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Biomedical subjects

M J Davis

Publications and source records attributed to M J Davis.

At least 37 records · Page 2Linked to original sources
PubMed2000

Transient increases in diameter and [Ca(2+)](i) are not obligatory for myogenic constriction.

Studies were performed to determine the significance of temporal variation in vascular smooth muscle Ca(2+) signaling during acute arteriolar myogenic constriction and, in particular, the importance of the stretch-induced intracellular Ca(2+) concentration ([Ca(2+)](i)) transient in attaining a steady-state mechanical response. Rat cremaster arterioles (diameter approximately 100 microm) were dissected from surrounding tissues, and vessel segments were pressurized in the absence of intraluminal flow. For [Ca(2+)](i) measurements, vessels were loaded with fura 2 and fluorescence emitted by excitation at 340 and 380 nm was measured using video-based image analysis. Ca(2+) and diameter responses were examined after increases in intravascular pressure were applied as an acute step increase or a ramp function. Additional studies examined the effect of longitudinal vessel stretch on [Ca(2+)](i) and arteriolar diameter. Step increase in intraluminal pressure (from 50 to 120 mmHg) caused biphasic change in [Ca(2+)](i) and diameter. [Ca(2+)](i) transiently increased to 114.0 +/- 2.0% of basal levels and subsequently declined to 106.7 +/- 4.4% at steady state. Diameter initially distended to 125.4 +/- 2.1% of basal levels before constricting to 71.1 +/- 1.2%. In contrast, when the same pressure increase was applied as a ramp function (over 5 min) transient vessel distension and transient increase in [Ca(2+)](i) were prevented, yet at steady state vessels constricted to 71.3 +/- 2.5%. Longitudinal stretch resulted in a large [Ca(2+)](i) transient (158 +/- 19% of basal) that returned to baseline despite maintenance of the stretch stimulus. The data demonstrate that the initial vessel distension (reflecting myocyte stretch) and associated global [Ca(2+)](i) transient are not obligatory for myogenic contraction. Thus, although arteriolar smooth muscle cells are responsive to acute stretch, the resulting changes in myogenic tone may be more closely related to other mechanical variables such as wall tension.

Abdominal Muscles↗
PubMed1999

Predictors of attrition from behavioral medicine treatments.

Despite the efficacy of a range of behavioral medicine interventions, high rates of attrition are a persistent problem in both clinical and research settings. Appropriately, studies have begun to focus on predictors of attrition with the hope of identifying important client or treatment characteristics. This article reviews attrition predictors in outpatient behavioral medicine treatments for headache, pain, stress, and weight management. Across all areas, psychological variables and severity of symptom variables were more predictive than demographic variables. However, as 13 of the 20 studies reviewed were in the area of weight management, generalizability of the findings to other treatment areas requires further investigation. Recommendations are made for improving attrition research by (a) developing clinically valid definitions of attrition, (b) recognizing important within-group differences among those who prematurely terminate treatment, and (c) focusing on theoretically grounded psychological and treatment process variables. A working definition of attrition based on the integration of clients' and clinicians' perspectives is also provided.

Adult↗
PubMed1999

Changes in coronary endothelial cell Ca2+ concentration during shear stress- and agonist-induced vasodilation.

Increases in intraluminal shear stress are thought to cause vasodilation of coronary arterioles by activation of Ca2+-dependent endothelial nitric oxide synthase followed by release of nitric oxide. We tested the hypothesis that endothelium-dependent vasodilation of isolated coronary arterioles to shear stress and agonists is necessarily preceded by an increase in endothelial cell Ca2+ concentration ([Ca2+]i). After selective loading of endothelium in isolated rabbit coronary arterioles with fura 2, simultaneous changes in diameter and [Ca2+]i were recorded. Vasodilations recorded in response to ACh, substance P, or shear stress were accompanied by significant increases in endothelial cell [Ca2+]i. Vasodilations to shear stress were accompanied by smaller changes in endothelial cell [Ca2+]i than equivalent dilations evoked by substance P or ACh. To test the role for Ca2+ as an activator of endothelial nitric oxide synthase, the endothelium was treated with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N', N'-tetraacetic acid. 1,2-Bis(2-aminophenoxy)ethane-N,N,N', N'-tetraacetic acid eliminated significant changes in endothelial cell [Ca2+]i and inhibited dilations to ACh and substance P but did not significantly affect shear stress-induced vasodilation. The data indicate that endothelium-dependent vasodilation of coronary arterioles in response to agonists and shear stress is mediated in part through a rise in endothelial cell [Ca2+]i but that a substantial component of the shear stress-induced response occurs through a Ca2+-insensitive pathway.

Acetylcholine↗
PubMed1999

Myogenic reactivity of rat epineurial arterioles: potential role in local vasoregulatory events.

Local control of neural blood flow is considered to reside in innervation of epineurial and endoneurial arterioles rather than in intrinsic autoregulatory mechanisms. With the use of an isolated vessel preparation and an in vivo approach, the present studies examined intrinsic vasomotor responsiveness of epineurial arterioles. Segments of epineurial arterioles, cannulated on glass micropipettes (40 micrometers) and pressurized in the absence of intraluminal flow, showed sustained pressure-dependent (30-90 mmHg) vasoconstriction and acute myogenic reactivity. Myogenic tone was unaffected by phentolamine (10(-6) M). Removal of extracellular Ca(2+) resulted in loss of spontaneous tone and passive behavior. Concentration-response curves for norepinephrine (10(-9)-3 x 10(-6) M) and relaxation to both acetylcholine (10(-8)-10(-5) M) and adenosine (10(-8)-10(-4) M) were obtained. Acetylcholine dilator responses were inhibited by N(G)-nitro-L-arginine methyl ester. Epineurial blood flow was measured in vivo using a laser-Doppler flow probe. Blood flow declined over a 2-h period after surgery, and during this time preparations developed responsiveness to the dilator acetylcholine. Phentolamine blocked vasoconstrictor responses to exogenous norepinephrine but only partially reversed the in vivo baseline tone. The time-dependent decline in epineurial blood flow was observed despite the presence of tetrodotoxin (1 microM), further confirming that tone was predominantly caused by myogenic rather than neurogenic mechanisms. It is concluded that because epineurial arterioles exhibit intrinsic myogenic reactivity, they have the potential to participate in local regulation of neural hemodynamics independently of their own innervation.

Acetylcholine↗
PubMed1999

Signaling mechanisms underlying the vascular myogenic response.

The vascular myogenic response refers to the acute reaction of a blood vessel to a change in transmural pressure. This response is critically important for the development of resting vascular tone, upon which other control mechanisms exert vasodilator and vasoconstrictor influences. The purpose of this review is to summarize and synthesize information regarding the cellular mechanism(s) underlying the myogenic response in blood vessels, with particular emphasis on arterioles. When necessary, experiments performed on larger blood vessels, visceral smooth muscle, and even striated muscle are cited. Mechanical aspects of myogenic behavior are discussed first, followed by electromechanical coupling mechanisms. Next, mechanotransduction by membrane-bound enzymes and involvement of second messengers, including calcium, are discussed. After this, the roles of the extracellular matrix, integrins, and the smooth muscle cytoskeleton are reviewed, with emphasis on short-term signaling mechanisms. Finally, suggestions are offered for possible future studies.

Animals↗
PubMed1999

Dating couples and their relationships: intimacy and contraceptive use.

Investigations of ineffective contraceptive use have generally focused on individualistic rather than dyadic factors. The present study used a sample of dating couples to investigate four intimacy dimensions in relation to contraceptive use. Fourteen consistent contraceptive use (CCU) couples and 16 inconsistent contraceptive use (ICU) couples participated. It was found that the two groups' expectations of intimacy did not differ significantly. However, the ICU couples reported experiencing significantly lower levels of emotional, social, and intellectual intimacy than did the CCU couples. Significant differences between realized and expected levels of intimacy were found only among ICU couples. The results indicate that partners with mutually dissatisfying levels of intimacy were more likely to use contraceptives inconsistently.

Adolescent↗
PubMed1999

Bone marrow transplants. Current applications & implications for oral health.

The application of bone marrow transplant (BMT) therapy to address a variety of pathologies has increased dramatically in the last decade. The list of diseases treated by this complex technology is quite lengthy. Side effects of BMT include a variety of documented untoward effects on oral health, many of which are age-dependent. With the increasing number of people, particularly children, receiving bone marrow transplants, it is entirely possible that these recipients may appear as "routine, healthy" patients in a general practice or other oral health care setting. They will present significant, unusual findings related to their history of BMT treatment. The purpose of this paper is to review this treatment modality, its current applications, and the short- and long-term effects that the oral health care practitioner must identify, understand and address.

Acute Disease↗
PubMed1998

Modulation of calcium current in arteriolar smooth muscle by alphav beta3 and alpha5 beta1 integrin ligands.

Vasoactive effects of soluble matrix proteins and integrin-binding peptides on arterioles are mediated by alphav beta3 and alpha5 beta1 integrins. To examine the underlying mechanisms, we measured L-type Ca2+ channel current in arteriolar smooth muscle cells in response to integrin ligands. Whole-cell, inward Ba2+ currents were inhibited after application of soluble cyclic RGD peptide, vitronectin (VN), fibronectin (FN), either of two anti-beta3 integrin antibodies, or monovalent beta3 antibody. With VN or beta3 antibody coated onto microbeads and presented as an insoluble ligand, current was also inhibited. In contrast, beads coated with FN or alpha5 antibody produced significant enhancement of current after bead attachment. Soluble alpha5 antibody had no effect on current but blocked the increase in current evoked by FN-coated beads and enhanced current when applied in combination with an appropriate IgG. The data suggest that alphavbeta3 and alpha5 beta1 integrins are differentially linked through intracellular signaling pathways to the L-type Ca2+ channel and thereby alter control of Ca2+ influx in vascular smooth muscle. This would account for the vasoactive effects of integrin ligands on arterioles and provide a potential mechanism for wound recognition during tissue injury.

Animals↗
PubMed1998

Current knowledge and significance of coronary artery ectasia: a chronologic review of the literature, recommendations for treatment, possible etiologies, and future considerations.

Coronary artery ectasia is the abnormal enlargement of the coronary artery. The prognosis, treatment, and etiology of this disease remain an enigma. There is some evidence to suggest that the incidence of ectasia is increasing, and therefore understanding of this entity needs to improve. This article reviews the current literature on coronary artery ectasia and summarizes the findings. A treatment plan that targets each of the suggested clinical complications is provided. Using multiple indirect observations and current understanding of endothelium-derived relaxation factor, a possible etiology that implicates overstimulation of endogenous nitric oxide is provided. Current literature suggests that ectatic coronary arteries, even without the presence of coronary stenosis, are subject to thrombus formation, vasospasm, and spontaneous dissection. Newer subgroups of ectasia are arising with the use of multiple interventional devices to dilate coronary artery stenosis. By design, these destroy the media of the coronary artery, and it is not clear whether these "iatrogenic" ectatic arteries are subject to the same complications as "idiopathic" coronary artery ectasia. Further investigation is necessary to help define the benefit of the proposed treatment regimen, to clarify the prognosis of these newer groups of "iatrogenic" ectasia, and to confirm or disprove the hypothesis targeting nitric oxide as an etiologic factor.

Anticoagulants↗
PubMed1998

Rickettsial relative associated with papaya bunchy top disease.

The phylogeny of a previously unidentified, obligate laticifer-inhabiting bacterium associated with the papaya bunchy top disease was investigated. Portions of genes corresponding to those for 16S rRNA, the flavoprotein subunit of succinate dehydrogenase (SdhA), citrate synthase (GltA), and the 17-kDa rickettsial common antigen were isolated and sequenced from the non-cultivable bacterium from diseased plants. Comparative sequence analyses consistently indicated that the bacterium is a member of the alpha-subdivision of the Proteobacteria and of the genus Rickettsia. The rickettsia was detected by polymerase chain reaction in diseased, but not healthy, papaya tissues and in the leafhopper vector, Empoasca papayae, providing further evidence of the possible etiological role of the bacterium in the disease. Although Rickettsia have been found naturally in arthropods and can be pathogenic to humans and other vertebrates, this is the first evidence of its kind implicating a Rickettsia as a plant pathogen.

Citrate (si)-Synthase↗
PubMed1998

Role of K+ channels in arteriolar vasodilation mediated by integrin interaction with RGD-containing peptide.

Integrins are transmembrane adhesion receptors found on most cells, including vascular smooth muscle cells. Several integrins bind to the conserved amino acid sequence Arg-Gly-Asp (RGD), and synthetic RGD-containing peptides can cause endothelium-independent arteriolar vasodilation by interacting with the alphavbeta3-integrin expressed by vascular smooth muscle. We hypothesized that RGD peptide-induced vasodilation involves K+ channels. Rat cremaster arterioles were treated with cRGD (GPenGRGDSPCA) in the presence or absence of the nonselective K+ channel inhibitor tetraethylammonium (TEA, 20 mM). TEA caused arterioles to constrict by 19 +/- 5% and inhibited cRGD-induced vasodilation (n = 7, P < 0.05). Vessels preconstricted with phenylephrine (5 x 10(-7) M) showed no significant inhibition of the dilatory response to cRGD, indicating that inhibition by TEA was not related to increased vasomotor tone. Further evidence for the involvement of K+ channels was obtained by addition of 100 mM KCl (n = 5), which inhibited vasodilation caused by cRGD. Inhibition of large and small conductance, Ca2+-activated K+ channels with iberiotoxin (100 nM) or apamin (25 nM), respectively, had no effect on cRGD-induced vasodilation. Partial inhibition of vasodilation was observed with inhibitors of voltage-gated (4-aminopyridine, 1 mM), ATP-sensitive (glibenclamide, 1 microM), and inward rectifying (barium, 50 microM) K+ channels. These data support the hypothesis that integrin-signaling pathways leading to arteriolar vasodilation may involve modulation of K+ channel function.

Animals↗
PubMed1997

Permanent pacing system malfunction due to hidden adjacent fractures of atrial and ventricular leads.

Periods of failure of ventricular pacing and atrial sensing were discovered on Holter recording in a 10-year-old boy 4 years after the implantation of a dual-chamber pacemaker with endocardial bipolar leads brought out through the right atrial wall. The old generator was explanted and the old leads tested. There was considerable atrial oversensing of an electrical artefact. The pacing threshold of ventricular lead was 1.8 V compared with 0.3 V 6 days post implantation. Post-operative lateral chest X-ray disclosed fractures of both atrial and ventricular leads at the approximate site of exit from the right atriotomy. Review of the preoperative lateral film showed that the fractures had been hidden by an ECG electrode.

Child↗
PubMed1997

Chlordiazepoxide counteracts activity-induced suppression of eating in rats.

Because benzodiazepines such as chlordiazepoxide increase food intake, the present experiments tested the effect of chlordiazepoxide on food intake in an animal model of anorexia nervosa, called activity anorexia (AA). To induce AA, rats (Rattus norvegicus) were maintained in activity wheels and restricted to a single 60-min feeding period each day. As previously found, this procedure suppressed food intake. After several days of this training, food intake was measured 30 min after the rats were injected with chlordiazepoxide (5 mg/kg) or saline. In 2 experiments, chlordiazepoxide counteracted the suppression of food intake produced by AA. Because benzodiazepines have been found to increase food intake in many mammalian species including primates, the present results suggest that benzodiazepines could be useful in the treatment of anorexia nervosa.

Animals↗
PubMed1997

Use of World Wide Web server and browser software to support a first-year medical physiology course.

We describe the use of a World Wide Web (Web) server to support a team-taught physiology course for first-year medical students. Our objectives were to reduce the number of formal lecture hours and enhance student enthusiasm by using more multimedia materials and creating opportunities for interactive learning. On-line course materials, consisting of administrative documents, lecture notes, animations, digital movies, practice tests, and grade reports, were placed on a departmental computer with an Internet connection. Students used Web browsers to access on-line materials from a variety of computing platforms on campus, at home, and at remote sites. To assess use of the materials and their effectiveness, we analyzed 1) log files from the server, and 2) the results of a written course evaluation completed by all students. Lecture notes and practice tests were the most-used documents. The students' evaluations indicated that computer use in class made the lecture material more interesting, while the on-line documents helped reinforce lecture materials and the textbook. We conclude that the effectiveness of on-line materials depends on several different factors, including 1) the number of instructors that provide materials; 2) the quantity of other materials handed out; 3) the degree to which computer use is demonstrated in class and integrated into lectures; and 4) the ease with which students can access the materials. Finally, we propose that additional implementation of Internet-based resources beyond what we have described would further enhance a physiology course for first-year medical students.

Computer Communication Networks↗
PubMed1997

Integrin-mediated reduction in vascular smooth muscle [Ca2+]i induced by RGD-containing peptide.

It has previously been shown that synthetic peptides containing the sequence arginine-glycine-aspartic acid (RGD) cause vasodilation by activation of alpha(v)beta3-integrin present on vascular smooth muscle (VSM) cells. The purpose of this study was to determine whether this dilatory effect is mediated by a reduction in VSM cytosolic Ca2+ concentration ([Ca2+]i). First-order arterioles from the rat cremaster were isolated, cannulated, and pressurized. [Ca2+]i was quantitated from the ratio of emitted fluorescence intensity during alternate excitation of fura 2-loaded vessels at 340 and 380 nm. Cyclo(-Arg-Gly-Asp-D-Phe-Val) (cycloRGD; 0.21-210 microM) produced a concentration-dependent dilation of arterioles that had developed basal myogenic tone. Over the entire concentration range tested, [Ca2+]i decreased from 91 +/- 6 to 27 +/- 4 nM (69.7 +/- 5.0% reduction). In association with the decrease in [Ca2+]i, arteriolar lumen diameter increased from 89 +/- 8 to 184 +/- 8 pm (89.8 +/- 1.8% dilation). At intermediate concentrations, cycloRGD induced rhythmic spiking of Ca2+ superimposed on the concentration-dependent lowering of basal [Ca2+]i. These data directly link integrin activation with alterations in Ca2+ regulation, the net effect of which is a reduction in [Ca2+]i. These data further suggest that integrins, through their role in mediating cellular attachment to the extracellular matrix and in cellular signaling involving Ca2+, could provide a logical link to mechanotransduction and myogenic phenomena.

Acetylcholine↗
PubMed1997

Calcium and mechanotransduction of the myogenic response.

The purpose of this study was to measure vascular smooth muscle (VSM) cytosolic calcium ([Ca2+]i) during the myogenic response. We examined the temporal and steady-state relationships between lumen diameter and VSM [Ca2+]i in isolated arterioles exposed to step changes in intravascular pressure. We also studied the relationship between step sizes in intravascular pressure and changes in [Ca2+]i. First-order arterioles from the hamster cheek pouch were isolated, cannulated, and pressurized. [Ca2+]i was quantified using the ratio of emitted fluorescence intensity (R340/380) during alternate excitation of fura 2-loaded vessels at 340 and 380 nm. Stepwise increases in transmural pressure elicited corresponding increases in steady-state [Ca2+]i and myogenic constriction. From a common baseline pressure, the initial rise in [Ca2+]i after a step change in pressure was directly related to the magnitude of the step size and of the distension caused by that pressure step. This supports the theory that there is a relationship between the initial distension of the vessel and the initial [Ca2+]i change. Also, increasing the size of the step change in pressure resulted in a greater myogenic response, yet no difference in the steady-state [Ca2+]i was detected, which suggests that Ca2+ is not the principal or only determinant of steady-state constriction. Finally, larger increases in [Ca2+]i do not necessarily augment the myogenic response, which suggests that some minimal rise in [Ca2+]i is required to elicit myogenic vasoconstriction. Collectively, these data suggest the presence of a separate, Ca(2+)-independent regulatory system.

Animals↗