillary involvement was restricted to the area nearest the graft while post-capillary venules were affected in more remote regions. Networks of newly formed vascular channels developed from the extremities of the tortuous loops. Altered permeability within the pre-existing vessels was related to the distension and tortuosity, with a pattern of vascular labelling quite unlike that induced by inflammatory mediators or tumour secreted vascular permeability mediator (VPM). These changes are considered to be the result of altered inter-endothelial cell adhesion and cellular rearrangement, and represent important antecedent stages in the formation of the new vascular structures.

Animals↗

PubMed2002

Spermine modulation of the glutamate(NMDA) receptor is differentially responsive to conantokins in normal and Alzheimer's disease human cerebral cortex.

The pharmacology of the N -methyl-d-aspartate (NMDA) receptor site was examined in pathologically affected and relatively spared regions of cerebral cortex tissue obtained at autopsy from Alzheimer's disease cases and matched controls. The affinity and density of the [(3)H]MK-801 binding site were delineated along with the enhancement of [(3)H]MK-801 binding by glutamate and spermine. Maximal enhancement induced by either ligand was regionally variable; glutamate-mediated maximal enhancement was higher in controls than in Alzheimer's cases in pathologically spared regions, whereas spermine-mediated maximal enhancement was higher in controls in areas susceptible to pathological damage. These and other data suggest that the subunit composition of NMDA receptors may be locally variable. Studies with modified conantokin-G (con-G) peptides showed that Ala(7)-con-G had higher affinity than Lys(7)-con-G, and also defined two distinct binding sites in controls. Nevertheless, the affinity for Lys(7)-con-G was higher overall in Alzheimer's brain than in control brain, whereas the reverse was true for Ala(7)-con-G. Over-excitation mediated by specific NMDA receptors might contribute to localized brain damage in Alzheimer's disease. Modified conantokins are useful for identifying the NMDA receptors involved, and may have potential as protective agents.

Aged↗

PubMed2004

Microinjection of the nitric oxide synthase inhibitor L-NAME into the lateral basal forebrain alters the sleep/wake cycle of the rat.

The effects of N(G)-nitro-L-arginine methyl ester (L-NAME) (0.19-0.74 micromol), a competitive inhibitor of the enzyme nitric oxide synthase (NOS); L-arginine (48.0-191.0 nmol), a nitric oxide (NO) precursor; and molsidomine (0.06-0.24 nmol), an NO donor, on spontaneous sleep were studied in adult rats implanted for chronic sleep recordings. Direct bilateral application of L-NAME into the nucleus of the horizontal limb of the diagonal band of Broca (HDB) increased waking (W) and reduced slow wave sleep (SWS). On the other hand, intra-HDB injection of L-arginine or molsidomine induced slight but inconsistent changes of sleep variables that did not attain significance. Pretreatment with L-arginine (191.0 nmol) or molsidomine (0.24 nmol) prevented the increase of W and the reduction of SWS induced by L-NAME (0.37 micromol), thus indicating that a decrease in the availability of NO may be involved in the effects of L-NAME on sleep variables. An increase in the release of acetylcholine (ACh) and/or a reduction in the output of gamma-aminobutyric acid (GABA) and adenosine could tentatively explain the effects of L-NAME on SWS and W.

Acetylcholine↗

PubMed1996

The contribution of NMDA receptors to the visual response in animals that have been partially monocularly deprived.

Kittens were monocularly deprived to give a partial shift in the ocular dominance histograms from their visual cortices. Responses were measured for the normal and deprived eyes at a variety of contrasts, and curves fitted to give measurements of background activity and peak visual response. The N-methyl-D-aspartate (NMDA) antagonist D-2-amino-5-phosphonovalerate (APV) was then applied, and the effect on the contrast-response curves was measured, and compared in the two eyes. In normal animals, the effect of APV on the contrast-response curve was similar in the two eyes. In monocularly deprived animals, on average, peak visual response was affected similarly in the two eyes, although there was wide variability from cell to cell. When the effect of APV on background activity was measured, there was difference between the normal and deprived eyes. APV reduced background activity in the normal eye more than it reduced background activity in the deprived eye. In other words, the NMDA contribution to background activity in the deprived eye was reduced compared to the NMDA contribution to background activity in the normal eye. This could represent a reduction of NMDA receptors in the pathway from the deprived eye, like the reduction of acetylcholine receptors associated with the losing input at the neuromuscular junction before the nerve is eliminated.

2-Amino-5-phosphonovalerate↗

PubMed2001

Inhibition of nitric oxide improves coronary perfusion pressure and return of spontaneous circulation in a porcine cardiopulmonary resuscitation model.

OBJECTIVE: During spontaneous circulation, nonspecific inhibition of nitric oxide synthase by N(G)-nitro-L-arginine methyl ester (L-NAME) increases systemic vascular resistance and, therefore, mean arterial pressure. If this effect can be extrapolated to cardiopulmonary resuscitation (CPR), administering L-NAME during CPR may be beneficial by maintaining or even improving coronary perfusion pressure, and hence successful defibrillation. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for hemodynamic variables, blood gases, and defibrillation attempt. SETTING: University medical center experimental laboratory. SUBJECTS: Ten domestic pigs. INTERVENTIONS: After 4 mins of ventricular fibrillation, ten animals were randomly assigned to receive L-NAME (25 mg/kg; n = 5) or saline placebo (n = 5) (given in two doses) after 3 and 13 mins of CPR, respectively. Defibrillation was provided 5 mins after the second dose of active drug or placebo. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem coronary perfusion pressure was significantly (p < .05) higher 90 secs (27 +/- 3 vs. 17 +/- 3 mm Hg), 10 mins (28 +/- 3 vs. 14 +/- 2 mm Hg), and 15 mins (21 +/- 5 vs. 7 +/- 3 mm Hg) after the first L-NAME administration compared with saline placebo. Mean +/- sem coronary perfusion pressure remained significantly higher 90 secs and 5 mins after the second L-NAME vs. saline placebo administration (19 +/- 4 vs. 6 +/- 4 mm Hg, and 17 +/- 3 vs. 4 +/- 4 mm Hg). After 22 mins of cardiac arrest, including 18 mins of CPR, four of five pigs in the L-NAME group were successfully defibrillated, and survived the 60-min postresuscitation phase. In the placebo group, none of five pigs could be defibrillated successfully (p < .05). CONCLUSIONS: Nonspecific blockade of nitric oxide synthase with L-NAME during CPR was associated with an increase in coronary perfusion pressure and resulted in significantly better initial resuscitation when compared with saline placebo.

Animals↗

PubMedDate not supplied

Oral administration of a nitric oxide synthase inhibitor enhances de novo mammalian angiogenesis mediated by TNF-alpha, saline and mast-cell secretion.

In healthy adult rats, the test tissue that is used in the mesenteric-window angiogenesis assay is natively vascularized, lacks physiological angiogenesis, and is unperturbed by surgical intervention. Using the rat MWAA oral treatment with the nitric oxide (NO) synthase inhibitor Nw-nitro-L-arginine methyl ester (L-NAME) enhanced the angiogenic response (compared with controls receiving the inactive enantiomer D-NAME) following i.p. injections of (i) TNF-alpha at an approximate physiological dose, (ii) Compound 48/80, which is a highly selective secretagogue causing mast-cell secretion in situ and a very strong angiogenic response, and (iii) saline of a grade not made for infusion, causing a weak angiogenic response. Angiogenesis was assessed quantitatively using microscopic morphometry and image analysis in terms of objective variables recording the microvascular spatial extension, microvascular density, number and length of microvessel segments (extending between two successive branching points) and the degree of microvessel tortuosity. The data strongly suggest that endogenous NO inhibits all three mammalian angiogenesis reactions, although to a markedly different extent. Notably, the present data are virtually the opposite of those that have been reported from other mammalian angiogenesis models, the test tissues of which display deranged homeostasis, such as surgical intervention and/or ischemia.

Administration, Oral↗

PubMed1994

L-NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs.

1. The effects of the inhibitor of nitric oxide (NO) synthesis, NG-nitro-L-arginine methyl ester (L-NAME), on systemic arterial blood pressure and jejunal motility, blood flow, and oxygen uptake have been investigated in anaesthetized dogs. 2. L-NAME (cumulative doses of 0.1-20 mg kg-1, i.v.) dose-dependently increased blood pressure and jejunal motility and decreased heart rate. The maximal response of these three variables occurred at doses, 3, 10 and 10 mg kg-1, respectively. L-NAME (cumulative doses of 0.5-5 mg kg-1) also dose-dependently induced jejunal vasoconstriction. The jejunal vascular resistance returned to control values as the cumulative doses reached 10 and 20 mg kg-1, which corresponded to the maximal increase in jejunal motility. 3. A single intravenous injection of L-NAME (10 mg kg-1) produced a prompt increase in blood pressure, which lasted for at least 50 min. 4. L-NAME (10 mg kg-1) produced a progressive rise in jejunal motility reaching its maximum (47 +/- 6 mmHg) 15 min after the administration, and lasting for 40-50 min. Both the basal lumen pressure and the amplitude of rhythmic contractions increased during this period. 5. L-NAME (10 mg kg-1) produced a triphasic change in jejunal vascular resistance and blood flow measured by timed collection of venous outflow. The blood flow decreased initially (-43% at 5 min), increased (+35%) and returned to control value between 15 and 35 min, then decreased (-35%) 40-50 min post-infusion. Jejunal vascular resistance reflected the blood flow response (+88% at both 5 and 50 min). The time during which the reversal of the vasoconstriction occurred (15-35 min) corresponded to the time of marked increase in motility, and was accompanied by a significant increase in jejunal oxygen uptake (+ 18%).6. The L-NAME-induced increase in motility was prevented by L-arginine (1 g kg-1, i.v.) but not by D-arginine pretreatment. The interim (15-35 min) changes in jejunal blood flow, vascular resistance and oxygen uptake were also prevented by L-arginine pretreatment.7. L-Arginine pretreatment attenuated L-NAME-induced hypertension for 5 min.8. The L-NAME-induced increases in jejunal vascular resistance and motility were inhibited by either local intra-arterial infusion of L-arginine (32 mM local arterial blood concentration) or topical application of 2 MicroM nitroglycerin. Infusion of D-arginine (32 mM local arterial blood concentration) had no such effect.9. The L-NAME-induced increase in blood pressure was not the mechanism by which jejunal motility was increased, because similar increases in blood pressure by mefenamate (10 mg kg-1, i.v.) had no such effect.10. Thus, inhibition of nitric oxide synthesis by L-NAME increased jejunal motility and vascular resistance and the marked increase in motility can abolish or reverse the vasoconstriction. Endogenous nitric oxide may play a role in regulating motility and blood flow in the resting canine jejunum.

Animals↗

PubMed2003

Transannular reactions of two parallel 1,3-butadiynes: syntheses, structures, and reactions of 1-azacyclotetradeca-3,5,10,12-tetrayne derivatives.

The synthesis of 1-alkyl and 1-aryl-1-azacyclotetradeca-3,5,10,12-tetraynes was achieved in a stepwise approach. The key intermediate was 1,13-dibromotrideca-2,4,9,11-tetrayne (18). Reaction with methyl- (19 a), ethyl- (19 b), isopropyl- (19 c), n-butyl- (19 d), and tert-butylamine (19 e) as well as aniline (19 f) and p-methoxyaniline (19 g) gave the corresponding 14-membered tetraynes 20 a-20 g. The ring inversion process of 20 b was studied by variable temperature (1)H NMR spectroscopy. From these measurements a value of 10.6 kcal mol(-1) was calculated for DeltaG(not equal). X-ray investigations on single crystals of 20 b, 20 c, and 20 f revealed the axial position for the substituent at each nitrogen atom. For 20 b we encountered the chair conformation, for 20 c both chair and boat conformations, and for 20 f the boat conformation in the solid state. The reaction of 20 c with concentrated HCl in ethanol yielded 2,10-dichloro-6-isopropyl-6-azatricyclo[9.3.0.0(4,8)]tetradeca-1(11),2,4(8),9-tetraene (25 c). Compound 25 c was oxidized by 2,3-dichloro-5,6-dicyano-1,4-benzoquinone (DDQ) to 27 c. The structure of the latter was confirmed by X-ray investigations. The reaction of 20 c in aqueous HCl lead to the formation of 10-chloro-2-isopropyl-1,3,4,6,7,8-hexahydro-2H-benzo[g]isoquinolin-9-one (37 c). The structure of 37 c was verified by X-ray studies on single crystals.

Journal Article↗

PubMed1993

Sublethal effects of three pesticides on Japanese medaka.

One- to 2-day-old medaka (Oryzias latipes) larvae were exposed for 4 days to the rice field pesticides methyl parathion, molinate, carbofuran and a mixture of all three. Pesticide concentrations were one-half the 96 h LC50 ("high concentration") and levels approximating those measured in receiving waters from rice field runoff ("low concentration"). Maximum swimming speed, spontaneous muscular activity, acetylcholinesterase activity, dry weight, RNA:DNA ratio, and five morphometric variables were determined at the end of the exposures. Larvae were retained for an additional 10 days in non-contaminated water, and the same measurements taken to investigate residual effects. Results are compared to a parallel study on striped bass larvae to evaluate the suitability of this species as a surrogate for the bass in toxicological studies involving sublethal exposures. There was no relationship between mortality rate and pesticide exposure either during the exposures or during the ten day subsequent period. Only the high concentration of carbofuran caused an impairment of swimming performance. Spontaneous activity was stimulated in the high concentration of molinate and the combined pesticides groups. Acetylcholinesterase was severely inhibited in parathion and molinate, and this persisted in some cases after 10 days in non-contaminated water. The pesticides had little effect on growth rate except for molinate which acted as a stimulant. Combining the three pesticides caused a less than additive effect. Except for decreases in acetylcholinesterase, the sublethal effects of the pesticides tested at the very low concentrations used were subtle. Apparently, larvae of this species are less sensitive to these pesticides than are striped bass larvae.

Animals↗

PubMed1996

Early enhancement but no late changes of motor responses induced by intracortical microstimulation in the ketamine-anesthetized rat.

The objectives of this study were to determine whether changes in electromyographic (EMG) responses observed during prolonged intracortical microstimulation (ICMS) were due to local plasticity of the motor system or to global changes in the preparation. Local effects would be expressed as changes only along the activated motor pathway, whereas global effects would be expressed as changes also appearing at distant cortical efferent microzones. The results of ICMS in the ketamine-anesthetized rat showed that the size of consecutive EMG responses increased gradually to a relatively stable magnitude over a period of four to six trains of stimuli. This early enhancement of EMG responses was maintained while continuously providing trains of stimuli at 1 Hz. However, it disappeared after a 5-min period of muscle inactivity. This response enhancement in the presence of ketamine (an NMDA, N-methyl-D-aspartate, receptor blocker) suggests that a neuronal mechanism involving non-NMDA-mediated homosynaptic short-term potentiation (STP) was responsible for the early enhancement of EMG responses. To compare ICMS effects at several time intervals it was necessary to average several evoked EMG responses because there was normal biological variability between single EMG responses. To determine the optimal number of EMG responses that would provide a reliable average EMG response, averages of 5, 10, 15, 20, and 25 EMG responses evoked from a single cortical site were collected at 5-min intervals. The results revealed that averages of 10 responses would provide reliable average EMG responses for all subsequent analyses. There were wide fluctuations in the average EMG responses when periodic injections of ketamine were used to maintain a low reflexive state in the animal. Switching to continuous infusion of ketamine abolished these fluctuations but there remained a small drift in the magnitudes of consecutive EMG responses. To test whether this drift reflected local plastic changes in the motor system induced by stimulation or some global changes, EMG responses evoked from another ICMS site were used as control. The rationale was that global effects would affect all motor output sites equally. The sizes of control EMG responses followed a similar time course to those evoked from the test site. Furthermore, standardizing the test EMG responses with respect to the control responses eliminated the drift in response magnitudes. Thus the drift was due to slow global changes in neuronal excitability possibly produced by the anesthesia. In conclusion, late changes occurring after hours of ICMS were not due to plasticity of the motor system but rather to global changes in the preparation, possibly resulting from the inability to set an ideal anesthetic infusion rate that could maintain a constant level of neuronal excitability over long periods of time. However, there was early enhancement of the EMG responses evoked by ICMS due to neuronal plasticity possibly mediated by a non-NMDA mechanism of homosynaptic STP such as post-tetanic potentiation (PTP). This early enhancement would favor recruitment of the previously activated motor pathway and lead to greater consistency in movement execution.

Anesthesia↗

PubMed2003

Spectroscopic and computational characterization of the nickel-containing F430 cofactor of methyl-coenzyme M reductase.

Methyl-coenzyme M reductase (MCR) catalyzes the terminal reaction in methanogenesis, the formation of methane from methyl-coenzyme M and coenzyme B. The active site of MCR binds the prosthetic group F(430), a unique nickel hydrocorphin cofactor. Here, spectroscopy and computations are employed in developing detailed electronic descriptions of the Ni(II) and Ni(I) forms of the free cofactor. Absorption, magnetic circular dichroism (MCD), and variable-temperature variable-field MCD data are analyzed within the framework of time-dependent DFT computations to assign key electronic transitions. DFT calculations are further employed to evaluate possible reduced F(430) models-a one-electron reduced Ni(I)F(430) model and a three-electron reduced Ni(I)F(red430) model (possessing a reduced hydrocorphin ligand)-on the basis of excited-state spectra and published EPR/ENDOR parameters. While calculations on both models yield spectroscopic parameters that are consistent with most experimental data, overall better agreement is achieved using the Ni(I)F(430) model, particularly with respect to electronic absorption and (1)H ENDOR. The experimentally validated bonding descriptions generated herein show that in Ni(II)F(430) the occupied Ni 3d orbitals are too low in energy to significantly perturb the dominant electronic transition involving the pi and pi* frontier MOs of the macrocycle (i.e., the HOMO-->LUMO transition). Upon one-electron reduction of the Ni(II) ion, the occupied Ni 3d orbitals are raised in energy, shifting between the HOMO and the LUMO of the oxidized cofactor. These ground-state changes have a dramatic effect on the excited-state structure, causing a blue shift of the dominant pi-->pi* transition and the appearance of numerous Ni 3d-->hydrocorphin pi* charge-transfer features in the vis/near-IR region.

Computational Biology↗

PubMed1989

Binding of a radiolabeled sea anemone cytolysin to erythrocyte membranes.

Stichodactyla helianthus cytolysin III, a 17 kDa basic polypeptide isolated from a Caribbean sea anemone, is one of the most potent hemolysins yet found in a living organism. This toxin has been reported to form new ion channels in artificial lipid bilayer membranes. The ability of this toxin to attack cell membranes is greatly enhanced by the presence of sphingomyelin. In order to investigate the mechanism by which the cytolysin causes cell lysis, we have prepared a highly active [3H]cytolysin derivative by reductive methylation with sodium cyanoborohydride and [3H]formaldehyde. A dimethylated toxin derivative was used to investigate the basis for the differential lytic activity of this polypeptide upon erythrocytes from six mammalian species. Using both direct [3H]toxin binding and indirect (Thron method) binding techniques, we found that the interspecies differences are due to variable membrane susceptibilities toward the bound toxin, rather than to differences in membrane affinity for the toxin. Similarly, we showed the enhanced lytic activity of the toxin for rat erythrocytes at elevated pH to be caused by enhanced activity of the bound toxin.

Alkylation↗

PubMed1986

Sulfated glucuronyl glycolipids reacting with anti-myelin-associated glycoprotein monoclonal antibodies including IgM paraproteins in neuropathy: species distribution and partial characterization of epitopes.

It was recently established that anti-myelin associated glycoprotein (MAG) IgM paraproteins associated with neuropathy and a substantial number of experimentally produced rat and mouse monoclonal antibodies that react with MAG (e.g. HNK-1) also bind to some sulfated glucuronic acid-containing sphingoglycolipids of human peripheral nerve. A species study revealed that these glycolipids could be detected readily by TLC overlay experiments in the acidic glycolipid fractions from human, monkey, bovine, cat and dog peripheral nerve. The glycolipids were also present in the nerves of rat, mouse, rabbit, guinea pig and chicken, but their concentration was about an order of magnitude lower. These antigenic glycolipids were present in the purified myelin fraction from cat nerve, but their level was not enriched over that in whole homogenate. Partial characterization of the epitopes in the glycolipids was accomplished by comparing binding of the human and experimental monoclonal antibodies to sulfated glucuronyl paragloboside (SGPG), to the desulfated lipid (GPG), and to the methyl ester of the desulfated lipid (MeGPG). All of the human, mouse and rat antibodies reacted with the intact SGPG, but none exhibited binding to MeGPG indicating that either the sulfate or the free carboxyl group on SGPG was required for reactivity. Five out of 11 human IgM paraproteins retained partial and variable reactivity with GPG showing that the sulfate was not absolutely required for binding, while the other 6 did not react with GPG. These results demonstrate idiotypic heterogeneity among the IgM paraproteins. Only 1 of 14 monoclonal antibodies produced experimentally in mice or rats retained reactivity with GPG.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Cardiovascular and muscle tone changes produced by microinjection of cholinergic and glutamatergic agonists in dorsolateral pons and medial medulla.

Cardiovascular and muscle responses to L-glutamic acid (Glut) and cholinergic agonists injected into the dorsolateral pontine tegmentum and medial medullary reticular formation (MMRF) were examined in unanesthetized, decerebrated cats. Glut, or cholinergic agonists acetylcholine (ACh) or carbachol (Carb), were injected into pons and MMRF at sites from which electrical stimulation produced bilateral suppression of muscle tone. Glut injection in MMRF produced hypotension without change in heart rate at doses as low as 1 mM. At higher doses (0.1-0.4 M), Glut induced hypotension with bradycardia in 23 out of 40 injections in both pons and MMRF. High concentrations of microinjected Glut decreased muscle tone or produced complete atonia in pons and rostral MMRF. Both N-methyl-D-aspartic acid (NMDA) and non-NMDA receptor blockers attenuated or completely blocked the cardiovascular response, while only non-NMDA antagonists blocked muscle inhibition to Glut injection. Microinjection of cholinergic agonists produced consistent hypotension in all of the injections in pons and MMRF, however, the heart rate response was variable with increase (27/42), decrease (2/42), or no change (13/42) in rate seen. Cholinergic injection produced muscle atonia in pons and caudal MMRF but not in rostral MMRF. Both muscle and cardiovascular responses were blocked by atropine but not by hexamethonium. The time course of muscle atonia and cardiovascular change differed in most of the experiments. We conclude that muscle tone suppression and cardiovascular response to Glut or cholinergic agonists use different receptor mechanisms and possibly different neurons. However, the co-localization of these mechanisms suggests that neuronal networks in the medial medulla and dorsolateral pons coordinate motor and cardiovascular responses.

Animals↗

PubMed2001

Mechanisms of the renal vasodilation caused by insulin in anesthetized pigs.

The present study was planned to determine the mechanisms involved in the renal vasodilation caused by insulin. Changes in flow caused by the intravenous infusion of 0.004 IU/kg/min of insulin at constant heart rate, aortic blood pressure, left ventricular contractility and blood levels of glucose and potassium in the left renal artery were assessed using an electromagnetic flowmeter. In ten pigs, infusion of insulin caused an increase in renal blood flow which averaged 12.8% of the control values. After hemodynamic variables had returned to control values, insulin infusion was repeated in five pigs following blockade of alpha-adrenergic receptors with injection of phentolamine into the renal artery and in the other five pigs following blockade of nitric oxide formation with injection in the same artery of Nomega-nitro-L-arginine methyl ester (L-NAME). After blockade of alpha-adrenergic receptors, insulin infusion caused an increase in renal blood flow which averaged 18.1% of the control values, being significantly enhanced with respect to the increase previously obtained in the same pigs. On the contrary, after blockade of nitric oxide formation insulin infusion caused a decrease in renal blood flow which averaged 6.5% of the control values. These responses were respectively abolished by the subsequent injection into the renal artery of L-NAME and phentolamine. The present study showed that the renal vasodilation caused by insulin in the anesthetized pig was the result of two opposite effects which involved a predominant vasodilation mediated by the release of nitric oxide from the endothelium and a sympathetic vasoconstrictor mechanism mediated by alpha-adrenergic receptors.

Animals↗

PubMed2003

Infrared and Raman spectra, conformational stability, vibrational assignment and ab initio calculations of methylvinyl silyl chloride.

The infrared spectra (3200-50 cm(-1)) of gaseous and solid and Raman spectra (3200-10 cm(-1)) of the liquid and solid methylvinyl silyl chloride, CH(2)=CHSiH(CH(3))Cl, and the Si-d isotopomer have been recorded. The three expected stable conformers (the three different groups eclipsing the double bond) have been identified in the fluid phase, but it was not possible to obtain an annealed solid with a single conformer. Variable temperature (-105 to -150 degrees C) studies of the infrared spectra of the sample dissolved in liquid krypton has been carried out. From these data the enthalpy differences between the most stable conformer with the hydrogen atom (HE) eclipsing the double bond to that with the chlorine atom (ClE) and the methyl group (ME) eclipsing the double bond have been determined to be 17+/-4 cm(-1) (203+/-48 Jmol(-1)) and 80+/-12 cm(-1) (957+/-144 Jmol(-1)), respectively. However in the liquid state the ME conformer is the most stable form with enthalpy differences of 13+/-4 and 27+/-7 cm(-1) to the HE and ClE rotamers, respectively. It is estimated that there is 39% of the HE conformer, 35% of the ClE conformer, and 26% of the ME conformer present at ambient temperature. A complete vibration assignment is proposed for the HE conformer which is based on infrared band contours and group frequencies, which is supported by normal coordinate calculations utilizing the force constants from ab initio MP2/6-31G(d) calculations. Additionally, several of the fundamentals for the other two conformers have been assigned. The optimal geometries, conformational stabilities, harmonic force fields, infrared intensities, Raman activities, depolarization ratios, and vibrational frequencies are reported for all three conformers from MP2/6-31G(d,p) ab initio calculations with full electron correlation. Optimized geometrical parameters and conformational stabilities have been obtained from MP2/6-311+G(d,p) calculations. At this highest level of calculations, the HE conformer is predicted to be more stable by 62 and 84 cm(-1) than the ME and ClE conformers, respectively. The coefficients from the potential function governing the conformational interchange have been obtained from the MP2/6-31G(d) ab initio calculations. By utilizing the frequency of the SiH stretching mode, the r(0)-H distance has been determined to be 1.481 A for the HE conformer. The ab initio calculated quantities are compared to the experimentally determined values where applicable, as well as to some corresponding results for some similar molecules.

Chlorides↗

PubMed2005

Chemometric characterization of the cypriot spirit "zivania".

In 42 alcoholic beverages produced in Cyprus and other countries, 26 chemical and physical-chemical variables were determined by HPLC and GC chromatography, (1)H NMR and ICP spectroscopy, and other techniques. Data were processed using multivariate chemometric techniques, involving principal component analysis, cluster analysis, regularized discriminant analysis, and classification and regression trees. Zivania can be differentiated from beverages from other countries. Using 2- and 3-methyl-butanol, 2-methyl-propanol, furfural, methanol, and the alcoholic grade and the chemical shift of -CH(3) in (1)H NMR spectra as features, a nearly correct classification for zivania was achieved. The reasons for diversions are given.

Alcoholic Beverages↗