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Biomedical subjects

L Bell

Publications and source records attributed to L Bell.

At least 73 records · Page 4Linked to original sources
PubMed1991

Hemodynamic effects of 1:2 ECG-coupled jet ventilation in the dog. A comparison with other modes.

In 16 closed-chest dogs the hemodynamics of ECG-coupled jet ventilation (JV) with frequencies of 1:1 (one breath for each cardiac systole) and 1:2 (one breath for every other cardiac systole) were compared to noncoupled JV and intermittent positive-pressure ventilation (IPPV). Cardiac output was similar during 1:2 coupling (1.6 +/- 0.2 L/min) and IPPV (1.6 +/- 0.2 L/min) but decreased during 1:1 coupling (1.2 +/- 0.2 L/min) and noncoupled JV (1.3 +/- 0.2 L/min), p less than 0.05. During 1:2 coupling and IPPV, systemic arterial and transmural left atrial pressures were increased, and pulmonary artery, pericardial, and right atrial pressures were decreased in comparison to the other JV modes. Pulmonary blood volume was preserved during 1:2 coupling but decreased during 1:1 coupling and noncoupled JV. Coupling at 1:2 preserves output by maintaining left ventricular preload via a decrease in right atrial pressure and subsequent maintenance of systemic venous return.

Airway Resistance↗
PubMed1990

Spatiotemporal segregation of endothelial cell integrin and nonintegrin extracellular matrix-binding proteins during adhesion events.

Bovine aortic endothelial cell (BAEC) attachments to laminin, fibronectin, and fibrinogen are inhibited by soluble arginine-glycine-aspartate (RGD)-containing peptides, and YGRGDSP activity is responsive to titration of either soluble peptide or matrix protein. To assess the presence of RGD-dependent receptors, immunoprecipitation and immunoblotting studies were conducted and demonstrated integrin beta 1, beta 3, and associated alpha subunits as well as a beta 1 precursor. Immunofluorescence of BAECs plated on laminin, fibronectin, and fibrinogen reveals different matrix-binding specificities of each of these integrin subclasses. By 1 h after plating, organization of beta 1 integrin into fibrillar streaks is influenced by laminin and fibronectin, whereas beta 3 integrin punctate organization is influenced by fibrinogen and the integrin spatial distribution changes with time in culture. In contrast, the nonintegrin laminin-binding protein LB69 only organizes after cell-substrate contact is well established several hours after plating. Migration of BAECs is also mediated by both integrin and nonintegrin matrix-binding proteins. Specifically, BAEC migration on laminin is remarkably sensitive to RGD peptide inhibition, and, in its presence, beta 1 integrin organization dissipates and reorganizes into perinuclear vesicles. However, RGD peptides do not alter LB69 linear organization during migration. Similarly, agents that block LB69--e.g., antibodies to LB69 as well as YIGSR-NH2 peptide--do not inhibit attachment of nonmotile BAECs to laminin. However, both anti-LB69 and YIGSR-NH2 inhibit late adhesive events such as spreading. Accordingly, we propose that integrin and nonintegrin extracellular matrix-binding protein organizations in BAECs are both temporally and spatially segregated during attachment processes. High affinity nonintegrin interaction with matrix may create necessary stable contacts for longterm attachment, while lower affinity integrins may be important for initial cell adhesion as well as for transient contacts of motile BAECs.

Acid Phosphatase↗
PubMed1990

Alpha-adrenergic regulation of splanchnic volume and cardiac output in the dog.

The present study examined whether alpha-adrenergic stimulation causes a change in splanchnic intravascular volume in the anaesthetized animal with an intact circulation, which region(s) mediate the volume change, and whether the splanchnic volume change influences cardiac output. In order to ascertain that a radionuclide imaging technique could be used to assess total splanchnic volume changes, drugs known to increase or decrease splanchnic volume were infused on 21 occasions in eight dogs studied under conditions of selective perfusion and drainage of the splanchnic vasculature with erythrocytes labelled with 99Tcm and a gamma camera placed over the abdomen. For these 21 infusions, volume and radionuclide count changes were related: r greater than or equal to 0.90 (n = 20), r = 0.76 (n = 1). After ascertaining tissue attenuation and blood radioactivity in four of the animals, the standard error for a single estimate of the absolute volume change using the radionuclide technique was determined to be 75 ml. In six animals with intact circulations, phenylephrine (40-80 micrograms min-1) for 20 min was associated with an increase in cardiac output of 12 +/- 2% (P less than 0.001) and a decrease in total splanchnic volume estimated to be 431 +/- 95 ml (P less than 0.001). The splanchnic volume decrease was due entirely to decreases in splenic and intestinal volume. In eight eviscerated animals, cardiac output decreased by 30 +/- 2% (P less than 0.001) during phenylephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Influence of splanchnic intravascular volume changes on cardiac output during muscarinic receptor stimulation in the anaesthetized dog.

The direct influence of systemic muscarinic receptor stimulation on total splanchnic intravascular volume and the splanchnic organs responsible for the total splanchnic volume change associated with muscarinic receptor stimulation in the animal with an intact circulation are unknown. Furthermore, the subsequent effect of these volume changes on cardiac output is not known. Thus, acetylcholine was infused at 5 micrograms kg-1 min-1 in 25 anaesthetized dogs in which nicotinic blockade of the ganglia was achieved with mecamylamine, while total and regional splanchnic intravascular volume changes were determined with a radionuclide imaging technique. Total splanchnic volume decreased by 4.9 +/- 1.0% (P less than 0.0001), splenic volume decreased by 10.3 +/- 2.0% (P less than 0.0001), hepatic volume increased by 5.8 +/- 1.4% (P less than 0.01), extrahepatosplenic volume increased by 6.6 +/- 1.6% (P less than 0.01) and cardiac output increased from 1960 +/- 190 to 2290 +/- 230 ml min-1 (P less than 0.001). After splenectomy (n = 13), the hepatic and extrahepatosplenic volume increments were abolished, and the increase in cardiac output was not attenuated (1600 +/- 260 to 2040 +/- 370 ml min-1). After subsequent evisceration (n = 5), the cardiac output increment associated with acetylcholine was still not attenuated. Acetylcholine-associated splanchnic volume changes were abolished after muscarinic receptor blockade with atropine. Thus, muscarinic receptor stimulation causes a decrease in total splanchnic volume due entirely to a decrease in splenic volume. The splanchnic volume changes do not influence cardiac output.

Acetylcholine↗
PubMed1990

Quantitative radionuclide assessment of total pulmonary vascular volume changes.

Current techniques do not permit continuous and noninvasive assessments of changes in total pulmonary intravascular volume. Hence, the present study was undertaken to determine whether quantitative radionuclide imaging can be used to determine the direction and estimate the magnitude of total pulmonary vascular volume changes. The pulmonary circulation was separately perfused at a constant rate via the pulmonary artery and drained at a constant pressure via the left atrium in nine dogs. Changes in pulmonary intravascular volume were recorded as reciprocal changes in extracorporeal reservoir volume during phenylephrine or isoproterenol administration, a 20% increase in pulmonary artery flow or a 5 mmHg (1 mmHg = 133.32 Pa) decrease in left atrial pressure. Erythrocytes were labeled with technetium-99m and pulmonary volume changes were determined from tissue attenuation, blood radioactivity, and changes in total pulmonary radioactivity obtained with a gamma-camera. During each of the interventions, count changes correlated with volume changes (r greater than or equal to 0.75). The technique reliably detected volume changes as small as 10 mL. For all 531 individual pairs of radionuclide- and reservoir-determined volume changes, the correlation between reservoir-determined and radionuclide-estimated pulmonary intravascular volume changes was 0.87. The standard error of the radionuclide estimate was 21 mL. Hence, the present study demonstrates that quantitative radionuclide imaging can be used to continuously and noninvasively determine total pulmonary vascular volume changes.

Animals↗
PubMed1990

Influence of the angiotensin system on endothelial and smooth muscle cell migration.

The blood vessel wall's response to injury is an important determinant of luminal size and vessel function. The physiologic migration of endothelial cells from the edges of a wound and the pathophysiologic migration of medial smooth muscle cells into the intima are two important components of the vessel wall's response to injury. The influence of the angiotensin system on endothelial and smooth muscle cell migration have not been examined. In the present study, the influence of angiotensin system components on bovine aortic endothelial cell (BAEC) and bovine aortic smooth muscle cell (BASMC) migration after release of cultured cell monolayers from contact inhibition was determined. The angiotensin-converting enzyme (ACE) inhibitor lisinopril increased BAEC migration 41% +/- 3% (P less than 0.001), as did the specific angiotensin II antagonist sar1, ile8-angiotensin II (SAR) (41% +/- 3% (P less than 0.001). Exogenous angiotensin I and angiotensin II did not affect BAEC migration. Exogenous angiotensin II abolished the effect of lisinopril on BAEC migration. Lisinopril increased cell-associated u-plasminogen activator (u-PA) 23% +/- 3% (P less than 0.001) in migrating BAEC and angiotensin II abolished this increase. SAR increased u-PA 33% +/- 0% (P less than 0.001). In contrast, these agents had the opposite effect on smooth muscle cells. Angiotensin II increased smooth muscle cell migration 40% +/- 3% (P less than 0.001), and this effect was abolished by SAR. Angiotensin II also increased cell-associated u-PA 83% +/- 7% (P less than 0.001) in migrating BASMC. The increase in BAEC migration with inhibition of endothelial cell angiotensin II stimulation, either with lisinopril or SAR, also was associated with an increase in cell-associated u-PA. These results indicate that lisinopril interrupts an autocrine pathway in endothelial cells, in which endothelial cell-derived angiotensin I is converted to angiotensin II by ACE, and imply that angiotensin-converting enzyme inhibitors in vivo would act to reduce vessel wall injury by directly increasing the rate of endothelial cell wound closure; by increasing the antithrombotic tendency of the endothelium via enhanced u-PA; and indirectly, by decreasing production of angiotensin II and thereby the rate of smooth muscle cell migration into the intima.

Angiotensins↗
PubMed1990

Influence of the new inotropic agent DPI 201-106 on the total capacitance vasculature in dogs.

Recent investigations have demonstrated that the piperazinyl-indole DPI 201-106 (DPI) acts to increase contractility independent of increases in cAMP or inhibition of Na+, K(+)-ATPase. Since associated changes in the capacitance vasculature would also be expected to influence ventricular performance, the influence of DPI on total intravascular volume (IV) was examined. In eight anesthetized dogs undergoing prior sinoaortic baroreceptor denervation and bilateral cervical vagotomy, blood from the venae cavae was drained to an extracorporeal reservoir and returned to the right atrium at a constant rate so that changes in IV could be recorded as reciprocal changes in reservoir volume. Racemic DPI at 50 micrograms/kg/min for 20 min was associated with a 65 +/- 7 ml (P less than 0.0001) decrease in total IV and a decrease in mean arterial pressure from 80 +/- 7 to 74 +/- 5 mmHg (P less than 0.0001). DPI administration was associated with a 67 +/- 9 ml (P less than 0.05) decrease in IV after beta adrenergic blockade and a 68 +/- 11 ml (P less than 0.05) decrease in IV after alpha and beta adrenergic blockade. Abdominal evisceration abolished the IV decrement due to DPI. Radionuclide imaging studies demonstrated that decreases in hepatic and splenic IV contributed to the decrease in splanchnic IV. Thus, DPI acts to decrease total IV. The IV decrement is due entirely to a decrease in splanchnic IV and is not mediated by baroreceptor stimulation or by adrenergic receptor stimulation. In the animal with an intact circulation, the total IV decrement would be expected to increase venous return and thereby act to maintain ventricular end diastolic pressure.

Animals↗
PubMed1989

The STE4 and STE18 genes of yeast encode potential beta and gamma subunits of the mating factor receptor-coupled G protein.

The STE4 and STE18 genes are required for haploid yeast cell mating. Sequencing of the cloned genes revealed that the STE4 polypeptide shows extensive homology to the beta subunits of mammalian G proteins, while the STE18 polypeptide shows weak similarity to the gamma subunit of transducin. Null mutations in either gene can suppress the haploid-specific cell-cycle arrest caused by mutations in the SCG1 gene (previously shown to encode a protein with similarity to the alpha subunit of G proteins). We propose that the products of the STE4 and STE18 genes comprise the beta and gamma subunits of a G protein complex coupled to the mating pheromone receptors. The genetic data suggest pheromone-receptor binding leads to the dissociation of the alpha subunit from beta gamma (as shown for mammalian G proteins), and the free beta gamma element initiates the pheromone response.

Amino Acid Sequence↗
PubMed1989

Influence of verapamil on total and regional intravascular volume in dogs.

Verapamil's influence on intravascular volume (IV) in the total capacitance circulation was examined in anesthetized dogs after mecamylamine or baroreceptor denervation. Blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that IV changes could be measured as reciprocal changes in reservoir volume. In 10 dogs, verapamil (50 micrograms/min) caused a decrease in total IV of 74 +/- 12 ml (P less than 0.0005) at 20 min and a decrease in arterial pressure from 79 +/- 5 to 66 +/- 3 mmHg (P less than 0.0005). After evisceration in nine animals, verapamil caused an extrasplanchnic (XSPL) IV decrease of 97 +/- 19 ml (P = 0.08). In 11 animals with separate perfusion and drainage of the splanchnic and XSPL circulations, verapamil caused an XSPL IV decrease of 74 +/- 20 ml (P less than 0.002) and a splanchnic IV increase of 19 +/- 9 ml (P = 0.06). In four animals on cardiopulmonary bypass, IV decreased 154 +/- 66 ml (P less than 0.002) during verapamil administration. Thus total IV decreases due to a decrease in systemic extrasplanchnic volume. Because pressure decreased while arterial flow and venous outflow pressure were constant, a decrease in the resistance to blood return to the central circulation mediates the XSPL volume decrement.

Animals↗
PubMed1989

Effect of platelet factors on migration of cultured bovine aortic endothelial and smooth muscle cells.

Endothelial cell (EC) injury and the response of EC and smooth muscle cells (SMCs) to injury contribute to the pathophysiology in patients with vascular disease and atherosclerosis. Since platelets have been suggested to play an important role in modulating vascular injury, the present study was undertaken to examine the influence and mechanism of action of individual platelet factors on bovine aortic EC and SMC migration using an in vitro wound assay system. Serotonin decreased EC proliferation and reduced EC migration 21 +/- 1% (p less than 0.005), which was attenuated by imipramine. Transforming growth factor-beta reduced EC proliferation and decreased EC migration 52 +/- 3% (p less than 0.005). Norepinephrine increased EC proliferation but decreased EC migration 26 +/- 2% (p less than 0.005), which was abolished by phenoxybenzamine. Histamine increased EC proliferation but reduced EC migration 29 +/- 2% (p less than 0.005), which was attenuated by diphenhydramine. Platelet-derived growth factor decreased EC proliferation and decreased EC migration 40 +/- 2% (p less than 0.005). In contrast, serotonin increased SMC proliferation and increased SMC migration 31 +/- 2% (p less than 0.005), which was abolished by ketanserin. Transforming growth factor-beta increased SMC migration 35 +/- 5% (p less than 0.005). Norepinephrine increased SMC proliferation and increased SMC migration 43 +/- 4% (p less than 0.005), which was abolished by propranolol. Histamine increased SMC proliferation and increased SMC migration 38 +/- 3% (p less than 0.005), which was abolished by cimetidine. Platelet-derived growth factor increased SMC proliferation and increased SMC migration 40 +/- 3% (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Syphilis detection in cerebrovascular disease.

To determine the importance of syphilis testing in cerebrovascular disease, we prospectively assessed 218 consecutive patients with either transient ischemic attack or completed stroke. The results from this study group were compared with those from a control group of 150 neurological patients without cerebrovascular disease. Of 275 patients from both groups specifically tested by the fluorescent treponemal antibody-absorption test, 34% of the study group were seropositive compared with 18% of the controls (chi 2 = 7.7, p less than 0.01). Fifty-four percent of the patients with a positive fluorescent treponemal antibody-absorption test underwent a cerebrospinal fluid examination; meningovascular syphilis was detected in one (0.4%) of these. This patient was a homosexual male with antibodies to the human immunodeficiency virus; a second patient, with possible meningovascular syphilis, also had antibodies to this virus. Despite the relatively high rate of syphilis seropositivity noted in our study group, syphilis was not found to be a common cause of cerebrovascular disease; therefore, routine screening is seen to be of low diagnostic yield. Attention to patients who are at higher risk for syphilitic infection, patients with clinical features suggestive of meningovascular syphilis, and the proper choice of serologic studies can help make the assessment of syphilis seropositivity more clinically appropriate and cost effective.

Cerebrospinal Fluid↗
PubMed1989

The interactions of vascular cells with solid phase (matrix) and soluble factors.

The vessel wall is composed of heterogeneous cell populations residing in a variety of vascular beds. Each cell type has different functions and morphologies but all of them have a role in the repair process following vascular injury. Responses to injury vary depending upon the type and extent of the injury and the vascular bed affected. The sheet migration and proliferation exhibited by large vessel endothelial cells is in striking contrast to the migration through soft tissues and tube formation exhibited by microvascular endothelial cells in response to injury. Vascular smooth muscle cells respond to injury by migrating into the intima, proliferating and synthesizing matrix, causing intimal thickening. The response to injury by vascular cells appears to be modulated, in part, by the composition and organization of the surrounding matrix and the various platelet factors and cytokines found at sites of injury. Furthermore, evidence has been accrued in culture, suggesting that solid phase (matrix) and soluble factors modulate each other's effects on local vascular cell populations following injury.

Animals↗
PubMed1989

Endothelial cell behavior after denudation injury is modulated by transforming growth factor-beta1 and fibronectin.

Endothelial denudation injury after endarterectomy, autologous and synthetic grafting and balloon angioplasty leads to exposure of thrombogenic vessel wall material and may elicit an atherogenic response in the media of the affected vessels in which complete reendothelialization may not occur. While the role(s) of extracellular matrix composition and organization in this process are only incompletely understood, it is widely accepted that endothelial cells respond to matrix components in specific, complex fashions. In this report we demonstrate that large vessel endothelial cell migration is affected by the surrounding matrix and the soluble factor, transforming growth factor-beta1, which may mediate its effects, in part, by modulating endothelial cell matrix synthesis. Specifically, large vessel endothelial cell migration is decreased on a fibronectin substratum and in the presence of transforming growth factor-beta1, which increases fibronectin mRNA and protein accumulation in culture. Inhibition of sheet migration is also elicited by the addition of soluble fibronectin to the cultures. These in vitro findings are consistent with our in vivo findings of increased staining of fibronectin luminally and in the intima in the chronically deendothelialized region of a balloon catheter denuded carotid artery. Thus, reendothelialization after iatrogenic and natural injury appears to be a complex process which can be modulated by the underlying matrix and soluble factors, which may themselves modulate the matrix synthesis of local vascular cells.

Animals↗
PubMed1989

Timing of ovulation for artificial insemination.

Two studies involving eighty women having treatment with artificial insemination by donor (AID) have demonstrated that the use of a urinary semi-quantitative assay for luteinising hormone (LH) gives pregnancy rates comparable to those obtained using plasma LH for the timing of insemination. The advantage of self test assay is evident in a scattered region such as Grampian.

Adult↗
PubMed1988

The presence and significance of intraepithelial mesenchymal cells in human foetal colon.

During an investigation of the morphogenesis of the human foetal colon, breaks in the basal lamina underlying the surface epithelium were frequently observed at 10 1/2-11 weeks. These occurred at those sites where the mesenchyme was sweeping up into the epithelium prior to the transformation of the epithelium from stratified to a single layer. At the same time numbers of mesenchymal cells appeared among the epithelial cells and some were observed actually in the process of passing through the gaps in the basal lamina. Close contact was apparent between some mesenchymal cells and basal epithelial cells through extended breaks in the basal lamina. Many of the mesenchymal cells within the epithelium contained numbers of apoptotic bodies. This suggests that one of the functions of the intra-epithelial mesenchymal cells is to remove the debris resulting from cell death which occurs in association with the re-arrangement of cells during development of the colon.

Basement Membrane↗
PubMed1988

Fetal growth and fetal lung phospholipid content in rats fed safflower oil, menhaden oil, or hydrogenated coconut oil.

The objective was to determine if dietary fish oil decreased the degree of fatty acid saturation in rat lung phosphatidylcholine (PC). A diet containing 12% of its energy as fat was fed for 3 wk to growing male Sprague-Dawley rats (trial I) or to pregnant rats for days 8-21 of gestation (trial II). The dietary fat treatments in trial I were safflower oil (SO), menhaden oil (MO), or hydrogenated coconut oil (HCO) and in trial II were SO, MO, HCO, or SO-MO (75%:25%). Polyunsaturated fatty acids reduced (p less than 0.05) hepatic fatty acid synthetase (MO greater than SO) in growing rats but the dietary lipids had no effect on lung palmitate content. Maternal consumption of MO vs SO reduced (p less than 0.05) fetal body weight and lung weight but not lung:body wt ratio. Dietary MO and SO-MO increased (p less than 0.05) disaturated PC content of fetal lungs. The fetal lung data indicate that maternal ingestion of fish oil improve fetal lung maturation.

Animals↗