Fibrinolytic System in Patients with Hypertensive Cardiovascular Disease

Prokopowicz, J; Worowski, K; A, Poplawski; Gabryelewicz, A; Niewiarowski, S

doi:10.1055/s-0038-1654078

Cited by 14 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a series of papers (Prokopowicz, Worowski, Poplawski, Gabryelewicz & Niewiarowski, 1967;Prokopowicz, Worowski, Poplawski, Mysliwiec & Niewiarowski, 1967;Prokopowicz, Worowski & Niewiarowski, 1969) have confirmed previous observations concerning the relationship between the state of activation of the fibrinolytic system and various pathological conditions and have shown that the treatment of angiotensin II with plasmin resulted in destruction of the pressor activity to about 50%. The present experiments were designed to determine the peptide bond(s) in angiotensin II cleaved by plasmin.…”

Section: Introductionsupporting

confidence: 57%

Degradation of angiotensin II by plasmin

Dudek

Latałło

Prokopowicz

et al. 1972

British J Pharmacology

View full text Add to dashboard Cite

show abstract

Section: Introductionsupporting

confidence: 57%

Degradation of angiotensin II by plasmin

Dudek

Latałło

Prokopowicz

et al. 1972

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…MHA again worsened (Fig. 1), and the presence of hemolysis was confirmed by 51 Cr-labeled red cell survival half-life values of 15 and 14 days being obtained during the fifth and seventh weeks of admission, respectively. A further course of intravenous heparin was given (days 47 to 51) without apparent effect.…”

Section: -131mentioning

confidence: 81%

“…Blood pressure decreased to the range of 120/60 to 160/85 mm Hg after operation, and the retinal abnormalities resolved. Two weeks after the operation T/2 51 Cr was normal at 23 days, and the platelet count had risen to 285,000/mm 3 . Most blood films since the operation have been normal (grade 0), although one showed slight fragmentation of red blood cells (grade I).…”

Section: -131mentioning

confidence: 96%

Microangiopathic Hemolytic Anemia and the Development of the Malignant Phase of Hypertension

Gavras¹,

Brown²,

Brown³

et al. 1971

Circ Res

View full text Add to dashboard Cite

Evidence of microangiopathic hemolytic anemia (MHA) was found in 14 of 22 patients with malignant phase hypertension, and in one of these, a patient with proliferative glomerulonephritis, MHA and malignant hypertension developed together during a three-month period of observation.Among 61 rats subjected to unilateral nephrectomy, injected with DOCA, and given 1% saline to drink, 42 developed evidence of MHA, Eighty-four per cent of these also had fibrinoid necrosis and/ or plasmatic vasculosis in the remaining kidney at autopsy. Blood pressure rose to 150 mm Hg or more in 72% of these DOCA-injected animals. In 29 control rats subjected to unilateral nephrectomy only, blood pressure rose to 150 mm Hg or more in 2135, MHA developed in 14%, and fibrinoid lesions were found in none.The significance of these observations is discussed in relation to the possibility that MHA is either a consequence of malignant hypertension or a contributory factor in its pathogenesis. KEY WORDSmicroangiopathic hemolytic anemia DOCA malignant hypertension fibrinoid lesions bilateral nephrectomy renal failure intravascular coagulation glomerulonephritis• An association between malignant phase hypertension and microangiopathic hemolytic anemia (MHA) is now well recognized. 1 " 5Since the association appears relatively common and since MHA, when it occurs in other states, is characterized by features similar to those of malignant hypertension, it seemed possible to us that MHA might at least contribute to the development of the malignant phase. 6 If this is so, MHA should be demonstrable when (or before) the malignant phase appears. Our earlier studies threw little light on this particular question since, by the time most patients presented, both the conditions were well established.

show abstract

“…Although several stimuli for t-PA release have been described such as exercise [1], venous occlusion [2] and cardiopulmonary bypass [3], the effect of blood pressure alterations on endothelial t-PA secretion re mains to be clarified. It has been attempted to correlate blood fibrinolytic activity with arterial blood pressure in a number of studies [4][5][6][7][8], but no clear-cut conclusions could be attained. Based on these considerations, the pre sent study was designed in order to compare the basal plasma t-PA levels in hypertensive and normotensive sub jects and to determine the effect of acute blood pressure reduction by sublingual nifedipine on plasma t-PA levels in essential hypertension.…”

mentioning

confidence: 99%

Tissue Plasminogen Activator in Essential Hypertension

Ank¹,

Tekin²,

Özdemir³

et al. 1992

Acta Haematol

View full text Add to dashboard Cite

Tissue plasminogen activator (t-PA) is regarded as the major activator of fibrinolysis. It is synthetised and stored in endothelial cells, from where it is released into the blood stream. Although several stimuli for t-PA release have been described such as exercise [1], venous occlusion [2] and cardiopulmonary bypass [3], the effect of blood pressure alterations on endothelial t-PA secretion re mains to be clarified. It has been attempted to correlate blood fibrinolytic activity with arterial blood pressure in a number of studies [4][5][6][7][8], but no clear-cut conclusions could be attained. Based on these considerations, the pre sent study was designed in order to compare the basal plasma t-PA levels in hypertensive and normotensive sub jects and to determine the effect of acute blood pressure reduction by sublingual nifedipine on plasma t-PA levels in essential hypertension.The study group included 18 previously untreated patients with diastolic blood pressure 105 mm Hg or higher, mean age 46 ± 2 years and 13 healthy age-and sex-matched normotensive patients. Blood samples were drawn without stasis, by means of an indwelling cathe ter placed in the antecubital fossa 30 min prior to test. The patency of the needle was maintained by slow saline infusion. Upon the comple tion of a 30-min period of recumbent rest, the baseline samples were drawn at 9:00 a.m. in both groups. Immediately after the baseline sampling, the hypertensive patients were given 10 mg nifedipine sub lingually. Additional samples were drawn 15,30 and 60 min after nife dipine. All subjects remained in the supine position during the study. Blood pressure measurements were performed at 0,15,30 and 60 min just after sampling. T-PA antigen levels were measured by the sand wich ELISA technique [9], The significance of the difference was analysed by the MannWhitney U and Wilcoxon rank tests for intergroup and intragroup measurements, respectively. The values were expressed as mean ± standard error of mean. Fig. 1. The effect of sublingual nifedipine on blood pressure and plasma t-PA antigen level in hypertensive patients (n = 18). Figure 1 shows the changes in mean systolic and dia stolic blood pressure and t-PA antigen levels after the ad ministration of sublingual nifedipine. The mean systolic and diastolic blood pressure in the hypertensive group at 0 min were 174.2 ± 6.0 mm Hg and 118.1 ± 2.8 mm Hg, respec tively. Gradual lowering of systolic and diastolic blood pressure was observed during the study period; minimal blood pressure values (systolic 155.0 ± 6.3 mm Hg, diastolic 103.6 ±3.2 mm Hg) were reached at 60 min (p <0.001).The mean baseline (0 min) t-PA antigen level of hyper tensive patients was 7.9 ± 1.6 ng/ml, which was not found to be significantly different from the mean t-PA antigen level

show abstract

Fibrinolytic System in Patients with Hypertensive Cardiovascular Disease

Cited by 14 publications

References 0 publications

Degradation of angiotensin II by plasmin

Degradation of angiotensin II by plasmin

Microangiopathic Hemolytic Anemia and the Development of the Malignant Phase of Hypertension

Tissue Plasminogen Activator in Essential Hypertension

Contact Info

Product

Resources

About