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Biomedical subjects

M L Foegh

Publications and source records attributed to M L Foegh.

At least 91 records · Page 5Linked to original sources
PubMed1988

Effects of CGS-13080, a thromboxane inhibitor, on pulmonary vascular resistance in patients after mitral valve replacement surgery.

Pulmonary hypertension with an elevated pulmonary vascular resistance was observed during the immediate recovery period in patients who underwent mitral valve surgery. In eight such patients, intravenous infusion of CGS-13080, imidazo(1,5-a)pyridine-5-hexanoic acid (a thromboxane synthetase inhibitor), at a dose range of 0.08-0.1 mg/kg/hr, effectively reduced pulmonary hypertension (from a mean pulmonary arterial pressure of 36 +/- 2 to 31 +/- 2 torr) and pulmonary vascular resistance (from 339 +/- 38 to 238 +/- 37 dynes.sec.cm-5) within 30 minutes and remained reduced for the entire infusion period (48 hours in five patients and 18 hours in three patients). Mean arterial pressure or systemic vascular resistance were not significantly affected by the drug infusion. Serum thromboxane B2 levels (a stable metabolic product of thromboxane A2) were significantly reduced after administration of the compound, with the maximum effect of greater than 90% reduction. All patients tolerated the drug infusion without significant side effects.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Urinary thromboxane excretion in cardiac allograft rejection in immunosuppressed rats.

Increased urinary excretion of immunoreactive thromboxane B2 (iTxB2) was found to have a high predictive value, with high sensitivity as an indicator of cardiac allograft rejection in both the immunosuppressed and nonimmunosuppressed rat. In the animals receiving an allograft, urinary iTxB2 excretion significantly increased prior to the onset of rejection, remained elevated, and returned to basal values following completion of the episode. Urinary iTxB2 remained at baseline values in the control animals. The association between rejection and iTxB2 excretion was preserved regardless of the presence or nature of immunosuppression. Urinary iTxB2 excretion increased significantly prior to the reduction of graft beat or histological evidence of rejection. Evaluation of urinary iTxB2 monitoring as a noninvasive indicator for surveillance of clinical cardiac allograft rejection appears to be warranted.

Animals↗
PubMed1987

The effect of prednisolone, thromboxane, and platelet-activating factor receptor antagonists on lymphocyte and platelet migration in experimental cardiac transplantation.

Three agents that significantly prolong cardiac allograft survival were tested in Lewis rats that were recipients of hearts from Lewis X Brown-Norway F1 hybrid donors. In the presence of azathioprine, the effects of daily administration of either the thromboxane antagonist (L 640,035), the platelet-activating factor (PAF) antagonist (BN 52021) or prednisolone were evaluated on the infiltration of cardiac allografts by syngeneic lymphocytes and platelets labeled with 111indium. As anticipated, platelet deposition was reduced by the thromboxane antagonist and unaffected by the PAF antagonist; the latter is likely due to the known absence of PAF receptors in rat platelets. In addition prednisolone had no effect. The increased accumulation of lymphocytes on days 4-5 was also unaffected by all three drugs. These experiments indicate that, in this model, graft survival is not necessarily related to lymphocyte and platelet infiltration of the graft. The data also provide evidence for the efficacy of the thromboxane receptor antagonist L 640,035 in preventing platelet deposition in vivo.

Animals↗
PubMed1987

Leukotrienes, thromboxane, and platelet activating factor in organ transplantation.

The antirejection eicosanoids--PGE2, (PGD2), and PGI2--have an attenuating effect on T-cell proliferation by inhibition of IL-1, IL-2, and class II antigen expression on macrophages, and the prorejection eicosanoids--TXA2, LTB4, LTC4, and LTD4--enhance T-cell proliferation. LTB4 stimulates IL-1 and IL-2 formation and expression of IL-2 receptor. The mechanism of enhancement of T-cell proliferation by TXA2 has not been demonstrated. LTC4 and LTD4 promote gamma-interferon release and can replace IL-2 as a stimulator of gamma-interferon. PAF at high concentrations inhibits lymphocyte proliferation. The eicosanoids interfere with the same mechanisms as CsA and corticosteroids on T-cell clonal expansion. In experimental organ transplantation, corticosteroids can be replaced by compounds preventing the formation or expression of the prorejection eicosanoids or analogs of antirejection eicosanoids as well as by PAF antagonists. In addition, these drugs exert synergistic effect with CsA and azathioprine.

Animals↗
PubMed1986

Coronary artery thrombosis and elevated urine immunoreactive thromboxane B2.

Immunoreactive thromboxane B2 (i-TXB2) was measured by radio-immunoassay (RIA) in urines collected over eight hours on the day of admission in 25 patients who were admitted with the diagnosis of myocardial infarction. In 16 of the patients myocardial infarction was confirmed by ECG and plasma enzymes. Another patient presented with pulmonary embolism and the remaining eight patients had angina pectoris. A further eight hour urine collection was obtained 24 hours later from eleven of the sixteen patients with myocardial infarction. In these eleven patients myocardial infarction was associated with five fold higher urine i-TXB2 (2.72 +/- 0.48 ng/ml) at the day of admission when compared to patients admitted under the same diagnosis but found to have angina only (0.51 +/- 0.08 ng/ml, p less than 0.001). In patients with myocardial infarction the urine i-TXB2 values were reduced 24 hours later (1.58 +/- 0.27 ng/ml, p less than 0.01). One patient was followed with urine i-TXB2 from three days prior to diagnosis of myocardial infarction and to one day prior to a second infarction. In this patient i-TXB2 was highest three days prior to infarction. We conclude that this early elevation of urine i-TXB2 three days prior to diagnosis of infarction and the increased i-TXB2 in patients with myocardial infarction when compared to patients with angina suggest thromboxane is probably released from activated platelets prior to infarction. We suggest that urine i-TXB2 may be of value in the differential diagnosis between myocardial infarction and angina.

Aged↗
PubMed1986

Implication of thromboxane in frusemide diuresis in rats.

Administration of the thromboxane A2 (TXA2) synthase inhibitor OKY 1581 to rats significantly increased the urine output elicited by the loop diuretic frusemide. The administration of the TXA2 receptor antagonist SQ 29548 significantly increased the diuretic effect of frusemide. Another TXA2 receptor antagonist L-640,035 increased significantly the diuretic effect of frusemide. Both the sodium excretion rate and urine osmolar excretion rate were significantly increased in rats treated with the TXA2 synthase inhibitor OKY 1581 and frusemide. The data suggest that TXA2 is released during frusemide-induced diuresis in rats, and the released TXA2 has an opposing antidiuretic effect. Key words: antidiuretic hormone, frusemide diuresis, thromboxane inhibitor and antagonists.

Animals↗
PubMed1986

Human peritoneal eosinophils and formation of arachidonate cyclooxygenase products.

Human peritoneal eosinophils were obtained from the waste dialysis bags of patients undergoing continuous ambulatory peritoneal dialysis. The number of eosinophils obtained from each bag varied from 3 X 10(7) to 288 X 10(7). The cells were incubated for 1 h in tissue culture medium and prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 (6-keto-PGF1), and thromboxane B2 (TXB2) were determined by radioimmunoassay of the supernatant. The basal release as well as the stimulated release from the purified eosinophils of TXB2 were five times greater than the release of PGE2 and thirty times greater than the release of 6-keto-PGF1. A dose-response curve was achieved for all three cyclooxygenase products with the calcium ionophore A23187. The release of TXB2 was inhibited in a dose-dependent manner by the specific thromboxane A2 (TXA2) synthase inhibitor OKY-1581 and a corresponding increase in PGE2 and 6-keto-PGF1 was obtained. Indomethacin (5.6 X 10(-6) M) inhibited the cyclooxygenase products to almost undetectable levels.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Eicosanoids, gamma-interferon and inflammatory cells in kidney transplant patients.

Urinary i-TXB2 of renal transplant patients was found to be unaffected by CsA administration. Thus CsA treatment is unlikely to contribute to false positive values in this diagnostic indicator of rejection. It is possible that CsA treatment may suppress the peak i-TXB2 attending rejection but this does not seem to be the case. Studies on rats with cardiac allografts show CsA not to attenuate the rejection i-TXB2 peak (8). The causal role of thromboxane in transplant rejection was further amplified by experimental studies in rats where the cardiac allograft was protected by thromboxane synthase inhibitors and receptor antagonists. The inflammatory cell infiltrate of clinical renal allografts correlated with urine i-TXB2. These data strengthens the diagnostic value of urine i-TXB2 as a non invasive indicator of transplant rejection. Serum gamma-interferon was studied in nine patients and detected for 14 and 10 consecutive days, respectively in 2 patients. Three of the remaining patients had mild rejection episodes. Of the two patients one rejected the kidney and the other had CMV infection. No correlation was found between gamma-interferon and urine-TXB2. Thus elevated serum gamma-interferon does not interfere with urine i-TXB2.

Animals↗