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H Boudoulas

Publications and source records attributed to H Boudoulas.

170 records · Page 10Linked to original sources

Time couse of the blockade effect of propranolol on sinus node and atrioventricular node.

The time course of the blockade effect of propranolol on the sinus node (SN) and the atrioventricular node (AVN) was studied in six normal volunteers. Serial isoproterenol infusions were done before and after oral propranolol administration, 160 mg daily for two days. The inhibition by propranolol of the heart rate increases due to isoproterenol was used to assess the blockade of the sinus node, and the diminution by propranolol of the shortening in the PR interval due to isoproterenol was used to assess the blockade of the atrioventricular node. The blockade effects on the sinus node and the atrioventricular node were identical and persisted more than 24 hours. There was no good relationship between plasma propranolol and blockade effect on sinus node and/or atrioventricular node as propranolol was no longer detectable in the plasma 24 hours after the last dose. A transient hypersensitivity to isoproterenol was present 36 to 48 hours after propranolol withdrawal. The explanation of these phenomena most likely lies in the peculiar nature of beta-adrenergic receptors.

Adult↗

Aortic pain.

With the exception of the pain of acute aortic dissection, the thoracic aorta is not usually considered as a pain-producing organ. However, nineteenth century clinicians considered the aorta as a source of cardiovascular pain in the presence of autopsy-documented inflammatory aortitis, aortic aneurysms, and arterial hypertension, whereas early in the twentieth century, aortic pain reactions were elicited in experimental studies involving distension of the ascending aorta or the application of stimulating substances to the outer surface of the aorta. More recently, increased attention to aortic elastic properties, and to aortic vascular biology at the molecular level refocused interest on the many facets of aortic function beyond that of a simple conduit. The recognition of pain of thoracic aortic origin now extends to patients with progressive aortic syndromes such as aortic intramural hematoma, aortic intimal tears, aortic penetrating ulcers, aortic root dilatation without dissection in connective tissue disorders, inflammatory aortopathies, and abnormalities of aortic distensibility. The occurrence of pain during balloon inflation at balloon angioplasty of aortic coarctation, which disappears immediately after deflation, is the modern equivalent of the early experimental studies. The authors present a consideration of thoracic aortic pain in light of contemporary concepts in cardiovascular medicine with roots in the rich historical reservoir of information about aortic function and disease.

Aortic Dissection↗

Expression of PDGF-A, TGFb and VCAM-1 during the developmental stages of experimental atherosclerosis.

PURPOSE: A considerable number of growth factors, cytokines, and adhesion molecules are implicated in the development of atherosclerotic lesions. These molecules interact in a complex network influencing the evolution of several processes, such as lipid metabolism, cellular proliferation and tissue repair. The aim of this study was to evaluate the expression of the growth factors PDGF-A, and TGFb, and the adhesion molecule VCAM-1 in the sequential steps of experimental atherogenesis. METHODS: Forty-two New Zealand white male rabbits were divided into 4 groups. The group A rabbits (n = 8) received normal diet and served as control animals. The remaining groups were fed with a diet enriched with 1% cholesterol and 6% corn oil. The rabbits of group B (n = 9) were sacrificed 1 month after the beginning of the study, of group C (n = 15) after 2 months and of group D (n = 10) after 3 months. In tissue sections of the aortic arch the antibodies of the prementioned factors were detected immunohistochemically. RESULTS: In group A only TGFb and PDGF-A were detectable. In lesions of the first month PDGF-A expression was high but declined towards the third month. VCAM-1 expression was getting more intense up to the second month and subsided thereafter. TGFb expression intensified towards the third month. Changes in the expression of these factors were statistically significant. CONCLUSION: PDGF-A, responsible for the uncontrollable growth of smooth muscle cells, and VCAM-1, regulating monocyte recruitment in the intima, acts mainly during the early stages of atherogenesis. TGFb, one of the main factors controlling the formation of connective tissue matrix, has a gradually increasing expression towards the third month contributing probably to the fibrous plaque formation.

Animals↗

Stereoselective pharmacokinetics of disopyramide enantiomers in man.

The plasma protein binding and pharmacokinetics of S(+)-disopyramide and R(-)-disopyramide following infusions of 100 mg were compared in five healthy human volunteers. The binding of S(+)-disopyramide was higher than that of R(-)-disopyramide at similar unbound concentrations in all subjects. The association constant characterizing the interaction between plasma protein and the S(+)- and R(-)-enantiomers was 17.1 X 10(5) M-1, and 7.68 X respectively. The unbound clearance and half-life of S(+)-disopyramide averaged 604 ml/min and 3.67 hr, respectively, and differed from that of R(-)-disopyramide, which averaged 401 ml/min and 4.62 hr, respectively. Both enantiomers appear to undergo active tubular secretion. The unbound renal clearance of the S(+)- and R(-)-enantiomers averaged 338 and 182 ml/min, respectively (p = 0.05). The unbound steady-state volume of distribution of S(+)- and R(-)-disopyramide averaged 172 and 141 liters, respectively (p = 0.14). The renal clearance of the mono-N-dealkylated metabolite of disopyramide following the administration of S(+)- and R(-)-disopyramide averaged 345 and 170 ml/min, respectively (p less than 0.05).

Blood Proteins↗

Effect of angiotensin-converting enzyme inhibitors on the power spectrum of heart rate variability in post-myocardial infarction patients.

BACKGROUND: Heart rate variability (HRV) time and frequency domain indices are strong predictors of malignant arrhythmias and sudden cardiac death. The effect of various angiotensin-converting enzyme (ACE) inhibitors on HRV in patients with acute myocardial infarction (AMI) has not been studied. METHODS: Ninety patients with uncomplicated AMI (age range 39-75 years, median 61 years) were assigned randomly to six groups of 15 patients each. They were treated with placebo or one of the following ACE inhibitors for 30 days: captopril, cilazapril, enalapril, lisinopril or quinapril. HRV was assessed 3 days after the onset of AMI (baseline), and 30 days after treatment. Fifteen patients with stable coronary artery disease and 15 healthy volunteers, age- and sex-matched with AMI patients, served as controls. RESULTS: At baseline, time and frequency domain HRV indices in the AMI groups were equally less than those in patients with stable coronary artery disease and normal volunteers. Compared with placebo, quinapril, lisinopril and captopril changed frequency domain HRV indices 30 days after initiation of treatment, indicating an increase in vagal tone, whereas enalapril and cilazapril had no significant effect on these indices. Most of the time domain HRV indices 30 days after initiation of treatment increased significantly in all patients treated with ACE inhibitors, but remained unchanged in the placebo group. Frequency domain and time domain HRV indices 30 days after treatment in the quinapril group did not differ statistically from those in patients with stable coronary artery disease, but were less than those in normal volunteers. CONCLUSIONS: Quinapril, lisinopril and captopril improved frequency domain HRV indices related to vagal tone, whereas cilazapril and enalapril had no effect on these indices. This influence of some ACE inhibitors on HRV may be beneficial in reducing the risk for sudden death in post-myocardial infarction patients.

Adult↗

Increased diastolic time: a possible important factor in the benefical effect of propranolol in patients with coronary artery disease.

Diastolic time (DT) calculated as the cycle length minus electromechanical systole (QS2) has a nonlinear relationship to heart rate (HR), increasing rapidly as rates fall below 75. The effect of propranolol on DT was studied in 150 patients with coronary artery disease. Patients were divided into three groups. Group I included patients with stable angina pectoris: propranolol (2.5 mg, i.v.) significantly increased DT from 411 +/- 18 to 527 +/- 22 msec (p less than 0.001) in 23 patients of group I; therapy with propranolol (mean daily dose 200 +/- 15 mg) increased DT from 446 +/- 29 to 766 +/- 26 msec (p less than 0.001) in 15 patients with stable angina. Group II was made up of patients with acute myocardial infarction: Propranolol (2.5 mg, i.v.) increased DT from 379 +/- 16 to 458 +/- 24 (p less than 0.001) in 18 of these patients. Group III included patients with recent coronary bypass surgery: propranolol (2.5 mg, i.v.) increased DT from 323 +/- 9 to 468 +/- 24 msec (p less than 0.001) in 14 patients 7 days after surgery. In addition, DT at 15 hr and 2 weeks after surgery was compared in 30 patients maintained on propranolol (mean daily dose, 155 +/- 11 mg preoperative and 68 +/- 9 mg postoperative) and 50 other patients who underwent coronary bypass surgery not on propranolol. DT was greater in propranolol patients (546 +/- 21 vs. 388 +/- 16 msec, p less than 0.001), preoperative and 396 +/- 15 vs. 320 +/- 12 msec, p less than 0.001, postoperative). Changes in DT after propranolol are mainly attributed to decreased HR. Changes in QS2 were much less profound and always less (p less than 0.01) than changes in DT. Thus propranolol significantly increased DT per beat in patients with coronary artery disease, which allowed more time for coronary perfusion; this effect of propranolol could well be as important as the reduction of myocardial oxygen consumption.

Adult↗