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S Degre

Publications and source records attributed to S Degre.

18 recordsLinked to original sources
PubMed1992

Effects of chronic congestive heart failure on 24-hour blood pressure and heart rate patterns: a hemodynamic approach.

For 29 patients with congestive heart failure (CHF), 24-hour noninvasive ambulatory blood pressure (ABP) and heart rate (HR) measurement profiles were described, using the periodogram method, and were compared with the same findings in 22 matched controls. Right-sided heart catheterization was performed in all patients. The mean cardiac index was 2.2 L/min/m2 (range 1.3 to 2.9 L/min/m2). More severe CHF, as assessed by cardiac index, pulmonary artery wedge pressure, and right atrial pressure, correlated significantly with a reduction in the amplitude of the circadian ABP and HR rhythms (0.38 less than r less than 0.63; p less than 0.05). Moreover, a reduced increase in cardiac index during cycloergometric exercise in 11 CHF patients correlated with a blunting of the circadian systolic ABP and HR profiles (0.57 less than r less than 0.90; p less than 0.05). Our results indicate that there is a reduction in the amplitude of the circadian BP and HR rhythms related to the severity of CHF.

Blood Pressure↗
PubMed1990

Increased platelet aggregability and prostacyclin biosynthesis induced by intense physical exercise.

Changes in platelet aggregability during maximal bicycle ergometry were studied in healthy untrained subjects. Ex vivo platelet aggregation in response to ADP and collagen was measured in whole blood by impedance aggregometry or by direct electronic counting in an Ultra-Flo 100 platelet counter. This last method revealed that the platelet aggregation induced by low concentration of ADP (0.5 - 1.0 microM) was significantly enhanced during exercise. The plasma level of beta-thromboglobulin and the urinary excretion of 2,3--dinor-6-keto prostaglandin F1 alpha were also increased. These data indicate that an intense physical exercise enhances the aggregability of human platelets and induces a compensatory increase in prostacyclin biosynthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Hemodynamic effects of SIN-1 in acute left heart failure.

To assess the hemodynamic effects of SIN-1, the active metabolite of the venodilator molsidomine, after acute as well as chronic intravenous administration, ten patients with exacerbation of chronic heart failure were studied. After a mean bolus dose of 2 mg of SIN-1, mean right atrial pressure (MRAP), mean pulmonary artery pressure (MPAP), and pulmonary capillary wedge pressure (PCAP) decreased significantly up to the 60th minute; pulmonary vascular resistance (PVR) decreased significantly up to the 30th minute, while cardiac index (CI) and systemic vascular resistance (SVR) remained unchanged. During a 24-hour continuous infusion of SIN-1, MRAP, MPAP, and PCAP decreased significantly, while CI, PVR, and SVR remained largely unaltered. No dose adjustment was required to maintain the hemodynamic effects over 24 hours. The absence of noteworthy side effects and tolerance during this prolonged administration indicate that SIN-1 is a potentially useful drug in the management of patients admitted with exacerbation of heart failure.

Aged↗
PubMed1989

Comparison of responses to acetylcholine and serotonin on isolated canine and human coronary arteries.

Canine and human coronary arteries were studied in organ baths to compare the responses to acetylcholine and serotonin in the two species. The human coronary rings were isolated from seven patients without cardiac disease (mean age 15 years, range 7-20). In one set of experiments canine and human preparations were incubated with phentolamine, propranolol and ketanserin (all at 1 mumol.litre-1 concentration) and precontracted with prostaglandin F2 alpha (PGF2 alpha 1-2 mumol.litre-1). Acetylcholine (0.1-10 mumol.litre-1) and serotonin (0.1-100 mumol.litre-1) relaxed canine preparations dose dependently, the maximum responses (expressed as % of depression of PGF2 alpha response) being 84 (SEM 6)% (n = 9) and 51(5)% (n = 6) respectively. In the same experimental conditions, acetylcholine and serotonin failed to relax the human coronary rings (n = 11) while substance P and bradykinin induced relaxations of 72(4)% (n = 11) and 66(7)% (n = 11) of PGF2 alpha response respectively. In another set of experiments, dose-contraction curves were constructed for acetylcholine or serotonin (in presence of phentolamine and propranolol). On human rings with endothelium, methylene blue (10 mumol.litre-1), a non-specific inhibitor of endothelium derived relaxing factor (EDRF), potentiated these dose-contraction curves: markedly for serotonin, the EC50 decreasing from 1.2(0.2) to 0.22(0.08) mumol.litre-1 (n = 11, p less than 0.01) with a significant increase in the maximal response); and slightly for acetylcholine, EC50 decreasing from 0.84(0.11) to 0.40(0.13) mumol.litre-1 (n = 10, p less than 0.05) without significant change in the maximal response.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

Alterations of beta-adrenoceptor mediated relaxations of atherosclerotic human coronary arteries.

Preliminary investigations suggest that atherosclerosis attenuates the beta-adrenergic relaxations of human coronary arteries. However, this finding could not be related specifically to the beta-agonists and responses to non-adrenergic relaxants could be also decreased. Therefore segments of coronary arteries were isolated from 35 human hearts (aged 18-58 years) with various degrees of atherosclerosis. On rings precontracted with KCl (15 mM) concentration-response curves were constructed for isoproterenol and were compared with the responses to three other vasodilators: forskolin, nitroglycerin and SIN1 (the active metabolite of molsidomine). At the end of each experiment, the degree of atherosclerosis was scored by histological examination. Moderate (class II) and severe (class III) lesions of atherosclerosis significantly altered the maximal response to isoproterenol, which was decreased from 76 +/- 5% (of KCl-induced contraction) to 33 +/- 6% in class II and 22 +/- 5% in class III. Conversely, the maximal relaxations to forskolin, nitroglycerin and SIN1 were not significantly modified. However, in class III, there was a significant shift to the right of the dose-response curves to nitroglycerin and SIN1 (but not to forskolin). Thus our results show that atherosclerosis markedly attenuates the relaxations of human coronary smooth muscles to isoproterenol, and that this abnormality is not related to an alteration in the intrinsic capacity of the atherosclerotic vessel to relax.

Adult↗
PubMed1988

Persistence of the response to SIN1 on isolated coronary arteries rendered tolerant to nitroglycerin in vitro or in vivo.

Experiments were performed on isolated canine and human coronary arteries to provide more insight into the mechanisms responsible for the vascular tolerance to nitroglycerin that is induced under in vitro or in vivo conditions. In vitro tolerance was produced after an incubation of coronary ring segments with nitroglycerin (10 microM for 30 min at physiological pH). After elevation of tone with KCl (15 mM), dose-response curves were constructed for nitroglycerin or SIN1 (3-morpholino-syndnonimin) on control and tolerant rings. On canine tolerant rings the dose-response curve for nitroglycerin-induced relaxations was significantly (p less than 0.001) shifted to the right, and 50% of the maximal relaxation (ED50) increased from 55 +/- 9 nM to 1.2 +/- 0.2 microM. Pretreatment of tolerant rings with N-acetylcysteine (NAC, 10 microM 10 min before KCl-induced contraction) partially restored the responsiveness to nitroglycerin, with ED50 reducing to 0.56 +/- 0.03 microM (p less than 0.02). On the other hand, the dose-response curves to SIN1 were not significantly altered. Similar results were obtained on human preparations. On isolated canine coronary rings rendered tolerant in vivo by subcutaneous injections of 15 mg/kg nitroglycerin (two times daily for 4 consecutive days), ED50 for nitroglycerin was 0.67 +/- 0.08 microM (p less than 0.001 versus control rings), and NAC again partially restored the responsiveness to nitroglycerin. As for the in vitro tolerance, the relaxations to SIN1 were not significantly altered on these canine rings rendered nitrate tolerant in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Comparison of the effect of beta adrenergic antagonists with different ancillary properties on isolated canine and human coronary arteries.

Experiments were performed on canine and human isolated coronary arteries to characterise human coronary beta adrenoceptors and to determine whether or not beta blocking agents with different ancillary properties unmask the alpha adrenergic effect of noradrenaline in a similar way. The inhibitory effects of atenolol (a beta1 selective antagonist), epanolol (a beta1 selective antagonist with modest intrinsic sympathetic activity), and propranolol (a non-selective antagonist) were assessed on isoproterenol concentration-response curves. Regression analysis provided slopes not significantly different from unity and similar pA2 values for each agent in both preparations. In a second group of experiments, the effects of noradrenaline (10 mumol.litre-1) were assessed in the absence and presence of beta blockade. At equipotent doses (1 log or 2 log units from the pA2 values) each beta blocking agent unmasked the alpha effect of noradrenaline in the same way. This alpha effect of noradrenaline (10 mumol.litre-1) was completely abolished by prazosin 1 mumol.litre-1 in canine coronary arteries but only partially antagonised in human coronary arteries. Thus the property of a beta blocking agent to unmask the alpha adrenergic effect of adrenaline is mainly related to its affinity for the coronary smooth muscle beta adrenoceptors. These beta adrenoceptors were very similar in both preparations and appear to be mainly beta1. The alpha adrenoceptors seem, nevertheless, to be different and resistant to prazosin in human preparations.

Adrenergic beta-Antagonists↗
PubMed1987

Calcium channel blockers cannot prevent pure vasospastic myocardial infarction.

Coronary artery spasm is a recognized cause of myocardial infarction. This report describes a case of myocardial infarction attributed to pure coronary spasm which was halted by a double perfusion with streptokinase and nitroglycerin. Further coronary artery spasm leading to a myocardial infarction could not be avoided several weeks later, although the patient was left on calcium channel blocker therapy. The two attacks were not preceded by warning angina pectoris, contrary to accepted belief. The best objective of end-point drug therapy and its assessment in vasospastic angina are discussed.

Calcium Channel Blockers↗
PubMed1986

[Hemodynamic effects of microencapsulated delayed-release nitroglycerin in acute myocardial infarction].

The hemodynamic effects following an oral dose of 19.5 mg of nitroglycerin microencapsulated to give prolonged release have been studied in 10 patients during the 48 hours which followed the establishment of a myocardial infarct complicated by moderate left cardiac insufficiency. The right auricular pressure and the pulmonary capillary pressure diminished significantly 20 minutes after the dose; 4 hours later the persistence of these effects is significant. A transient diminution of the systolic arterial pressure was observed initially (p less than 0.05). We observed that the cardiac index tends to increase although the increase did not attain the threshold of significance. No difference was observed in cardiac frequency, diastolic and mean arterial pressure and in the systemic vascular resistance. We conclude that in the patient presenting an acute myocardial infarct, 19.5 mg of NTG, microencapsulated to give prolonged release, essentially produce a reduction of the preload, with an early onset of action and a hemodynamic efficacy lasting at least 4 hours.

Aged↗
PubMed1979

Functional evaluation of a physical rehabilitation program including breathing exercises and bicycle training in chronic obstructive lung disease.

20 patients suffering from chronic obstructive lung disease (COLD) were submitted to a 6-month rehabilitation program including breathing exercises only (A) or coupled with bicycle training (B). Functional results obtained at rest were the following: for A: nonsignificant changes in FRC, RV, FEV1, Raw, Pa O2, pH, Pp, VO2 max SL but significant changes (p less than 0.05)for TLC (+ 214 cm3), VC (+ 171 cm3), DL CO (+ 1.79 ml), Pa CO2 (-2.9 mm Hg). For B: similar changes as for A with additional significant changes in PaO2 (+ 7.4 mm Hg) VO2 max SL (+ 250 ml) and Pp (-4 mm Hg). These results, although minimal, are attributed to improved respiratory muscle strength and improved alveolar ventilation. Exercise training adds an increased ability to sustain higher loads.

Breathing Exercises↗
PubMed1977

[Exercise retraining].

Among the essential positive facts resulting from the physical training of patients with moderate to severe obstructive bronchopneumopathy, the following should be noted:-- the maximal capacity for work increases on average by 10%;-- physiologically this increment of work maximal capacity corresponds simply to a better extraction of oxygen by the muscles;--no specific central haemodynamic modification is usually observed at maximum or sub-maximum level;-- after training there is a favourable evolution of the PaO2 at rest. In the absence of spirographic modification and diffusion capacity, this increase of PO2 seems to result from an improvement of the ratio ventilation/perfusion.

Carbon Dioxide↗
PubMed1975

[Cardio-respiratory assistance with the extracorporeal membrane oxygenator for massive pulmonary embolism].

A 39 year old pneumectomized patient presents a massive pulmonary embolism, dies within 3 hours and is supported inefficiently by cardiac massage with recurrent mydriasis during 2 hours. At that time, under extracorporeal cardiopulmonary bypass with a membrane oxygenator, the cardiac activity recovers immediatly due to right decompression and coronary perfusion. The patient is conscious within 5 hours. The cardiopulmonary bypass with a membrane oxygenator appears to be the best therapy when the cardiac massage fails to restitute a normal myocardial function. No embolectomy was performed. The patient died when the bypass was stopped after 48 hours. We conclude that the prolonged peripheral extracorporeal bypass followed by embolectomy is the best therapy of pulmonary embolism.

Adult↗