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Biomedical subjects

D A Haas

Publications and source records attributed to D A Haas.

At least 37 records · Page 2Linked to original sources
PubMed1994

Molecular dynamics in liquids: spin-lattice relaxation of nitroxide spin labels.

Time domain pulsed saturation recovery and electron-electron double resonance spectroscopies were used to measure the spin-lattice relaxation rates of the electron and the nitrogen nucleus in nitroxide spin labels in liquids. The rotational correlation time range covered is from picoseconds to milliseconds. These rates are quantitatively explained by isotropic rotational Brownian dynamics, which modulate the interactions between the electron spin and the molecular angular momentum; the nitrogen and electron spins; and the solvent protons with both the electron and the nitrogen spins. This solves a 20-year-old problem that has limited scientific applications of nitroxides.

Cyclic N-Oxides↗
PubMed1993

Using nitroxide spin labels. How to obtain T1e from continuous wave electron paramagnetic resonance spectra at all rotational rates.

Historically, the continuous wave electron paramagnetic resonance (CW-EPR) progressive saturation method has been used to obtain information on the spin-lattice relaxation time (T1e) and those processes, such as motion and spin exchange, that occur on a competitive timescale. For example, qualitative information on local dynamics and solvent accessibility of proteins and nucleic acids has been obtained by this method. However, making quantitative estimates of T1e from CW-EPR spectra have been frustrated by a lack of understanding of the role of T1e (and T2e) in the slow-motion regime. Theoretical simulation of the CW-EPR lineshapes in the slow-motion region under increasing power levels has been used in this work to test whether the saturation technique can produce quantitative estimates of the spin-lattice relaxation rates. A method is presented by which the correct T1e may be extracted from an analysis of the power-saturation rollover curve, regardless of the amount of inhomogeneous broadening or the rates of molecular reorientation. The range of motional correlation times from 10 to 200 ns should be optimal for extracting quantitative estimates of T1e values in spin-labeled biomolecules. The progressive-saturation rollover curve method should find wide application in those areas of biophysics where information on molecular interactions and solvent exposure as well as molecular reorientation rates are desired.

Biophysical Phenomena↗
PubMed1993

An anaphylactoid reaction following local anesthesia: a case report.

A case report of an adverse reaction to a preparation of an amide local anesthetic, prilocaine with epinephrine, is presented. Signs and symptoms were consistent with an anaphylactic reaction and the patient responded positively to treatment based on this assumption. Treatment included administration of epinephrine injected sublingually and oxygen by inhalation. However, subsequent skin testing failed to confirm this diagnosis. A number of explanations are possible and a final diagnosis of an anaphylactoid reaction was made. Local anesthetic allergies and their management are reviewed. The literature demonstrates that an allergic reaction to amide local anesthetics can occur and a thorough history, intradermal testing, and subcutaneous challenge are reasonable approaches to determine a safe agent for subsequent use.

Adult↗
PubMed1992

Development of an orofacial model of acute inflammation in the rat.

An appropriate model was created by the paraperiosteal injection of mustard oil (20% allyl isothiocyanate dissolved in mineral oil) into the periarticular temporomandibular tissue of anaesthetized rats. Inflammation was assessed by the plasma extravasation of Evans' blue dye bound to plasma protein. This was confirmed visually and compared spectrophotometrically with the contralateral untreated control site (p less than 0.0005). A time-course study of the effect of mustard oil on Evans' blue extravasation revealed a gradually increasing effect that was maximal at 30 min after administration, with no further increase at 60 min. A dose-response study showed that giving 30 microliters of 20% mustard oil produced the maximal effect, with no further increase from 50 microliters. To confirm induction of inflammation, polymorphonuclear neutrophil infiltration was assessed morphometrically and found to increase in the treated tissue compared with the contralateral untreated control (p less than 0.001).

Acute Disease↗
PubMed1992

Ketamine: a review of its pharmacologic properties and use in ambulatory anesthesia.

The administration of intravenous agents is the most commonly used method in Canada and the United States to produce sedation or general anesthesia for dental procedures. Ketamine, a dissociative anesthetic, has several advantageous physical, pharmacokinetic, and pharmacodynamic properties. It can be used to induce anesthesia, sedation, analgesia, and amnesia. Ketamine can maintain functional residual capacity, induce bronchodilation, and avoid cardiovascular depression. However, adverse effects have been demonstrated, such as cardiovascular stimulation and unpleasant emergence phenomena, both of which may be modulated by supplementation with benzodiazepines. An increase in the use of ketamine for ambulatory anesthesia has recently been advocated. This review of the literature supports the use of ketamine as an effective agent for selected anesthetic procedures.

Ambulatory Surgical Procedures↗
PubMed1992

Malignant hyperthermia and the general dentist: current recommendations.

Malignant hyperthermia is a potentially fatal disease that may be triggered by the administration of specific drugs or by stress. Although most often associated with general anesthesia, stress can be a significant stimulus and is therefore of concern to the general dentist. The decision as to how and where to treat these patients is complicated by conflicting recommendations from various sources. The aim of this article is to propose a protocol for the dentist to use in the treatment of patients with a history of malignant hyperthermia. The dentist must assess the patient for both their susceptibility to a crisis and the degree of stress of the planned procedure. For non-stressful treatment, it is reasonable to assume that the general dental practitioner can treat these patients in his office. For stressful treatment, advanced preparation is advised.

Anesthesia, Dental↗
PubMed1991

Lack of differential effect by Ultracaine (articaine) and Citanest (prilocaine) in infiltration anaesthesia.

It has been claimed that anaesthesia of mandibular pulpal and lingual soft tissue, as well as maxillary palatal soft tissue, results following buccal infiltration of the local anaesthetic Ultracaine (articaine HC1). However, this has never been scientifically proven and the aim of this investigation was to test these claims by comparing articaine to a standard anaesthetic, Citanest (prilocaine HC1). In order to study this, a double blind, randomized trial was conducted in healthy adult volunteers. In these subjects, the ability to induce maxillary and mandibular anaesthesia following buccal infiltration with articaine (as compared to prilocaine given contralaterally), was determined by measuring sensation to electrical stimulation at the tooth, buccal and lingual soft tissue at each of the four non-carious, non-restored, second molars. Results showed that there were no statistically significant differences between articaine and prilocaine in their ability to induce anaesthesia for any tissue at any of the six sites (p greater than 0.05) as determined by chi-square analysis. Analysis of effect on sensation for 25 minutes post-administration also failed to demonstrate a difference between the two drugs. Therefore, these data are not consistent with superior anaesthesia efficacy by articaine at any site, including the mandibular pulpal, lingual or maxillary palatal tissues, in the second molars studied.

Administration, Buccal↗
PubMed1990

Differential alpha-1 and alpha-2 adrenergic effects on hypothalamic corticotropin-releasing factor and plasma adrenocorticotropin.

There is presently no consensus as to the nature of the catecholaminergic influence on the regulation of corticotropin-releasing factor. The potential role that the alpha-adrenergic system plays was investigated by measuring hypothalamic corticotropin-releasing factor-like immunoreactivity and plasma adrenocorticotropin, following manipulation of alpha-1 and alpha-2 adrenergic receptor activation. Administration of the alpha-1 agonist methoxamine did not significantly alter either plasma adrenocorticotropin or hypothalamic corticotropin-releasing factor. Administration of the alpha-2 agonist clonidine resulted in a 24-fold increase in plasma adrenocorticotropin and a significant decrease in median eminence corticotropin-releasing factor, consistent with its release. Corticotropin-releasing factor in the remainder of the hypothalamus was not altered. Concurrent administration of clonidine with the selective alpha-2 antagonist yohimbine prevented the clonidine-induced changes in plasma adrenocorticotropin and hypothalamic corticotropin-releasing factor, consistent with the clonidine effect being mediated through alpha-2 receptors. Concurrent administration of clonidine with methoxamine did not prevent these effects, suggesting that the effect of clonidine was not mediated through presynaptic inhibition of noradrenergic adrenergic neurotransmission. Inhibition of protein synthesis by anisomycin induced changes in corticotropin-releasing factor and adrenocorticotropin which were not altered by combined treatment with methoxamine or clonidine. These data suggest differential roles for alpha-1 and alpha-2 systems in the regulation of corticotropin-releasing factor. Results from alpha-2 adrenergic activation were consistent with stimulation of corticotropin-releasing factor release, an effect mediated by a postsynaptic alpha-2 mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1990

Effect of protein synthesis inhibition on brain corticotropin-releasing factor and plasma adrenocorticotropin.

The effect of inhibiting protein synthesis on concentrations of corticotropin-releasing factor (CRF) in rat brain and plasma adrenocorticotropin (ACTH) was assessed following the administration of the general protein synthesis inhibitor anisomycin. Compared with vehicle-injected controls, protein synthesis inhibition resulted in significantly reduced CRF immunoreactivity (CRF-ir) in median eminence within 1 h (p less than 0.01), remained decreased after 4 h (p less than 0.025), and was nonsignificantly decreased after 24 h. Plasma ACTH levels were greatly increased within 1 h posttreatment (p less than 0.0005), continued elevated after 4 h (p less than 0.01), and returned to normal levels after 24 h. CRF-ir measured in other brain areas 24 h after anisomycin showed decreased levels in medulla-pons (p less than 0.025) and neurointermediate lobe of pituitary (p less than 0.05), with no change noted in frontal cortex, hippocampus, midbrain-thalamus, or cerebellum. Overall these data show that blockade of normal protein synthesis with anisomycin can elicit changes in CRF-ir and ACTH content.

Adrenocorticotropic Hormone↗
PubMed1990

Adrenergic regulation of hypothalamic proenkephalin neurons: evidence for opposite effects in subpopulations terminating in median eminence and neurointermediate pituitary.

The effect of adrenergic influences on Met-enkephalin concentrations in median eminence, neurointermediate pituitary and hypothalamus outside median eminence were examined. Met-enkephalin levels in median eminence were augmented by administration of the alpha 1-adrenergic agonist methoxamine acutely or chronically and decreased by the selective depletion of adrenergic transmitters by 6-hydroxydopamine. Met-enkephalin levels in neurointermediate lobe were decreased by methoxamine but unaffected by depletion of noradrenaline/adrenaline. These results indicate that adrenergic mechanisms maintain Met-enkephalin concentrations tonically in median eminence and deplete Met-enkephalin concentrations in neurointermediate lobe. These results suggest differential adrenergic regulation of hypothalamic proenkephalin neurons terminating in median eminence and neural lobe of pituitary.

Animals↗
PubMed1989

Neuropeptide Y-induced effects on hypothalamic corticotropin-releasing factor content and release are dependent on noradrenergic/adrenergic neurotransmission.

Neuropeptide Y (NPY) administration increases both hypothalamic corticotropin-releasing factor-like immunoreactivity (CRF-ir) and plasma adrenocorticotropin (ACTH). The dependence of these effects on noradrenaline and adrenaline was investigated by selectively depleting these neurotransmitters with 6-hydroxydopamine (6-OHDA) prior to administration of NPY. This combined treatment decreased hypothalamic CRF-ir (P less than 0.025), an effect isolated to the median eminence (P less than 0.025), whereas plasma ACTH increased greatly compared to 6-OHDA treatment alone (P less than 0.0005). In order to further investigate the potential mechanism of this NPY effect, the alpha 2-adrenergic agonist clonidine was administered to normal rats. This treatment increased plasma ACTH (P less than 0.005) and decreased hypothalamic CRF-ir (P less than 0.025), an effect localized to the median eminence (P less than 0.01). The results from both of these treatments are consistent with increased release of hypothalamic CRF. These data imply that the NPY-induced effects are dependent on normal noradrenergic/adrenergic neurotransmission. Depletion of these neurotransmitters allowed NPY to profoundly stimulate CRF release with no evidence for alteration in synthesis, a result common to alpha 2 stimulation.

Adrenocorticotropic Hormone↗
PubMed1989

Estradiol or ovariectomy decreases CRF synthesis in hypothalamus.

Gonadectomy and gonadectomy plus chronic estradiol administration decrease the content of hypothalamic corticotropin-releasing factor-like immunoreactivity (CRF-ir). This investigation was conducted to determine whether this was a result of chronic inhibition of CRF synthesis or stimulation of release. Administration of the protein synthesis inhibitor anisomycin one hour prior to sacrifice in otherwise untreated controls resulted in a 21% decrease in median eminence CRF-ir (p less than 0.01). Rats were ovariectomized and then administered either estradiol or vehicle daily for 3 weeks. Compared to vehicle-treated controls, estradiol treatment decreased CRF-ir in median eminence (p less than 0.01). In contrast to controls, administration of anisomycin to these ovariectomized rats did not significantly decrease median eminence CRF-ir in either the vehicle or estradiol-treated groups, implying that CRF synthesis was already depressed. Plasma adrenocorticotropin (ACTH) was increased by anisomycin treatment in all groups whether intact, ovariectomized or estradiol-treated (p less than 0.0005). Adrenal weights did not differ between these groups, or in comparison to sham-ovariectomized rats, indirectly implying lack of chronically elevated plasma ACTH. These data suggest that the mechanism for both the ovariectomy and chronic estradiol-induced decrease in CRF-ir content is an inhibition of CRF synthesis as opposed to a stimulation of CRF release.

Adrenocorticotropic Hormone↗
PubMed1988

Single or repeated mild stress increases synthesis and release of hypothalamic corticotropin-releasing factor.

The effect of a specific mild stress on the levels of corticotropin-releasing factor immunoreactivity (CRF-ir) in the hypothalamus of adult male rats was determined using a radioimmunoassay specific for rat CRF. A single 5 min restraint significantly increased CRF-ir in the median eminence 24 h later compared to appropriate controls (P less than 0.025), with no change detected earlier. Plasma ACTH, an indirect index of CRF release, was significantly elevated within 15 min (P less than 0.025). Repetition of a mild stress daily for 9 days (P less than 0.01), or a single episode of handling (P less than 0.05), both resulted in significantly increased CRF-ir in the whole hypothalamus 24 h later. Blockade of axonal transport by intracisternal colchicine decreased CRF-ir in the median eminence 24 h later (P less than 0.005). Inhibition of protein synthesis by anisomycin during a single 5 minute restraint resulted in significantly decreased CRF-ir in the median eminence 24 h later compared to vehicle-injected stressed rats (P less than 0.005) or to anisomycin-injected unstressed controls (P less than 0.025). These data show that mild stress increased net hypothalamic CRF content as a result of the balance between augmented synthesis and augmented release.

Adrenocorticotropic Hormone↗
PubMed1988

Gonadal regulation of corticotropin-releasing factor immunoreactivity in hypothalamus.

The effect of gonadectomy and subsequent gonadal steroid administration on hypothalamic corticotropin-releasing factor immunoreactivity (CRF-ir) in male and female rats was determined using a radioimmunoassay specific for rat CRF. When compared to appropriate controls, gonadectomy resulted in significantly decreased CRF-ir in both males and females (p less than 0.025). Short-term replacement with testosterone or estradiol did not significantly alter hypothalamic CRF-ir. Acute IC administration of gonadotropin-releasing hormone to male rats significantly decreased CRF-ir in the median eminence 15 minutes later. Chronic administration of estradiol for 3 weeks significantly reduced CRF-ir in ovariectomized rats (p less than 0.005). This decrease was shown not to correlate to the marked increase in anterior pituitary weight (r2 = 0.063, not significant). Chronic administration of estradiol to hypophysectomized female rats significantly decreased hypothalamic CRF-ir (p less than 0.01), an effect localized to the median eminence (p less than 0.005). These data imply that the gonadectomy-induced reduction in hypothalamic CRF-ir was not directly mediated by the loss of gonadal steroids. Chronic estradiol treatment decreased hypothalamic CRF-ir, by a non-pituitary mechanism. These data show significant effects of the gonadal axis in the regulation of CRF in the hypothalamus in both sexes.

Animals↗
PubMed1988

Effect of dopaminergic and alpha-adrenergic modulation on corticotropin-releasing factor immunoreactivity in rat hypothalamus.

The potential role that dopaminergic mechanisms have in the regulation of corticotropin-releasing factor (CRF) in the hypothalamus was investigated. Adult male rats were administered bromocriptine, a potent dopamine agonist, for periods ranging up to 51 days. Overall, bromocriptine treatment resulted in a significant decline in CRF-like immunoreactivity (CRF-ir). The dopamine antagonist, haloperidol, was administered for similar periods and resulted in no overall significant effect, except for a transient decrease. Treatment with reserpine, known to deplete monoamines including dopamine, induced a significant decrease in CRF-ir 24 h post-treatment. The possibility that the original results were due to alpha-adrenergic inhibition by bromocriptine and haloperidol was studied next. alpha 1-Stimulation by administration of methoxamine had no significant effect. alpha 2-Stimulation by clonidine significantly reduced hypothalamic CRF-ir. Selective depletion of neurotransmitter from noradrenergic and adrenergic neurons by 6-hydroxydopamine also resulted in a significant reduction of hypothalamic CRF-ir, an effect localized entirely to the median eminence. These results show a reduction in CRF-ir subsequent to either bromocriptine administration, generalized monoamine depletion, alpha 2-stimulation, or selective noradrenaline-adrenaline depletion. No direct dopaminergic effects could be confirmed. These data are consistent with a constant, near-maximal alpha 1-adrenergic effect maintaining hypothalamic CRF concentrations, presumably by inhibition of CRF release from the median eminence.

Adrenergic alpha-Agonists↗
PubMed1987

Neuropeptide Y administration acutely increases hypothalamic corticotropin-releasing factor immunoreactivity: lack of effect in other rat brain regions.

The effect of acute central administration of Neuropeptide Y (NPY) to adult male rats on the brain content of corticotropin-releasing factor immunoreactivity (CRF-ir) was investigated. The brain regions studied included frontal cortex, hippocampus, medulla-pons, midbrain-thalamus, cerebellum, neurointermediate lobe of pituitary, median eminence and the remaining hypothalamus. CRF-ir was determined in each of these regions using a radioimmunoassay specific for rat CRF. CRF-ir was found to be significantly increased in the major site of CRF localization in the brain, the hypothalamus, in NPY-treated rats as compared to vehicle-treated controls either 15 minutes (p less than 0.025) or 45 minutes (p less than 0.005) post-injection. This increase was localized to the median eminence (p less than 0.05 after 15 minutes, p less than 0.01 after 45 minutes). No statistically significant differences were noted in any of the other brain regions assessed. Plasma adrenocorticotropin levels were also found to increase following NPY treatment, an effect which became significant after 45 minutes (p less than 0.05). These data show that NPY can alter the content of hypothalamic CRF and may play a role in its regulation.

Adrenocorticotropic Hormone↗