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Biomedical subjects

G Thorgeirsson

Publications and source records attributed to G Thorgeirsson.

52 records · Page 3Linked to original sources
PubMed1989

Desensitization of inositol phosphate production after agonist stimulation of endothelial cells is not mediated by protein kinase C.

To investigate the possible role of protein kinase C activation in the desensitization of inositol phosphate production in endothelial cells we compared desensitization induced by agonists to that induced by the phorbol ester TPA. While histamine or thrombin induced desensitization of inositol phosphate production is homologous TPA induced desensitization is heterologous. The protein kinase C inhibitor H-7 reduced TPA desensitization but had no effect on the agonist induced desensitization. While downregulation of protein kinase C by long term (24 hr) treatment of the cells with TPA reduced the desensitization mediated by short term TPA-treatment it did not affect the agonist induced desensitization. These results suggest that desensitization of inositol phosphate production after agonist stimulation of endothelial cells is not mediated by protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Additive effects of moderate dietary salt reduction and captopril in hypertension.

In a randomized, cross-over study 27 patients had diastolic blood pressure of greater than or equal to 96 mmHg during four visits without treatment. Following captopril 25 mg b.i.d. nine patients' blood pressure was less than or equal to 90 mmHg. The remaining 18 were randomized into two treatment modalities, captopril and moderate dietary salt reduction, and captopril and hydrochlorothiazide 25 mg daily. Following a wash-out period the groups crossed over to the alternative treatment. At the end of the control period the average blood pressure was 151/100 +/- 12/6 mmHg recumbent and 140/91 +/- 11/7 standing, following captopril 144/94 +/- 13/5 and 132/92 +/- 12/6, respectively, with low salt diet added to captopril 140/91 +/- 12/6 and 128/89 +/- 11/6 and with hydrochlorothiazide and captopril 133/86 +/- 12/7 and 120/84 +/- 11/7 mmHg supine and erect, respectively. It is concluded that moderate dietary salt reduction, which is easily advised, will significantly potentiate the blood pressure fall following captopril treatment in moderate arterial hypertension.

Adult↗
PubMed1987

Chronic atrial fibrillation--epidemiologic features and 14 year follow-up: a case control study.

In a randomly selected population of 9067 individuals, 32-64 years of age in 1967-1970, 25 (0.28%) had chronic atrial fibrillation (CAF). Eight had lone atrial fibrillation. In 1984 the cases were compared with an age- and sex-matched control group of 50 and found to have more cerebrovascular accidents (6 versus 2; P less than 0.05), congestive heart failure (9 versus 1; P less than 0.001), and valvular rheumatic heart disease (3 versus 0) or history consistent with rheumatic fever (6 versus 0; P less than 0.01). The mortality in the CAF group was 60% higher due to an excess in cardiovascular (relative risk 6.1; P less than 0.05) and cerebrovascular (relative risk 12.2; P less than 0.05) causes. The prevalence or incidence of ischaemic or hypertensive heart disease or the presence of coronary risk factors did not significantly differ in the two groups. By M-mode echocardiography the left atrial size, left ventricular enddiastolic dimension and left ventricular mass were increased in the CAF patients, while the systolic left ventricular shortening was significantly less. Thus, the prevalence of CAF is low in a randomly selected population 32-64 years of age and CAF is not strongly associated with ischaemic heart disease or hypertension. The CAF patients have an increased risk of dying prematurely particularly from cerebrovascular causes, even in the absence of valve disease.

Adult↗
PubMed1985

Acute thoracic inlet obstruction in achalasia with adenoid cystic and squamous cell carcinoma.

Respiratory symptoms due to compression of the trachea by the dilated esophagus in achalasia are extremely rare. A patient is presented whose respiratory manifestations included engorged neck veins and a neck swelling that fluctuated with respiration. He also had two malignant tumors in his dilated esophagus, a squamous cell carcinoma and an adenoid cystic carcinoma.

Acute Disease↗
PubMed1984

Diltiazem-like effect of thioridazine on the dihydropyridine binding site of the calcium channel of rat myocardial membranes.

The phenothiazine thioridazine enhances the binding of [3H]-nitrendipine to cardiac membranes and antagonizes the inhibition of [3H]-nitrendipine binding by other classes of calcium channel blockers. These effects are similar to those of diltiazem. The increased binding of [3H]-nitrendipine in the presence of thioridazine or diltiazem is due to increased binding affinity rather than an increased number of binding sites. Increased affinity is due in part to a decrease in the dissociation rate of nitrendipine in the presence of either thioridazine or diltiazem. Thioridazine also reverses the blocking effect of tiapamil (a phenylalkylamine) on [3H]-nitrendipine binding to rat heart membranes, as does diltiazem, suggesting that thioridazine binds to the same site as diltiazem. Thioridazine may have calcium channel blocking effects in the high therapeutic and toxic dose ranges that could be responsible for some of its adverse cardiovascular effects.

Animals↗
PubMed1979

Migration of human vascular endothelial and smooth muscle cells.

Migration of endothelial and smooth muscle cells was studied in vitro by measuring the increase in surface area at specific time intervals of confluent cell colonies advancing under agarose gels that contained both Morgan's medium 199 and variuos types of sera. First passage cultures of endothelial cells or 3 to 6 passage smooth muscle cells were plated into wells punched in agarose gels, at a seeding density of 50,000 cells per well. At zero time the size of the cell colonies was 35.4 sq. mm. +/- standard error 0.1. Irradiation (1500 rads) did not affect the expansion of the cell colonies although 3H-thymidine uptake was inhibited. Endothelial cells migrated under the agarose gels concentrically as contiguous sheets. When exposed to either 20 per cent platelet-poor plasma serum, platelet-rich plasma serum, or whole blood serum, the average increase in surface area was approximately 9 sq. mm. per day. In contrast, arterial smooth muscle cell colonies expanded with an increment of approximately 9 sq. mm. per day when exposed to 10 per cent platelet-poor plasma serum but 12 sq. mm. per day when exposed to 10 per cent platelet-rich plasma serum (p less than 0.001). Platelet factors also had stimulatory effects on the migration of venous smooth muscle cells. Cytochalasin B, dibutyryl cyclic AMP, and theophylline inhibited the migration of both endothelial and smooth muscle cells, but the latter responded more to the inhibitory effects of all three agents. It is concluded that in contrast to vascular smooth muscle, endothelial cells do not require platelet factors for migration and are less responsive to specific inhibitors affecting cell movement.

Blood Platelets↗
PubMed1978

Platelet factors and the human vascular wall: variations in growth response between endothelial and medial smooth muscle cells.

In the present investigations, the effects of platelet factors on DNA-synthesis by human arterial and venous smooth muscle and venous endothelial cells were compared. Also studied was the role of such factors in restimulating quiescent endothelial cultures and in endothelial reaction to injury. Aortic smooth muscle cells grown in medium containing 10% human serum prepared from plasma poor in platelets (PPPS) reached 9.7%+/-SE 0.65 labelling index when continuously exposed to [3H] thymidine (1 muCi/ml). When lysate from gel-filtered platelets was added, the index was 19.4% +/- SE 1.13 (P less than 0.01) and in the presence of serum derived from platelet rich plasma (PRPS) it reached 24.6% +/- SE 1.22 (P less than 0.01). Similar results were obtained with smooth muscle cells from umbilical veins. In constrast, platelet factors did not significantly affect DNA-synthesis in endothelial cultures. They reached 25.6% +/- SE 1.97 when grown in medium containing PPPS as compared to 21.9% +/- Se 2.53 (P greater than 0.05), when exposed to PRPS. The ability of sera to stimulate DNA-synthesis in endothelial cultures rendered quiescent by 24 h exposure to medium containing 1.4% serum albumin (labelling index 1.83% +/- SE 0.14) was not affected by platelet factors. Platelet lysates alone were not sufficient to restimulate the quiescent cells (labelling index 3.03% +/- SE 1.06) (P greater than 0.05). Platelet factors did not affect the proliferative response following experimental mechanical injury to endothelial monolayers in vitro. We conclude that while platelet factors are essential for human vascular smooth muscle cells to achieve optimal growth, they are not indispensable for endothelial cell proliferation. It is suggested that these cellular differences in growth requirements may play an important role in human atherogenesis.

Aorta↗
PubMed1978

Platelet factors and the human vascular wall. Part 2. Such factors are not required for endothelial cell proliferation and migration.

The effects of platelet factors on human umbilical venous endothelial cell DNA-synthesis at various serum concentrations were studied. While [3H]thymidine uptake of these cells was almost linearly related to the concentration of serum in the culture medium, no significant differences were found at any serum level between cultures treated with sera derived from either platelet-rich or platelet-poor plasma. The role of platelet factors in cellular migration into standardized mechanical "wounds" was also investigated following inhibition of the proliferative response by irradiation of endothelial monolayers. Repopulation of such "wounds" was not affected by platelet factors. We conclude that endothelial cells proliferate and migrate in vitro independently of platelet factors.

Blood Coagulation Factors↗
PubMedDate not supplied

Mesothelioma of the AV node.

A 21-month-old boy died suddenly six months after presenting with heart murmur and second-degree atrioventricular (AV) block. Autopsy revealed a mesothelioma completely replacing the AV node and extending into the central fibrous body. The bundle of His and bundle branches were not involved. Mesothelioma of the AV node is a rare cause of supra-His (AV) block, arrhythmias, and sudden death.

Atrioventricular Node↗
PubMedDate not supplied

An association between chronic eosinophilic pneumonia and histiocytic lymphoma.

An association between chronic eosinophilic pneumonia and non-Hodgkin's lymphoma previously has not been reported in adults. We describe a woman with chronic eosinophilic pneumonia documented by chest roentgenogram, elevated total eosinophil count, and transbronchial biopsy demonstrating eosinophilic pneumonitis. The illness was controlled with corticosteroids for ten months after which time lymphadenopathy appeared and diffuse, histiocytic lymphoma was diagnosed.

Chronic Disease↗
PubMedDate not supplied

Aortic stiffness in insulin-dependent diabetics: an echocardiographic study.

To assess the aortic stiffness (AS) in young (15-35 year old) insulin-dependent diabetics without manifestations of atherosclerotic disease or hypertension, M-mode echocardiography was used to measure relative changes in aortic diameter expressed as Aortic strain = Diameter change/Diastolic diameter-100% Aortic stiffness can be calculated from the formula AS = Pulse pressure/Aortic strain. Fifty-seven diabetics were investigated, 31 men (aged 23.6 +/- 5.6 years, mean +/- SD) and 26 women (aged 25.7 +/- 6.4 years). There were 26 healthy controls with similar blood pressure, 14 men (aged 25.0 +/- 5.5 years) and 12 women (aged 24.6 +/- 7.1). The AS in diabetic men was 14 +/- 8.0 (mean +/- SD) compared to 3.6 +/- 0.7 in controls (p less than 0.001). In diabetic women the AS was 5.8 +/- 3.1 compared to 4.3 +/- 1.3 in controls (p less than 0.05). Diabetic men also had much stiffer aortas than diabetic women (p less than 0.001). There was a linear correlation between AS and duration of diabetes in men (R = 0.70; (p less than 0.001). For females no such correlation was found, the AS frequently being within the range of the controls in spite of long duration of the disease. In males there was a significant correlation between AS and retinopathy (R = 0.49; p less than 0.01) and an inverse correlation with HDL-cholesterol/total cholesterol ratio (R = 0.51; p less than 0.01). In diabetic females AS was significantly greater in smokers (7.0 +/- 3.7) than in non-smokers (4.2 +/- 2.2; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Role of phosphoinositides in the regulation of endothelial prostacyclin production.

To elucidate the role of the phosphoinositide signal transduction system in endothelial endothelial prostacyclin production, endothelial cells from human umbilical veins previously labelled with 3H-inositol were incubated with thrombin or histamine. Water-soluble inositol phosphates were separated on anion exchange columns. Both agonists evoked transient bursts of inositol phosphate production with inositol trisphosphate peaking at 15 seconds in histamine-stimulated cells and at 60 seconds in thrombin-stimulated cells. The inositol phosphate production was closely linked to prostacyclin production. After stimulation, there was concurrent desensitization to prostacyclin production and formation of inositol phosphates. Arachidonic acid and the Ca2+-ionophore A23187 did not affect inositol phosphate production in concentrations sufficient to increase prostacyclin production 20-fold, and they did not affect desensitization to a subsequent thrombin stimulation. The phorbol ester 12-o-tetradecanoyl phorbol 13-acetate, a stimulator of protein kinase C, inhibited thrombin-induced generation of inositol phosphates, enhanced A23187-mediated prostacyclin production, and had complex effects on thrombin-mediated prostacyclin production, but had no effect on its production from extrinsic arachidonic acid. The current data suggest that production of inositol phosphates is a link in receptor stimulation of endothelial cells to produce prostacyclin and that associated activation of protein kinase C affects both the generation of second messengers and the release of arachidonic acid.

Arachidonic Acid↗