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Biomedical subjects

M Olausson

Publications and source records attributed to M Olausson.

At least 127 records · Page 7Linked to original sources
PubMed1991

Metabolic risk factors for cardiovascular disease in pancreas and kidney transplant recipients.

Hyperinsulinaemia when combined with insulin resistance and hypertriglyceridaemia is a risk factor for cardiovascular disease. We have studied the serum lipid profile and glycaemic control in 27 uraemic diabetic patients, 23 Type 1 (insulin-dependent) diabetic kidney recipients, 18 non-diabetic kidney recipients, and 30 recipients of kidney and pancreas transplants at 6 months post-transplantation. Fasting serum triglycerides were increased in the uraemic diabetic patients and nondiabetic kidney transplanted patients but not in diabetic kidney transplanted patients whether or not they had received a pancreas. Total cholesterol was increased only in the uraemic diabetic patients while HDL cholesterol was normal in all groups. Within the pancreas and kidney transplanted group triglyceride values correlated with glomerular filtration rate (r = -0.55) but not with plasma insulin, glycated haemoglobin or kG-value following an intravenous glucose load. Plasma insulin was increased. Whether such isolated hyperinsulinaemia confers an increased risk of cardiovascular disease is not known. There may be adaptive feed-back mechanisms to protect target cells. Increasing the surgical risk in attempts to secure insulin delivery to the portal circulation does not seem warranted.

Adult↗
PubMed1991

Echocardiographic findings in kidney transplanted type 1 (insulin-dependent) diabetic patients with and without a pancreas transplant.

Echocardiography with Doppler recordings was carried out in 14 Type 1 (insulin-dependent) diabetic recipients of pancreas and kidney transplants and in 14 Type 1 diabetic kidney transplanted control patients, matched for age, sex, duration of diabetes, extent of other late complications, time since transplantation, dose of prednisolone, and renal function. HbA1c was 5.5 +/- 0.6 vs 8.7 +/- 1.4% (pancreas transplanted vs kidney only). Both groups had a slight increase in interventricular septum thickness. Left ventricular mass was equal. The ejection fraction as a measure of systolic function was normal and equal, 0.71 +/- 0.05 vs 0.69 +/- 0.07. Diastolic function was also equal in two out of three parameters, isovolumic relaxation time and deceleration time. The A/E ratio, however, tended to be lower in the pancreas transplanted group, 0.94 +/- 0.20 vs 1.06 +/- 0.18 (p = 0.04). This indicates more frequent occurrence of impaired diastolic filling in the recipients of kidney only. Follow-up will show whether diastolic dysfunction increases and may be related to the increased cardiovascular mortality in kidney transplanted Type 1 diabetic patients.

Adult↗
PubMed1990

Blood lymphocyte subsets in ATG-treated and allografted rats.

A single dose of rabbit antithymocyte globulin (ATG) was given as the sole immunosuppressive therapy in a model of strong MHC barrier rat heart allotransplantation. PVG/c hearts transplanted to Wistar/Kyoto (WKy) rats resulted in long-term surviving (LTS) grafts and cell-mediated lympholysis (CML) unresponsiveness in 50% of the animals. The effects of ATG treatment on the peripheral blood lymphocyte subsets were studied by flow cytometry. The absolute T-lymphocyte levels decreased to less than 5% and were normalized after 2 weeks. CD8-positive cells were normalized within 1 week, whereas CD4- and CD5-positive cells remained low. Rats with LTS grafts had low levels of all T-lymphocyte markers, especially the CD4- and CD5-positive cells. Rats rejecting their grafts showed an eightfold increase in levels of CD8- and CD5-positive lymphocytes and a twofold increase in levels of CD4-expressing lymphocytes. It is concluded that ATG treatment causes the immediate elimination of large lymphoid populations as well as long-lasting immunomodulation detectable in peripheral blood.

Animals↗
PubMed1990

24-hour intragastric acidity and plasma gastrin after omeprazole treatment and after proximal gastric vagotomy in duodenal ulcer patients.

The relationship between suppressed gastric acidity and the increase in plasma gastrin levels after pharmacological and surgical treatment of peptic ulcer disease were compared in this study. Eight patients with chronic duodenal ulcer and referred for proximal gastric vagotomy were studied. 24-hour intragastric acidity and plasma gastrin levels were investigated in the same patients on three consecutive occasions: preentry without any treatment; after 4 weeks of administration of 20 mg of omeprazole daily, and 4-6 months after proximal gastric vagotomy. Intragastric acidity was slightly more reduced by omeprazole (94%) than after proximal gastric vagotomy (78%), with no difference found during the day or night with either. Plasma gastrin levels increased slightly more after proximal gastric vagotomy [284% (median, 2120 pmol.h/L; range, 733-2831 pmol.h/L)] than after omeprazole administration [186% (median, 1586 pmol.h/L; range, 495-2573 pmol.h/L)]. There is strong evidence that the increased plasma gastrin concentration following omeprazole treatment is caused by the reduced intragastric acidity. The slight increase in plasma gastrin concentration following proximal gastric vagotomy despite a lesser reduction in intragastric acidity may be the result of additional effects on gastrin release by the vagotomy. Both treatments resulted in a modest increase in plasma levels of gastrin that were far below the gastrin levels observed in achlorhydric patients, e.g., patients with pernicious anemia.

Adult↗
PubMed1990

Transplantation in patients with diabetic nephropathy. Outcome of combined pancreas and kidney transplantation compared with kidney transplantation only.

Detailed results of 12 combined pancreas and kidney transplantations (Comb) were compared with those of two matched diabetic controls per patient--one living donor kidney recipient (LD) and one cadaveric donor kidney recipient (CD--who, though eligible for pancreas transplantation also, preferred kidney transplantation only. Mean follow-up was 22, 23, and 21 months in the three groups. There was no mortality in the LD group, but two CD and one Comb patient died from cardiovascular disease. Two kidneys were lost in both the Comb and the LD group, compared to five in the CD group. Ten major vascular events occurred and three of them were lethal. The only LD case was one below-knee amputation; the other nine were equally distributed in the Comb and CD groups. The time spent in the hospital was shorter for the LD group. Thus, in the short run, LDs confer the best results, whereas in the long term the better metabolic control in the Combs may prove favorable.

Adult↗
PubMed1989

Effect of omeprazole on gastric acid secretion and plasma gastrin in man.

Single doses of omeprazole inhibit pentagastrin-stimulated gastric acid secretion and almost complete inhibition can be achieved for 4-6 hours with a single dose of 80 mg. Acid secretion then slowly returns and reaches normal levels after 3-4 days. Omeprazole also dose-dependently inhibits basal acid secretion as well as acid secretion stimulated with histamine, peptone and modified sham feeding, with similar efficiency. During repeated once-daily dosing with an enteric-coated granule capsule formulation, inhibition of acid secretion increased initially, and stabilized within about 4 days. Dose-response studies in patients with duodenal ulcers and healthy subjects have shown that 20-40 mg/day results in a peak reduction (80-100%) of pentagastrin-stimulated acid secretion 6 hours after dose. Studies of 24-hour intragastric acidity in duodenal ulcer patients have shown that 4 weeks of treatment with omeprazole, 20 mg once daily, resulted in a reduction of median intragastric acidity by 97%, which was superior to the 57% median reduction achieved with ranitidine, 150 mg b.d., for 4 weeks in the same patients. During omeprazole treatment, fasting plasma gastrin increased in relation to the degree of inhibition of acid secretion. After discontinuation of treatment, plasma gastrin normalized. Treatment with omeprazole, 20 mg, increased 24-hour plasma gastrin to the same extent as after highly selective vagotomy. Long-term treatment with omeprazole, 20-40 mg, for up to 2 years has not been associated with any progressive rise in fasting plasma gastrin.

Dose-Response Relationship, Drug↗
PubMed1989

Effect of omeprazole on gastric acid secretion and plasma gastrin.

Omeprazole represents a new class of gastric acid inhibitors, which inhibits the H+, K(+)-ATPase in the secretory membrane of the parietal cell. Single oral doses inhibited pentagastrin stimulated acid secretion with an ED50 of 27 mg. Almost complete inhibition could be achieved with a single dose of 80 mg. Acid secretion then slowly returned and reached normal levels after 3-4 days. Omeprazole also inhibited basal, histamine peptone and vagally stimulated acid secretion with similar potency. For clinical use omeprazole has been formulated as enteric coated granules. During repeated once daily dosing with this formulation the degree of acid suppression increased over the first days after the start of treatment but stabilized within about 4 days. Dose-response studies in both DU-patients and healthy subjects have shown that daily doses of 20-40 mg result in 80-100% reduction of stimulated acid secretion when measured 6 h after dose. Due to the long duration of action the inhibition was still 50-80% when measured 24 h after dose. Studies of 24 h intragastric acidity in DU-patients have shown that once daily treatment with 20 mg omeprazole results in a reduction of intragastric acidity by 97% which in the same study was superior to the 57% reduction caused by treatment with ranitidine, 150 mg twice daily. During omeprazole treatment, plasma gastrin increased in relation to the degree of acid suppression. The level of increase of 24 h plasma gastrin during once daily treatment with 20 mg omeprazole was slightly higher than for ranitidine, 150 mg twice daily, but similar to that seen after highly selective vagotomy.

Dose-Response Relationship, Drug↗
PubMed1988

Morphology of rat cardiac allografts with permanent survival induced by antithymocyte globulin.

In a rat heart transplantation model, permanent graft survival was achieved by anti-thymocyte globulin (ATG) treatment of Wistar Kyoto (WKy) recipients before grafting with PVG/c hearts. Nine hearts with palpable and electrocardiographic (ECG) function 8-20 months after transplantation were studied with histological and immunohistochemical methods. The dominating findings were fibrosis, intimal thickening, thrombosis of vessels, cellular infiltrates, and a high number of cells expressing class II antigens. These findings suggest that reactions compatible with a chronic rejection can be found in long-term surviving rat heart allografts. This rat model may thus be used in further studies of a chronic rejection process.

Animals↗
PubMed1988

Characteristics of the induction phase of antithymocyte-globulin-induced heart allograft tolerance in the rat.

Transplantation tolerance was induced in 50% of Wky rats treated with antithymocyte globulin (ATG) 2 days prior to transplantation of a PVG/c heart. The induction period immediately following ATG treatment and transplantation was characterized by instability, with 50% of the allografts being lost in rejection within 30 days after transplantation. Second syngeneic transplantation to ATG-treated recipients 5 days after the first transplantation facilitated tolerance induction and permanent acceptance of both transplants. Thirty days after ATG treatment and the primary transplantation, 50% of second syngeneic allografts were accepted. During the early period after transplantation a continuous antigen presence together with ATG was necessary. Graft removal and absence of the transplant for 3 days, close to ATG administration, resulted in rejection of a second PVG/c transplant. Furthermore, the induction phase could easily be manipulated by the addition of sensitized or tolerized spleen cells to the recipient, causing allograft rejection or tolerance, respectively. Sixty days after ATG treatment and transplantation, a longer period between graft removal and retransplantation was required to break tolerance. Injection of sensitized spleen cells at this time did not affect graft survival, indicating an increased stability of the unresponsive state 60 days after ATG treatment and transplantation.

Animals↗
PubMed1988

Relationship between reduction of gastric acid secretion and plasma gastrin concentration during omeprazole treatment.

We have studied the relationship between reduction of gastric acid secretion and fasting plasma gastrin concentrations during once daily omeprazole treatment. Healthy subjects were given omeprazole for 5 days in daily doses of 5, 10, 20, 40, or 80 mg. Acid secretion and fasting gastrin concentration were measured 6 h (maximal omeprazole effect) and 24 h (minimal omeprazole effect) after the fifth omeprazole dose. Omeprazole in doses lower than 20 mg daily did not suppress pentagastrin-stimulated acid secretion in all subjects 6 h after dosing on the 5th day. Doses of 20-80 mg omeprazole, however, significantly reduced acid secretion 24 h after the fifth dose, the range being 36-76%. A relationship between degree of acid inhibition and fasting gastrin concentration was observed. However, acid secretion needed to be reduced by more than 80% before gastrin levels were clearly affected. This degree of acid inhibition was only achieved 6 h after administration of omeprazole in doses of 20 mg and higher. The inhibitory effect of omeprazole on acid secretion decreased 24 h after dosing. Thus, fasting gastrin concentrations were moderately increased in the beginning and normalized at the end of each 24-h period during treatment with daily doses of 20-80 mg omeprazole.

Adult↗
PubMed1987

Evidence of donor-specific cellular suppressor activity in donor-specific cell-mediated lympholysis unresponsiveness in renal transplant patients.

Twenty patients with well-functioning kidney grafts from one-haplotype-mismatched related donors, were studied 1-10 years after transplantation (A). Another group of six patients were studied at various times after transplantation (B). The presence of donor-specific transplantation tolerance, using mixed lymphocyte culture (MLC) and cell-mediated lympholysis (CML) tests was investigated, as well as the possible existence of cells with suppressive activity. All recipients were transfused prior to transplantation and treated with conventional immunosuppression. The patients in group A showed MLC reactivity against donor and third-party cells, indicating a allogeneic response capacity. The CML activity against the donor was low, however, and remained low also following removal of adherent cells. The CML activity toward third-party cells was within the normal range of unmatched individuals. In group B, two of six recipients and high postoperative CML activity against the donor. Both recipients showed clinical signs of rejection. In the remaining four recipients, the antidonor CML reactivity one week after transplantation was lower than the preoperative level. The decrease was even more pronounced at 12 months, although the reactivity against third-party cells was unaltered. The CML reactivity from unrelated fourth-party individuals toward donors was suppressed when cells from recipients with long-term functioning kidneys were added to the cell cultures. The results suggest the presence of a donor-specific cellular suppressor mechanism underlying the donor-specific CML unresponsiveness in recipients with long-term-functioning kidney allografts.

Adolescent↗
PubMed1987

Mechanisms maintaining transplantation tolerance in antithymocyte globulin-treated rats.

A model for induction of permanent PVG/c heart allograft survival in adult WKy rats, following antithymocyte globulin (ATG) treatment, was studied. Attempts to induce acute rejection of permanently accepted grafts, by injection of presensitized spleen cells, were successful only if the tolerant recipients had been pretreated with cyclophosphamide. Tolerance against second allografts from the primary donor strain could not be abrogated by injection of presensitized cells shortly after grafting. After removal of the permanently accepted graft, the tolerant recipients regained their capacity for acute rejection within 100 days. Tolerance was adoptively transferred with spleen cells, obtained from tolerant rats, to syngeneic sublethally irradiated recipients. The transferred unresponsiveness was donor-specific, antigen-dependent, and could again be transferred to irradiated recipients. The transferred suppression was abolished by the addition of presensitized, but not by naive, syngeneic spleen cells. The results indicate that donor-specific, antigen-dependent suppressor cells are essential for the maintenance of ATG-induced allograft acceptance. The suppression may influence the generation and activation, as well as the function, of alloreactive cells.

Animals↗
PubMed1987

Twenty-four-hour intragastric acidity and plasma gastrin concentration in healthy subjects and patients with duodenal or gastric ulcer, or pernicious anaemia.

Twenty-four-hour intragastric acidity and plasma gastrin concentration were measured in healthy subjects (n = 16), and patients with duodenal (n = 12) or gastric (n = 10) ulceration, or pernicious anaemia (n = 8). Median integrated 24-hour intragastric acidity was highest in duodenal ulcer patients and lowest in pernicious anaemia patients (1148 and 0 mmol.hour litre-1, respectively). Median integrated 24-hour plasma gastrin was highest in pernicious anaemia and lowest in the healthy subjects (9886 and 238 pmol.hour litre-1, respectively). Pernicious anaemia patients have unremitting hypergastrinaemia throughout the 24 hours. The results of this study not only provide a reference range of acidity and plasma gastrin in health and disease, but also will act as a baseline for future studies using antisecretory drugs.

Adult↗
PubMed1987

Twenty-four-hour intragastric acidity and plasma gastrin concentration before and during treatment with either ranitidine or omeprazole.

Simultaneous 24-hour intragastric acidity and plasma gastrin concentrations were measured in 12 duodenal ulcer patients before and on the twenty-eighth day of treatment with either ranitidine 150 mg b.d. or omeprazole 20 mg o.m. Median integrated 24-hour intragastric acidity was decreased significantly from 1148 to 490 and 36 mmol.hour litre-1 during treatment with ranitidine and omeprazole, respectively, whilst median intragastric 24-hour plasma gastrin was raised significantly from 328 to 799 and 1519 pmol.hour litre-1 respectively. When the results of all 48 experiments were considered together, there was a significant inverse correlation between the 24-hour integrated values for intragastric acidity and plasma gastrin concentration. Both drugs caused a significant elevation of plasma gastrin throughout the 24 hours, although ranitidine had no effect on intragastric acidity from 1900 to 2200 hours. When compared with similar profiles of acidity and gastrin in pernicious-anaemia patients, the modest elevations of plasma gastrin observed in this study suggest that neither drug will be associated with clinically relevant enterochromaffin-like cell proliferation in duodenal ulcer patients.

Adult↗