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Biomedical subjects

L Linder

Publications and source records attributed to L Linder.

At least 37 records · Page 2Linked to original sources
PubMed1995

Femoral component migration in total knee arthroplasty: randomized study comparing cemented and uncemented fixation of the Miller-Galante I design.

The Miller-Galante I knee replacement was inserted in 25 women and three men (33 knees) with osteoarthrosis. All patients received a TiAlV femoral component with a commercially pure titanium fiber-mesh undersurface. Cemented or cementless fixation was used based on a randomization protocol. Micromotions of the femoral components were recorded with roentgen stereophotogrammetric analysis during the first 2 postoperative years. The magnitude of migration did not differ between cemented and uncemented fixation. The number of nonmigrating prostheses decreased from 21 (12 cemented and nine uncemented) at 3 months to six (three cemented and three uncemented) at 24 months. In both groups, the magnitude of prosthetic tilting about the longitudinal axis (internal-external rotation) was as large as that about the transverse axis (flexion-extension). Rotation into extension was as common as rotation into flexion. The largest translations were recorded at either of the posterior condyles. In 10 uncemented components, radiolucent lines were seen at the distal interface postoperatively. Proximal migration of the femoral component was recorded in these knees, and the width of the lines decreased or the lines disappeared totally at 24 months. After 2 years, lines were noted around four cemented and four uncemented replacements, mainly anteriorly or distally. All of these prostheses migrated. One prosthesis, revised because of malalignment, displayed pronounced migration after an initial period of stability. Bone ingrowth was observed anteriorly and anterodistally despite the presence of motions of 1 mm or more.

Aged↗
PubMed1995

Neuropeptide Y in human hand veins: pharmacologic characterization and interaction with cyclic guanosine monophosphate-dependent venodilators in vivo.

The dorsal hand vein compliance technique was used to study direct vascular effects of human neuropeptide Y in vivo. Human neuropeptide Y is an endogenous vasoconstrictor peptide that is costored with norepinephrine in sympathetic nerve endings and coreleased with the catecholamine under various physiologic and pathologic conditions. Compared with the alpha 1-adrenergic agonist phenylephrine (geometric mean dose-rate that produces the half-maximal response [ED50]: 1.05 nmol/min; maximum venoconstriction [Emax] +/- SEM, expressed as a percentage of baseline compliance: 91% +/- 3%), human neuropeptide Y was nine times more potent (geometric mean ED50: 0.122 nmol/min; p < 0.001) but markedly less efficacious (Emax: 58% +/- 4%; n = 12; p < 0.001). Venoconstrictor effects of human neuropeptide Y lasted several hours and were unchanged by simultaneous administration of alpha-adrenergic antagonists but were readily reversed by nitroglycerin or bradykinin. The high responsiveness of subcutaneous veins to human neuropeptide Y indicates that human neuropeptide Y may regulate venous compliance and filling of the venous subcutaneous capacitance bed in vivo.

Adult↗
PubMed1995

Infection adjacent to titanium and bone cement implants: an experimental study in rabbits.

A pure titanium cylinder or a piece of bone cement was implanted in each upper tibial metaphysis of 20 rabbits. After 4 months radiograms were taken and 10(4), 10(6), or 10(8) Staphylococcus aureus were injected into each leg through central holes in the implants in three groups of animals. Four weeks later new radiograms, bacteriological and histological biopsies were obtained. Three animals died before the end of the experiment. In animals which received 10(6) or 10(8) S. aureus radiographic signs of infection were found in 11/22 legs with both titanium and bone cement implants. No radiolucent zones developed around the implants. Bacteriological cultures from bone close to the implants were negative in all legs with titanium implants and positive in four legs with cement implants. Seven cultures were negative in spite of radiographic changes. It is concluded that after a proper time for wound healing the bone around unloaded implants of both titanium and bone cement is fairly resistant to infection. In some cases, healing of an infection in the surrounding bone seems possible.

Animals↗
PubMed1995

Periodontal healing and periopathogenic microflora in smokers and non-smokers.

The aim of the present study was to monitor the clinical and microbiological effects of non-surgical therapy in smokers and non-smokers. The subject material included 32 patients (age range 32-61 years), 11 men and 21 women with moderate to severe periodontitis. 17 patients were smokers ( > or = 15 cigarettes/day) and 15 non-smokers. All patients were subjected to non-surgical periodontal therapy performed by a dental hygienist. Periodontal variables (plaque index, gingival index and probing depth) were registered and bacterial samples were collected before and 2 months after treatment. The treatment resulted in significant reductions towards very low plaque and gingival indices in smokers and non-smokers alike (p < 0.05). Although probing depth was reduced in both smokers and non-smokers, the probing pocket depth reduction was significantly smaller in smokers than non-smokers (p < 0.05). Microbiologically, the same therapeutical efficacy was attained in both smoking groups, indicating an almost total eradication of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Concerning Prevotella intermedia, out of 14 smokers and 10 non-smokers positive at baseline, 9 and 5, respectively, remained positive after treatment. The results suggest a less favourable clinical outcome of non-surgical therapy in smokers than non-smokers in spite of the fact that the therapy was equally effective with regard to reducing the alleged periopathogens A. actinomycetemcomitans, P. gingivalis and P. intermedia.

Adult↗
PubMed1995

Role of basal and stimulated release of nitric oxide in the regulation of radial artery caliber in humans.

Although it is well established that nitric oxide contributes to the regulation of resistance arterial tone in humans, its role at the level of large arteries is less clear. Therefore, we assessed in healthy volunteers the effect of local administration of the inhibitor of nitric oxide synthesis NG-monomethyl-L-arginine (L-NMMA) on basal radial artery diameter (transcutaneous A-mode echotracking) and radial blood flow (Doppler) as well as on the radial response to acetylcholine and the nitric oxide donor sodium nitroprusside. A catheter was inserted into the brachial artery for measurement of arterial pressure and infusion of L-NMMA (2, 4 and 8 mumol/min for 5 minutes, n = 11), acetylcholine (3, 30, 300 and 900 nmol/min for 3 minutes, n = 8), and nitroprusside (2.5, 5, 10, and 20 nmol/min for 3 minutes, n = 6). None of the treatments affected arterial blood pressure or heart rate. L-NMMA dose-dependently decreased radial blood flow (from 31 +/- 6 to 17 +/- 3 10(-3) L/min after 8 mumol/min, P < .01) but did not affect radial artery diameter (from 2.93 +/- 0.11 to 2.90 +/- 0.14 mm). Acetylcholine dose-dependently increased radial blood flow (154 +/- 43% after 900 nmol/min) and radial artery diameter (16 +/- 4%), and both effects were markedly reduced after L-NMMA (increase in radial blood flow and radial artery diameter: 22 +/- 20% and 3 +/- 2%, respectively; both P < .01 versus controls). Nitroprusside also dose-dependently increased radial artery diameter (14 +/- 4% after 20 nmol/min) but only moderately affected radial blood flow (47 +/- 21%).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

[Role of nitric oxide in the regulation of the mechanical properties of peripheral muscular arteries in man].

Although several experiments have demonstrated the existence of a basal NO-dependent vasodilatory tone at the arteriolar level, the contribution of NO to the mechanical properties of large arteries has not been investigated in humans. To evaluate the effect of NO-synthase inhibition on these mechanical properties, radial artery internal diameter (d, mm) and wall thickness (h, mm) were measured continuously in 11 healthy volunteers (age: 24 +/- 1 years), using an A-mode echo-tracking system coupled to a Doppler device for the measurement of radial blood flow (RBF, ml/min). A catheter was inserted in the brachial artery for measurement of arterial pressure (AP, mmHg), and infusion of the inhibitor of NO synthesis NG-monomethyl L-arginine (L-NMMA: 4 mumol/min for 5 min, infusion rate 0.8 ml/min). Arterial compliance C, 10(-3) mm2/mmHg), distensibility (D, 10(-3)/mmHg), mid-wall stress (sigma, 10(5) dynes/mm2) and incremental modulus (Ei, 10(7) dynes/mm2) were calculated before and after L-NMMA. After L-NMMA, RBF decreased from 31 +/- 6 to 23 +/- 4 (p < 0.05), radial vascular resistance increased from 2.70 +/- 0.35 to 3.77 +/- 0.55 (p < 0.05), without changes in AP or heart rate. Table shows mechanical parameters, assessed at fixed AP (80 mmHg) (*: p < 0.05 vs baseline): [table: see text] Thus, the L-NMMA-induced decrease in radial arterial wall stiffness (Ei) without changes in arterial diameter or stress demonstrates that NO-synthase inhibition induces an isometric relaxation of vascular muscle cells, which explains the increase of arterial compliance at constant mid-wall stress. These results demonstrate that NO contributes to the regulation of peripheral muscular arterial mechanics in humans. At the level of large arteries, the isometric relaxation observed after NO-synthase inhibition is probably the consequence of compensatory vasodilator mechanisms.

Adult↗
PubMed1995

Indirect evidence for stimulation of nitric oxide release by tumour necrosis factor-alpha in human veins in vivo.

OBJECTIVES: The detrimental haemodynamic changes observed in septicaemia are generalised vasodilation, arterial hypotension, and hyporesponsiveness to vasopressor compound, all of which could be explained by the release of an endogenous vasodilator. Experimental and clinical evidence suggests that tumour necrosis factor-alpha (TNF) induces the expression of vascular nitric oxide (NO) synthase within hours and that NO released from smooth muscle cells could be involved in the pathogenesis of septic shock. The aim of this study was to investigate the role of NO in the vascular effects of TNF. METHODS: Using the dorsal hand vein compliance technique, the effect of the NO synthase inhibitor L-NG-monomethyl-arginine (L-NMMA) on alpha 1-adrenergic responsiveness (phenylephrine 1.25-8000 ng/min) was studied after prolonged local venous infusion of TNF (8.7 micrograms in 5 h) in 9 volunteers and in 6 volunteers without previous cytokine exposure. RESULTS: Mean (+/- s.e.) maximum phenylephrine constriction (Emax) was 73 +/- 6% and log dose-rates exerting 50% of Emax (log ED50) were 3.2 +/- 0.09 (geometric mean: 1535 ng/min). Local co-administration of L-NMMA at a dose sufficiently high to block NO formation (3.4 mumol/min) increased venous sensitivity to phenylephrine threefold (log ED50 2.8 +/- 0.1, P < 0.015; geometric mean: 574 ng/min) whereas Emax was similar (73 +/- 5%). In the controls the phenylephrine dose-response relationship remained unaffected by simultaneous administration of L-NMMA. CONCLUSIONS: As no basal release of NO occurs in hand veins without previous exposure to TNF these results provide direct evidence for induction of NO formation in the human vasculature and consecutive resistance to alpha-adrenergic venoconstriction. NO might, therefore, be a key mediator of haemodynamic impairment in humans under conditions with known elevations of circulating TNF, such as a septic shock.

Adult↗
PubMed1994

A study in vitro of threaded titanium pins used for retrograde obturation of root canals.

The microleakage of four retrograde filling materials was compared in vitro. Fifty-three single rooted teeth were instrumentated and root filled with resin chloroform and gutta-percha. The gutta-percha cones were left extruding from the access opening. All teeth were apicected and retrograde fillings placed. The materials used were a non gamma 2 amalgam (Amalcap), a glass ionomer cement (ChemFil II), threaded titanium pins cemented with a glass ionomer cement (ChemFil II) and identical titanium pins cemented with a silicone material (Adheseal). After removal of the gutta-percha with tweezers, a radioactive isotope solution was placed in the teeth. Extraradicular samples were taken at 3, 7, 28, 77 and 104 days. All retrograde fillings showed some microleakage. The group with titanium pins cemented with silicone showed the least leakage: significantly less than the teeth with glass ionomer cement (P < 0.01) and with amalgam (P < 0.01). No significant differences were found between other groups.

Dental Amalgam↗
PubMed1994

Diminished vascular response to inhibition of endothelium-derived nitric oxide and enhanced vasoconstriction to exogenously administered endothelin-1 in clinically healthy smokers.

BACKGROUND: Smoking is a major risk factor for the development of atherosclerosis. Because endothelial dysfunction may be a marker for future atherosclerosis, we investigated the effects of smoking on endothelium-dependent control of vascular tone. METHODS AND RESULTS: The effects of brachial arterial infusions of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide synthesis inhibitor; sodium nitroprusside; endothelin-1; and norepinephrine on forearm blood flow (strain-gauge plethysmography) were compared in 29 long-term smokers and 16 nonsmokers. The acute effects of smoking on systemic hemodynamics, plasma catecholamines, and forearm vascular responses to these compounds were investigated in smokers only. Smokers did not differ from nonsmokers (n = 16) regarding the vascular effects of sodium nitroprusside (n = 13) or vasoconstriction due to norepinephrine and endothelin-1 (n = 16). Low-dose endothelin-1-induced vasodilation, believed to reflect endothelial prostacyclin or nitric oxide release, was absent in smokers (n = 16), and their increase of forearm vascular resistance (FVR) after L-NMMA (n = 13) was impaired (35.6 +/- 27.9% versus 118.8 +/- 43.2%, P < .001). Short-term smoking (n = 11) increased blood pressure, heart rate, and plasma epinephrine concentrations (P < .05 or less); enhanced endothelin-1-induced vasoconstriction (delta FVR, 457 +/- 192% versus 254 +/- 143%, P < .01); and decreased norepinephrine-induced vasoconstriction (P < .05), but had no effect on the other interventions. CONCLUSIONS: Long-term smoking is associated with a diminished nitric oxide-dependent component of basal vascular tone and an impaired endothelium-dependent vasodilator response to low-dose endothelin-1 and short-term smoking enhances endothelin-1-induced vasoconstriction. Impaired endothelial control of vascular tone might reflect impairment of normal antiatherosclerotic endothelial functions in smokers, but the relevance of smoking-induced enhancement of endothelin-1 vasoconstriction remains to be determined.

Adult↗
PubMed1994

Site-related streptococcal attachment to buccocervical tooth surfaces. A correlative micromorphologic and microbiologic study.

Scanning electron (SEM) microscopy of epoxy replicas made from dental impressions has shown that in buccal gingival recession the root surfaces are devoid of cementum, leaving the dentin exposed. In this study replication techniques were applied to correlate the micromorphology of the buccocervical region with early streptococcal attachment. The subjects were 27 healthy young adults. The buccocervical surfaces of all the premolars were meticulously cleaned. The subjects fasted for 2 h before impression-taking. Replicas were made from impressions in hydrophilic A-silicone, and streptococcal attachment was visualized by light microscopy of mitis-salivarius agar replicas incubated anaerobically for 48 h. The surface micromorphology was documented by SEM of corresponding epoxy replicas. Colonization only 2 h after cleaning was very sparse. Sites with healthy or inflamed gingivae had markedly different colonization patterns in the sulcular region. In 4 subjects with a total of 12 sites where gingival recession, undetected clinically, was disclosed by SEM, representative colonies were retrieved and identified microbiologically to species level. Two healthy sites per subject were also sampled. Streptococcus mutans and S. sobrinus were identified from eight sites with exposed root dentin. S. oralis predominated on the enamel surfaces. The method offers a valuable complement to in situ and in vitro microbiologic studies of exposed dentin and a novel technique for sampling clinical isolates of streptococci.

Adolescent↗
PubMed1994

Implant stability, histology, RSA and wear--more critical questions are needed. A view point.

I discuss the radiostereometry (RSA) of prosthetic micromovement from clinical and histological viewpoints. Even in non-migrators there is a wide variety of interfaces with various resistances to trigger factors, such as mechanical forces and sequels of wear. I suggest that the various forms of bone resorption seen with conventional radiography are caused by such trigger factors and that their anatomical appearance is determined by the structure of the interface obtained at surgery.

Biomechanical Phenomena↗
PubMed1994

Osseointegration of titanium implants in the tibia. Electron microscopy of biopsies from 4 patients.

We studied the ultrastructure of bone tissue around implants of pure titanium inserted into the tibia in 4 patients with arthrosis or rheumatoid arthritis. Three main appearances of the interface were noted. First, a close contact between titanium and calcified bone with living osteocytes inside the newly-formed bone was observed in all samples. Secondly, a close contact was also seen between the implant and osteoid, the newly formed collagenous matrix being either uncalcified or calcifying. Thirdly, a loose extracellular matrix with fibrillar and nonfibrillar materials was sometimes observed between bone mineral and implant. There was no inflammatory reaction at the interface. We concluded that the titanium implants were osseointegrated, but the calcification of the bone tissue was not complete even after 20 months. However, mineralization of osteoid and living bone cells revealed the presence of an active tissue.

Arthritis, Rheumatoid↗
PubMed1994

[Role of nitric oxide in flow-dependent vasodilation of human peripheral arteries in vivo].

Experiments performed in isolated arteries or in animals suggested that flow-dependent dilatation of conduit arteries is mediated through the release of endothelium-derived nitric oxide (NO). The present study was designed to assess whether NO also contributes to flow-dependent dilatation of conduit arteries in humans. Radial artery internal diameter was measured in 8 healthy volunteers (age 22 +/- 1 years), using a transcutaneous A-mode echo-tracking system, coupled to a Doppler device for the measurement of radial blood flow. A catheter was inserted in the brachial artery for measurement of arterial pressure and infusion of the L-arginine analogue NG-monomethyl L-arginine (L-NMMA (8 mumol/min for 7 min, infusion rate 0.8 ml/min). Flow-dependent dilatation was evaluated before and after L-NMMA as the response of the radial artery to an acute increase in flow (reactive hyperemia after a 3 min distal cuff occlusion). Release of the occlusion induced a significant increase in radial blood flow (from 27 +/- 4 to 82 +/- 13 ml/min; p < 0.01) followed by a delayed increase in radial diameter (flow-mediated dilatation; from 2.77 +/- 0.13 to 2.85 +/- 0.13 min; p < 0.01), without any change in heart rate or arterial pressure. L-NMMA induced a significant decrease in basal forearm blood flow (from 27 +/- 4 to 14 +/- 2 ml/min; p < 0.05), without affecting basal radial artery diameter, heart rate or arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Vascular effects of endothelin-1 in humans and influence of calcium channel blockade.

AIM: To investigate the effects of brachial artery infusions of endothelin-1 on forearm blood flow in normal healthy volunteers. METHODS: Brachial artery cannulation was used for a direct assessment of blood pressure and for intra-arterial regional drug infusions. Drug-induced forearm blood flow changes were measured by venous occlusion plethysmography. RESULTS: Low-dose endothelin-1 infusions resulted in a significant increase in forearm blood flow, indicating vasodilation, which was significantly attenuated by cyclo-oxygenase inhibition using aspirin. High-dose endothelin-1 infusions resulted in transient vasodilation, followed by dose-dependent and long-lasting vasoconstriction. In the human forearm the vasoconstrictor potency of endothelin-1 was approximately 10-15 times greater than that of norepinephrine. Maximal cyclic GMP-dependent vascular muscle relaxation, after muscarinergic stimulation by acetylcholine (endothelium-dependent) or after infusion of sodium nitroprusside (endothelium-independent), did not prevent endothelin-1 induced vasoconstriction. However, calcium channel blockade by brachial artery infusions of maximally vasodilating doses of either verapamil or nifedipine not only abolished the endothelin-induced vasoconstriction but also unmasked the vasodilator potency of high-dose endothelin-1 infusions. The infusion of lower doses of nifedipine indicated that endothelin-1 induced vasoconstriction was reversed by plasma concentrations estimated to be in the therapeutic range. CONCLUSIONS: These results demonstrate a dual action of luminally applied endothelin-1 in human resistance vessels in vivo, consisting of transient initial vasodilation followed by pronounced vasoconstriction, and suggest that blockade of voltage-operated calcium channels can effectively counter the vasoconstrictor effects of endothelin-1.

Adult↗
PubMed1993

Biocompatibility of polyoxymethylene (Delrin) in bone.

The bone tissue reaction to bulk polyoxymethylene (Delrin) was studied in eight adult albino rabbits followed for up to 5 months after insertion of implants into the tibial metaphyses. Each animal received two implants, one of pure Delrin, the other a 'mosaic' plug with alternating areas of commercially pure titanium and Delrin. At the passage through the cortex, a direct bone-Delrin contact was seen in more than half of the cases, but the contact was usually limited in extent. At the same time, in virtually all sections, a foreign-body reaction with macrophages and giant cells was prominent. It was concluded that bulk Delrin has inferior biocompatibility to titanium, and the advisability of using Delrin as a biomaterial for bone anchorage is questionable.

Animals↗
PubMed1993

Effects of angiotensin converting enzyme inhibition on endothelial vasodilator function in primary human hypertension.

Hypertension in animal models and in humans is associated with a decreased vasodilator response to acetylcholine which causes vascular relaxation by release of endothelium-derived relaxing factor from the endothelium. Since lowering of blood pressure, particularly with angiotensin converting enzyme inhibitors, improved the response to acetylcholine we investigated the effects of brachial artery infusions of ascending dosages of acetylcholine on forearm blood flow before and after 5 months of therapy with the angiotensin converting enzyme inhibitor, cilazapril, in 10 patients with mild to moderate primary hypertension. Cilazapril decreased blood pressure from 150.8 +/- 14.4/98.9 +/- 4.3 mmHg during placebo to 138.8 +/- 15.6/88.6 +/- 8.9 mmHg (P < 0.01). Brachial artery acetylcholine infusions increased forearm blood flow from 2.95 +/- 1.5 to a maximum of 22.8 +/- 11.5 ml.min-1.100 ml-1 forearm tissue and decreased forearm vascular resistance from 48.1 +/- 34.1 to 6.9 +/- 6.9 units before cilazapril. This response did not change after cilazapril therapy. Our findings in patients with primary hypertension, therefore, do not support the concept that angiotensin converting enzyme inhibition influences endothelium-dependent vascular relaxation to acetylcholine to a significant degree. Whether this lack of effect on endothelial vasodilator function is specific for the vascular bed chosen for study or whether it represents a fundamental difference between animal models and human hypertension remains an important issue to be clarified.

Acetylcholine↗