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Biomedical subjects

L Linder

Publications and source records attributed to L Linder.

At least 55 records · Page 3Linked to original sources
PubMed1993

Impacted cancellous allografts and cement for revision total hip arthroplasty.

We report the results of using impacted cancellous allografts and cement for fixation of the femoral component when revision arthroplasty is required in the face of lost bone stock. In 56 hips reviewed after 18 to 49 months there were few complications and a majority of satisfactory results with evidence of incorporation of the graft. Further study and review are necessary, but the use of the method appears to be justified.

Aged↗
PubMed1993

Histology of cancellous impaction grafting in the femur. A case report.

We report the histology of a femur retrieved 3.5 years after a cemented revision of a hip replacement in which impaction allografting had been used to fill two large cortical defects. The allograft chips had largely been replaced by viable cortical bone, and the interface between cement and tissue resembled that seen after primary cemented arthroplasty.

Bone Regeneration↗
PubMed1992

Reversal of endothelin-1-induced vasoconstriction by nifedipine in human resistance vessels in vivo in healthy subjects.

The influence of blockade of voltage-operated calcium channels by nifedipine on endothelin-1-induced vasoconstriction was investigated in 10 healthy volunteers. Brachial artery infusions of nifedipine (0.25, 0.5, 1 and 3 micrograms/min/100 ml forearm tissue) resulted in dose-dependent increases (mean +/- SD) in forearm blood flow (103 +/- 63% to 833 +/- 426%). Intraarterial infusions of endothelin-1 (50 ng/min/100 ml) resulted in transient increases in forearm blood flow (2.6 +/- 0.9 vs 3.9 +/- 2.0 ml/min/100 ml, p less than 0.01) in the first minute of infusion and subsequent decreases (to 1.0 +/- .5 ml/min/100 ml, p less than 0.01) in the third minute of infusion. Endothelin-1-induced vasoconstriction was reversed by the lowest dose of nifedipine, whereas the higher dosages of nifedipine further increased forearm blood flow to 12.5 +/- 6.4 ml/min/100 ml. The percent increase of forearm blood flow during co-infusion of endothelin-1 and the highest dosage of nifedipine was significantly greater compared with nifedipine alone (1,204 +/- 531% vs 833 +/- 426%, p less than 0.05). The results demonstrate a dual action of luminally applied endothelin-1 in human resistance vessels in vivo (e.g., transient initial vasodilation followed by pronounced vasoconstriction) and suggest that blockade of voltage-operated calcium channels can effectively counteract the vasoconstrictor effects of endothelin-1.

Adult↗
PubMed1992

[Endothelin-induced vasoconstriction in man: variable modification caused by endothelium-derived relaxing factor, Sodium nitroprusside and calcium antagonists].

The vascular effects of endothelin-1 (ET) were investigated in 25 healthy volunteers by measuring changes of forearm blood flow in response to brachial artery ET infusions. ET in a low dose (0.5 ng/min/100 ml tissue) resulted in a small but significant increase of forearm blood flow (FBF) from 2.3 +/- 1.5 to 2.5 +/- 1.5 ml/min/100 ml (n = 25, p less than 0.05) while higher dosages (25 and 50 ng/min/100 ml) resulted in significant decreases of FBF to 1.78 +/- 1.3 and 1.1 +/- 0.9 ml/min/100 ml (p less than 0.01). Neither sodium nitroprussid (n = 6) nor acetylcholine (n = 7) prevented ET-induced vasoconstriction. In contrast, both verapamil (n = 6) and nifedipine (n = 6) not only prevented ET-induced vasoconstriction but resulted in additional vasodilatation to values above those seen with the calcium antagonists alone. Thus, in human resistance vessels ET has a dual action with vasodilation occurring at low dosages and vasoconstriction at high dosages. Blockade of voltage-operated calcium channels prevents ET-induced vasoconstriction and unmasks the vasodilatory effects of high ET-dosages. Blockade of voltage-operated calcium channels but not cyclic GMP dependent vasodilation appears to be an effective tool in preventing ET-induced vasoconstriction.

Acetylcholine↗
PubMed1992

Quantitative radioactive analysis of microleakage of four different retrograde fillings.

Sealing properties of four different retrograde filling materials were investigated in vitro. Radioactive isotopes were applied in the root canal, and leakage into an extraradicular fluid was measured at regular intervals. The method permitted repeated observation of the specimens over prolonged periods of time. Forty single-rooted human teeth were biomechanically instrumented and obturated using calcium-hydroxide paste. Following obturation, an apicectomy was performed and retrograde cavities were filled with four different materials: group 1, non gamma 2 amalgam (Amalcap); group 2, glass ionomer cement (Ketac Silver); group 3, calcium-hydroxide-based root canal sealer (Sealapex); group 4, composite resin (Palfique Light-S). After removal of the calcium hydroxide, the teeth were immersed in a fluid. An isotope solution was then placed in the root canals. Samples were taken from the fluid at 0, 3, 7, 28, 56, 105, 210, 285 and 376 days to determine the radioactivity. It was found that Sealapex and Palfique Light-S showed significantly less leakage than amalgam and glass ionomer cement, which had the highest apical leakage.

Analysis of Variance↗
PubMed1992

Actinobacillus actinomycetemcomitans, Capnocytophaga and Porphyromonas gingivalis in subgingival plaque of adolescents with Down's syndrome.

Levels of Actinobacillus actinomycetemcomitans, Capnocytophaga and Porphyromonas gingivalis were determined in subgingival plaque samples from 37 adolescents with Down's syndrome and 37 healthy controls matched with respect to age and sex. Gingival inflammation, supra- and subgingival calculus, periodontal pockets ( > 4 mm) and alveolar bone loss were registered. Alveolar bone loss was more frequent in Down's syndrome subjects (32%) than in the controls (3%). A. actinomycetemcomitans was detected in the subgingival plaque in 35% of the Down's syndrome adolescents and in 5% of the controls. On site level, A. actinomycetemcomitans and Capnocytophaga were more frequent in the subgingival plaque samples of Down's syndrome children than in those of controls. Comparing Down's syndrome subjects positive or negative for A. actinomycetemcomitans and Capnocytophaga, no significant differences were found in terms of gingival inflammation, periodontal pockets ( > 4 mm) or number of sites with alveolar bone loss. The results indicate an altered microbial composition of the subgingival plaque of Down's syndrome subjects compared with healthy controls, with higher frequency of A. actinomycetemcomitans.

Adolescent↗
PubMed1992

Blood pressure control by the renin-angiotensin system in normotensive subjects. Assessment by angiotensin converting enzyme and renin inhibition.

BACKGROUND: The participation of the renin-angiotensin system in the control of blood pressure in normal, sodium-replete subjects is not clear. The use of a specific inhibitor of human renin should allow a better delineation of the importance of this system. METHODS AND RESULTS: Blood pressure responses were measured 1 hour after randomized, double-blind administration of the renin inhibitor Ro 42-5892 (600 mg p.o.) or the angiotensin converting enzyme inhibitor captopril (50 mg p.o.) in 20 healthy men on an ad libitum sodium diet. Effective inhibition of the renin-angiotensin system by either compound was indicated by increases of immunoreactive renin associated with an increase of angiotensin I production rate of 67.8 +/- 33.6% after captopril and a decrease of 79.5 +/- 16.4% after Ro 42-5892. Furthermore, Ro 42-5892 decreased plasma renin activity by 64%. Whereas intra-arterial diastolic (60 +/- 5.1 to 51.4 +/- 7.2 mm Hg, p less than 0.01) and mean arterial (77.7 +/- 6.0 to 71.4 +/- 8.5 mm Hg, p less than 0.001) pressures decreased after captopril, they remained unchanged after Ro 42-5892. Captopril, but not Ro 42-5892, increased forearm blood flow (2.4 +/- 0.8 versus 1.9 +/- 0.8 ml/min/100 ml, p less than 0.01) and significantly enhanced the increase of forearm blood flow to brachial artery infusions of bradykinin (0.15, 1.5, 5, 15, and 50 ng/min/100 ml; 5 minutes each) from 744 +/- 632% to 1,383 +/- 514% (p less than 0.01). Furthermore, repeat bradykinin infusions resulted in further decreases of blood pressure (from mean pressure of 71.4 +/- 8.5 to 63.2 +/- 7.6 mm Hg, p less than 0.01) only after captopril. Changes of blood pressure after captopril were unrelated to baseline plasma renin activity but correlated with captopril-induced enhancement of vasodilation to bradykinin (r = 0.68, p less than 0.05). CONCLUSIONS: The lack of blood pressure effects of renin inhibition in contrast to angiotensin converting enzyme inhibition suggests that the renin-angiotensin system does not contribute significantly to blood pressure control in normotensive, sodium-replete subjects. The hypotensive activity of angiotensin converting enzyme inhibitors may result from additional hormonal effects, for example, inhibition of bradykinin degradation and/or subsequent increases of vasodilating prostaglandins or endothelium-derived relaxing factor(s).

Adult↗
PubMed1992

Endothelin-induced vasoconstriction and calcium antagonists.

Endothelial cells can produce contracting factors; endothelin, a 21-amino acid peptide, is one of the most potent of these factors, which can control local vascular tone. The peptide is formed from its precursor, big endothelin, via the activity of the endothelin converting enzyme. The basal production of the peptide is stimulated by epinephrine, angiotensin II, arginine vasopressin, transforming growth factor beta, thrombin, interleukin-1 and the calcium ionophore A23187. In vascular smooth muscle cells, endothelin binds to its specific receptor (ETA-receptor and possibly ETB-receptor) which activate phospholipase C and lead to the formation of inositol trisphosphate, diacylglycerol and increased intracellular calcium levels. In certain blood vessels, the endothelin receptor is linked to voltage-operated calcium channels via a Gi-protein. This linkage may explain why calcium antagonists inhibit endothelin-induced contractions in certain, but not other blood vessels. In large conduit arteries, such as the human internal mammary artery, endothelin-induced contractions are primarily mediated by release of intracellular calcium and hence, calcium antagonists do not markedly affect the response. In contrast, in the human forearm circulation, calcium antagonists of different classes do prevent endothelin-induced contractions. Similarly, in mesenteric resistance arteries of the rat, calcium antagonists can reverse endothelin-induced contraction suggesting that calcium antagonists are particularly potent in inhibiting endothelin-induced contraction in resistance arteries, where peripheral vascular resistance and hence, blood pressure is regulated.

Animals↗
PubMed1992

Ultrastructure of the bone-cement and the bone-metal interface.

A review is given of the methods used to demonstrate the bone-implant interface by transmission electron microscopy (TEM). Neither method is yet refined enough to permit demonstration without artifacts of the contact between implant, cells, and organic and inorganic matrix. Published studies on certain metallic implants and bone cement demonstrate a direct contact between bone matrix and implant, without a continuous interposed layer of cells. The 1000 nm closest to the implant surface show a variable structure, the interpretation of which is unknown. The degree of mineralization within this distance of the implant has not yet been adequately studied. Without completely reliable analytic methods and comparable implantation protocols, the gradation of implant biocompatibility, based on the TEM appearance of the interface, should be performed with great caution.

Animals↗
PubMed1991

Endothelin-1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor.

The vascular effects of endothelin-1 (ET) in humans were investigated by brachial artery infusions of ET into 25 healthy volunteers. Forearm blood flow increased from a mean +/- SD value of 2.3 +/- 1.5 to 2.5 +/- 1.5 ml/min/100 ml forearm tissue (n = 25, p less than 0.05) in response to low dose (0.5 ng/min/100 ml forearm tissue) ET infusion and decreased to 1.78 +/- 1.3 and 1.1 +/- 0.9 ml/min/100 ml forearm tissue (p less than 0.001) during higher dosages (25 and 50 ng/min/100 ml forearm tissue). Sodium nitroprusside (0.6 micrograms/min/100 ml forearm tissue, n = 6), acetylcholine (16 micrograms/min/100 ml forearm tissue, n = 7), nifedipine (6 micrograms/min/100 ml forearm tissue, n = 6), and verapamil (80 micrograms/min/100 ml forearm tissue, n = 6) were infused alone and in combination with ET to evaluate the interactions between ET-induced vasoconstriction and stimulation of vascular muscle cyclic GMP levels by sodium nitroprusside, release of endothelium-derived relaxing factor by acetylcholine, and blockade of voltage-operated calcium channels by nifedipine and verapamil. Neither the vasodilator nor the vasoconstrictor response to ET was influenced by sodium nitroprusside or acetylcholine. In contrast, both calcium antagonists converted ET-induced vasoconstriction (e.g., delta forearm vascular resistance to ET 50 ng/min/100 ml forearm tissue, 151 +/- 100% and 164 +/- 92% in verapamil and nifedipine groups, respectively) to vasodilation (-35 +/- 12% and -21 +/- 16%, p less than 0.05). Our results demonstrate both ET-induced vasodilation (at low dosages) and vasoconstriction (at high dosages) in resistance vessels of normal humans. Blockade of voltage-operated calcium channels prevented ET-induced vasoconstriction and unmasked the vasodilator effect of high ET dosages. In human resistance vessels, blockade of voltage-operated Ca2+ channels but not cyclic GMP-dependent vasodilation may be an effective tool to inhibit ET-induced vasoconstriction.

Adult↗
PubMed1990

Arterial vasodilator effects of the dihydropyridine calcium antagonist amlodipine alone and in combination with verapamil in systemic hypertension.

The arterial vasodilator properties of the dihydropyridine calcium antagonist amlodipine were compared with the effects of vascular muscle cyclic guanosine monophosphate production by sodium nitroprusside and with the effects of a combined infusion of amlodipine and the nondihydropyridine calcium antagonist verapamil in 8 untreated patients with primary hypertension. Arterial vasodilation was assessed by measurement of changes of forearm blood flow by mercury in Silastic strain-gauge plethysmography during brachial artery drug infusions. Forearm blood flow increased during amlodipine infusions (0.4 to 45 micrograms/min/100 ml forearm tissue) from 2.9 +/- 1.7 to a maximum of 23.6 +/- 7.6 ml/min/100 ml (687%), while sodium nitroprusside caused an increase from 3.0 +/- 1.8 to 16.2 +/- 5.4 ml/min/100 ml (449%), attesting to the importance of transmembrane calcium influx for the maintenance of vascular tone. The addition of verapamil 40 micrograms/min/100 ml to an infusion of amlodipine 44.5 micrograms/min/100 ml resulted in a further increase of forearm blood flow, from 23.6 +/- 7.6 to 34.4 +/- 9.8 ml/min/100 ml (p less than 0.05). The precise mechanisms of this finding have yet to be elucidated but may be due to interactions of the effects of the binding of these 2 chemically and pharmacologically different calcium antagonists to distinct binding sites at calcium channels. The clinical relevance of this observation for the treatment of coronary artery disease and systemic hypertension needs further study.

Amlodipine↗
PubMed1990

Indirect evidence for release of endothelium-derived relaxing factor in human forearm circulation in vivo. Blunted response in essential hypertension.

In isolated blood vessels, acetylcholine releases endothelium-derived relaxing factor (EDRF). In vivo, the vasodilator action of acetylcholine may be mediated by EDRF, but prostacyclin or prejunctional inhibition of adrenergic neurotransmission may also be involved. Therefore, we investigated whether acetylcholine releases EDRF in humans in vivo and, if so, whether the response altered in essential hypertension. Acetylcholine was infused into the brachial artery, and forearm blood flow measured by venous occlusion plethysmography. In control subjects, acetylcholine (0.02-16 micrograms/min/100 ml tissue) increased flow from 2.4 +/- 5.0 to 20.6 +/- 5.2 ml/min/100 ml tissue (n = 14; p less than 0.05) and decreased forearm vascular resistance from 42.0 +/- 4.1 to 6.0 +/- 1.4 units (p less than 0.03), a response comparable to that of sodium nitroprusside (0.6 micrograms/min ml tissue). Acetylsalicylic acid (500 mg i.v.) given to block vascular prostacyclin production did not alter the response (n = 14). alpha-Adrenoceptor blockade by phentolamine (12 micrograms/min/100 ml tissue) did not prevent the increase in flow evoked by acetylcholine. In hypertensive patients, the decrease in forearm vascular resistance induced by acetylcholine but not evoked by sodium nitroprusside was reduced as compared with controls (14.5 +/- 3.1 and 6.1 +/- 1.6 units, respectively; n = 8; p less than 0.05). Thus, the vascular effects of acetylcholine in the human forearm circulation are independent of prostaglandins and adrenergic neurotransmission and therefore are most likely to be mediated by EDRF; the acetylcholine-induced release of EDRF is blunted in patients with essential hypertension.

Acetylcholine↗
PubMed1990

Arterial vasodilator and antihypertensive effects of diltiazem.

The arterial vasodilator properties of the calcium antagonist diltiazem were investigated by measurement of changes of forearm blood flow during brachial artery infusions of eight dosages of diltiazem in eight hypertensive patients. Forearm blood flow increased and calculated forearm vascular resistance decreased dose-dependently (maximum decrease of 83.5 +/- 8.6%). When comparing the effects of calcium influx inhibition by diltiazem with stimulation of the vascular cyclic guanosine monophosphate (GMP) system by sodium nitroprusside, the vasodilation by diltiazem was approximately 1.6 times greater, attesting to its potent arterial vasodilator activity. The clinical efficacy and feasibility of diltiazem monotherapy was evaluated in 40 patients with mild to moderate essential hypertension treated with a slow-release formulation of diltiazem, 90 mg twice daily over 8 weeks, and in a subgroup of 21 patients with two tablets of 90 mg once daily in the morning over a period of 2 weeks. Blood pressure was lowered significantly and to a similar extent by either twice- or once-daily administration of diltiazem. This effect was maintained during open long-term therapy over a mean of 11 months. Heart rate and body weight did not change. Thus, the vasodilator properties of diltiazem can be utilized for effective long-term treatment of hypertension. The possibility of once-daily dosing may prove useful with respect to drug compliance in the long-term treatment of a generally asymptomatic disease such as hypertension.

Adult↗
PubMed1989

On the correlation between micromotion and histology of the bone-cement interface. Report of three cases of knee arthroplasty followed by roentgen stereophotogrammetric analysis.

The bone-cement interface from the tibial components in three clinically successful unicompartmental Marmor arthroplasties was studied histologically. The migratory behavior of the prostheses had been followed by roentgen stereophotogrammetic analysis (RSA) since their insertion 5-7 years prior to retrieval for reasons other than mechanical loosening. The prostheses migrated during the first 3 years, after which no further migration occurred. Clinical and RSA data thus suggest stable fixation. All interfaces were made up entirely of soft tissue. In the sagittal portion, between the prosthesis and the tibial eminence there was mostly fibrous tissue, while the region underneath the prostheses consisted largely of highly differentiated fibrocartilage. This histologic picture is compatible with a migratory pattern, as measured by RSA, of stable fixation after an initial remodelling period, which the authors believe has the potential of good long-term results.

Aged↗
PubMed1989

Experimental and clinical experience with the calcium antagonist diltiazem in hypertension.

The arterial vasodilator properties of the calcium antagonist diltiazem were investigated by measurement of changes in forearm blood flow during brachial artery infusions of eight dosages of diltiazem in eight patients with mild to moderate hypertension. Forearm blood flow increased and calculated forearm vascular resistance decreased dose dependently. Comparison with the vascular effects of verapamil did not show any difference between the two drugs, attesting to their powerful vasodilator action. The clinical efficacy and feasibility of diltiazem monotherapy was evaluated in 40 patients with mild to moderate essential hypertension who were treated with a retarded formulation of 90 mg of diltiazem twice daily over 8 weeks. A subgroup of 21 patients were treated with two tablets of 90 mg of diltiazem once daily in the morning over 2 weeks. Blood pressure was lowered significantly as a result of either mode of diltiazem administration. This effect was maintained during open long-term therapy over a mean of 11 months. Heart rate and body weight did not change. Thus, the vasodilator properties of diltiazem can be utilized for effective long-term treatment of hypertension. The possibility of once-daily administration may prove useful for long-term treatment of a generally asymptomatic disease such as hypertension.

Diltiazem↗
PubMed1989

Microvascular response to locally injected collagenase. An experimental investigation in hamsters and rabbits.

Collagenase was injected into the ears of rabbits and the cheek-pouches of hamsters. The acute and long-term microvascular effects were studied by vital microscopy and microangiography. The enzyme was injected at three different concentrations: 120 units/ml, 600 units/ml and 3,000 units/ml. The medium (600 units/ml) and high (3,000 units/ml) concentrations induced effects on the microcirculation such as blood flow impairment and microbleedings. The magnitude of these effects was related to the concentration of the enzyme. Generally, these microvascular effects were of low magnitude as compared with other substances tested using the same experimental models.

Animals↗
PubMed1989

Osseointegration of metallic implants. I. Light microscopy in the rabbit.

Thirty-eight adult albino rabbits received one implant of pure titanium and one implant of another, test, material in each tibia. The test materials were titanium-aluminum-vanadium alloy, chrome-cobalt alloy, and stainless steel. Observation times were 4 months and 11 months. Light microscopy of the interface revealed a direct contact between bone and implant surface (osseointegration) in 73 of the 76 cases. The exceptions were two implants of pure titanium and one of stainless steel. Thus, given identical healing conditions, the modern implant metals were accepted by the bone in the same way. It is suggested that osseointegration should be regarded not as an exclusive reaction to a specific implant material, but as the expression of a nonspecific and basic healing potential in bone.

Alloys↗