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Biomedical subjects

M Condorelli

Publications and source records attributed to M Condorelli.

At least 217 records · Page 12Linked to original sources

Hemodynamics of the splanchnic and systemic circulation after hypotonic water load-comparison between normal subjects and patients with congestive heart failure.

The authors investigated the changes in cardiovascular and splanchnic hemodynamic, diuresis and urinary and hepatic veins osmolarity induced by hypotonic water load in five normal subjects and in five patients with congestive heart failure (CHF). Pulmonary wedge pressure increased significantly only in CHF patients while cardiac index, total pulmonary resistances and peripheral vascular resistances remained unchanged in both groups. Hepatic blood flow increased significantly in control group while in CHF showed a significant reduction 15 and 30 minutes after water load. Hepatic veins osmolarity decreased significantly in control group only at the 45th minute. Diuresis was significantly higher in normals which eliminated water load with a lower urinary osmolarity. The authors conclude that: water loading is particularly interesting in so much it resembles the physiological conditions of the absorption of the alimentary hypotonic bolus; the failing heart responds to the water load on a depressed function curve; the hepatic blood flow is reduced in CHF patients and is probably responsible for some humoral abnormalities found in these subjects; CHF patients eliminate a water load slower than a normal subject and with a higher osmolarity.

Aged↗

[Effectiveness of the aorto-coronary by-pass procedure in elderly patients].

This study was undertaken to evaluate the efficacy of coronary artery by-pass grafting (CABG) in elderly patients with coronary artery disease. A consecutive series of 79 patients, 65 years of age and older, who underwent CABG from 1975 to 1981 was analysed and their follow up status ascertained. This group was compared with a consecutive series of 397 patients under the age of 65 who underwent CABG during the same period. The patients aged 65 years or greater had a higher incidence of unstable angina pectoris (p less than 0.05). Coronary angiographic and left ventriculographic features were comparable in both age groups; also comparable were the number of saphenous veins graft utilized and the number of left ventricular aneurysmectomies and mitral valve replacements performed. The hospital mortality rate for patients aged 65 years and older was 12.6%, for those aged less than 65, it was 8.3%; if the other cardiac procedures are excluded mortality rates become 12.5% and 6.0% respectively (n.s.). Survival at 6 years was 92% for patients in both age groups. However, the symptomatic status was less favourable in older patients, compared with that obtained in younger patients (p less than 0.05).

Aged↗

Possible role of arachidonic acid and of phospholipase A2 in the control of lysosomal enzyme release from human polymorphonuclear leukocytes.

We have studied the role of arachidonic acid (AA) metabolism in the release of lysosomal enzymes (beta-glucuronidase and lysozyme) from human polymorphonuclear leukocytes (PMNs). 5,8,11,14-Eicosatetraenoic acid (ETYA), which inhibits both the cyclo-oxygenase and the lipoxygenase pathways of AA metabolism, was found to cause a dose-dependent inhibition of lysosomal enzyme release from human PMNs induced by immunological (i.e., serum-treated zymosan: Zx) and nonimmunological stimuli (i.e., formyl methionine-containing peptide and the Ca2+ ionophore A23187). In contrast, the non-steroidal anti-inflammatory drugs (indomethacin, meclofenamic acid and aspirin), which only block the cyclo-oxygenase pathway of AA metabolism, had little effect on enzyme release from PMNs induced by the same stimuli. 5,8,11-Eicosatriynoic acid (ETI), a selective inhibitor of the lipoxygenase pathway of AA metabolism, caused a dose-dependent inhibition of lysosomal enzyme release elicited by Zx, f-met peptide, and A23187. p-Bromophenacyl bromide (BPB), which inhibits the phospholipase A2 (PLA2) activity in several tissues, was found to cause a dose-dependent inhibition of lysosomal enzyme release induced by the same immunological and non-immunological stimuli. The inhibitory effect of BPB on enzyme release was irreversible and extremely rapid. It appears that activation of PLA2 and the products of the AA metabolism, generated via a lipoxygenase pathway, play an essential role in the biochemical control of human PMNs activation and secretion.

5,8,11,14-Eicosatetraynoic Acid↗

The autonomic nervous tone abnormalities in the genesis of the impaired baroreflex responsiveness in borderline hypertensive subjects.

1. The effects of intravenous administration of neostigmine and propranolol, individually or in combination, on baroreflex responsiveness have been evaluated in 18 borderline hypertensive subjects and in 14 age-matched control subjects. 2. Baroreceptor sensitivity was tested by evaluating both heart rate response to phenylephrine-induced increase in arterial pressure, and heart rate and blood pressure changes induced by increasing neck-tissue pressure by means of a neck-chamber. 3. In borderline hypertensive subjects a reduced baroreflex responsiveness was demonstrated with both stimuli as compared with normal subjects. Neostigmine administration improved consistently both reflex responses. Similarly, after propranolol treatment, borderline hypertensive subjects showed a significant enhancement of the baroreflex sensitivity. Finally, the combined administration of neostigmine and propranolol restored the baroreflex responses. In fact, both the mean slopes of the regression lines between blood pressure and R-R interval after phenylephrine and the increase in mean arterial pressure and heart rate induced by the reduction in carotid transmural pressure in borderline hypertensive subjects were similar to those observed in normals. 4. These findings indicate that in borderline hypertensive subjects the impairment of baroreflex responsiveness is mainly due to abnormalities of autonomic regulation.

Adult↗

Effects of oral salt loading on beta-adrenergic receptor responsiveness in normal and hypertensive subjects.

The effect of oral salt loading (400 mmol per day of NaCl for 7 days) on cardiac and pancreatic beta-receptor responsiveness has been evaluated in 12 patients with established essential hypertension and in seven age-matched control subjects. Cardiac beta-receptor responsiveness was evaluated by assessing the dose of isoprenaline which increased a stable heart rate by 25% (chronotropic dose 25%, CD 25%). Pancreatic beta-receptor responsiveness was measured by the incremental areas of insulin secretion induced by iv infusion of increasing amounts of isoprenaline. Before salt load, CD 25% was significantly higher in hypertensives compared with controls (7.84 +/- 1.34 micrograms vs 3.9 +/- 0.48 micrograms, P less than 0.05) while there was no difference in the isoprenaline-induced insulin secretion between the two groups of subjects. After salt loading, CD 25% was significantly reduced in hypertensive patients but was not modified in normal subjects. Therefore, the difference in CD 25% was no longer detectable between the two groups (5.5 +/- 1.42 micrograms vs 3.2 +/- 0.48 micrograms in normal subjects and in hypertensives, respectively, NS). Furthermore, salt loading failed to induce any change in isoprenaline-induced insulin secretion in either groups. These results support the existence of a relationship between sodium intake and adrenergic beta-receptor responsiveness in human hypertension.

Adolescent↗

Effects of combined alpha- and beta-blockade by labetalol in patients with coronary artery disease.

1 The effect of labetalol 100 mg orally twice daily on exercise tolerance has been compared with placebo in 19 normotensive subjects with angiographic evidence of coronary artery disease. 2 Labetalol, at the same work load as during placebo exercise, significantly reduced systolic and diastolic blood pressures, as well as heart rate and rate-pressure product. 3 Similarly, ST segment depression was reduced by labetalol from 2.0 +/- 0.4 to 1.36 +/- 0.6 mm (P less than 0.001), thus enabling an increase in exercise tolerance from a control value of 83.7 +/- 18 to 95.3 +/- 19 W (P less than 0.005). 4 In seven other patients, also with coronary artery disease, the haemodynamic effects of a single 0.6 mg/kg intravenous dose of the drug was evaluated during exercise. 5 Compared with conditions during control exercise, labetalol induced a significant reduction in rate-pressure product from 17228 +/- 2375 to 13445 +/- 2404 mmHg/min (P less than 0.005) and in peripheral vascular resistance from 612.0 +/- 61.2 to 512.7 +/- 36.2 dyn cm-5 m-2 (P less than 0.0025). These events were not accompanied by any change in cardiac index and in dP/dT left ventricular end-diastolic pressure (LVEDP) ratio. 6 These data suggest that labetalol may induce reduction in myocardial oxygen consumption, thereby increasing exercise tolerance in patients with coronary artery disease, without impairment of left ventricular performance.

Adult↗

Renal function in borderline hypertensive first-degree relatives of essential hypertensives. Effects of sodium load.

Renal function in the basal state and after sodium load has been investigated in 21 borderline, hypertensive, first-degree relatives of established hypertensives and in 21 age- and sex-matched, normal subjects with no family history of hypertension. During intravenous infusion of inulin and p-aminohippurate in saline, both groups showed a decrease in plasma aldosterone levels (p less than 0.05) but renal plasma flow (595 +/- 48 vs. 750 +/- 59 ml/min, p less than 0.05), diuresis (1.4 +/- 0.2 vs. 2.2 +/- 0.5 ml/min, p less than 0.05), natriuresis (0.21 +/- 0.02 vs. 0.3 +/- 0.02 mEq/min, p less than 0.05) and sodium clearance (1.05 +/- 0.1 vs. 2.4 +/- 0.4 ml/min, p less than 0.05) in borderline hypertensives were higher than in the control group. After the salt load (NaCl, 1.35% i.v., 5 ml/min for 2 h) there was an increase in blood pressure and a decrease in plasma aldosterone and potassium levels in both groups. However, borderline hypertensives showed higher diuresis, natriuresis, sodium clearance and also kaliuresis compared to normotensives. These results suggest that borderline hypertensives already present the changes in renal function which are characteristics of established hypertensives.

Adolescent↗

Further observations on the electrophysiologic effects of oral amiodarone therapy.

A case is presented of a reversible intra-Hisian block occurring under amiodarone treatment for atrial tachycardia in a patient without clear intraventricular conduction abnormalities. His bundle recordings showed an atrial tachycardia with intermittent exit block and greatly prolonged BH and HV intervals (40 and 100 msec, respectively). Thirty days after amiodarone discontinuation, His bundle electrograms showed atrial flutter without intra-Hisian or infra-Hisian delay. Amiodarone should be used with caution during long-term oral therapy in patients with or without clear intraventricular conduction defects.

Adult↗

Quantitative assessment of infarct size in isoproterenol-infarcted rats.

The authors performed a number of experiments aiming at quantifying the infarct size in Sprague-Dawley male rats. The experimental model employed was isoproterenol (ISP) induced, infarctlike myocardial lesions. In quantifying the extent of the infarct area they compared the cross reliability of enzymatic and histological methods. ISP was administered in two subcutaneous injections (50 mg/100 Gm body weight) at a 24 hour interval. At the peak of the necrotic process (48 hrs after the first injection), the heart was subjected to enzymatic or histological studies. Thus, a group of infarcted animals (n = 25) and their controls (n = 15) underwent the assessment of creatine kinase (CK) content in the homogenate of the myocardium. Another group of animals (n = 15) was used for histological observations, including measurement of infarct size by planimetry from histological sections. A good relationship was observed between the percentage of necrotic tissue calculated on the basis of CK values (69.11 +/- 2.39%) and the infarction area assessed by planimetry (72.37 +/- 2.69%) (mean +/- standard error of the mean [SEM]). Thus, the present study confirms that ISP-induced myocardial lesions are a simple and reliable model for experimental infarct. Moreover, the assessment of the CK content in the heart is correlated with histological studies by planimetry, and is suggested as a direct enzymatic method to quantify the extent of myocardial necrosis.

Animals↗