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Biomedical subjects

A Virdis

Publications and source records attributed to A Virdis.

65 records · Page 4Linked to original sources
PubMed1992

Adenosine activates a vascular renin-angiotensin system in hypertensive subjects.

In vitro data indicate that the activation of A2 adenosine receptors increases renin release by the accumulation of cyclic AMP. Because in human forearm vessels beta-adrenergic receptor stimulation causes the local release of renin and angiotensin II through the increase of cyclic AMP, we evaluated in six essential hypertensive subjects whether adenosine can release vascular angiotensin II. Adenosine was infused into the brachial artery at cumulatively increasing doses (0.5, 1.5, and 5 micrograms/100 ml forearm tissue per minute for 5 minutes each) during saline infusion and in the presence of the adenosine antagonist theophylline (100 micrograms/100 ml forearm tissue per minute for 15 minutes), while venous (ipsilateral deep forearm vein) and arterial (brachial artery) angiotensin II (picograms per milliliter) were measured at the end of each infusion period, and forearm angiotensin II net balance (picograms per minute) was calculated by venous-arterial differences corrected for forearm blood flow (strain-gauge venous plethysmography) and hematocrit. In control conditions, adenosine, at higher doses, caused a dose-dependent vasodilation and increased venous angiotensin II without affecting arterial values; therefore, the calculated angiotensin II net balance showed an adenosine-mediated dose-dependent release. Theophylline pretreatment blunted adenosine-mediated forearm blood flow increments and angiotensin II release. The local origin of angiotensin II was further confirmed in another group of six hypertensive subjects in whom the angiotensin converting enzyme inhibitor captopril, locally infused at the rate of 2.5 micrograms/100 ml forearm tissue per minute for 15 minutes, abolished the adenosine-mediated venous angiotensin II increments. Our data indicate that exogenous adenosine can stimulate the production of angiotensin II in the forearm vessels of hypertensive patients.

Adenosine↗
PubMed1990

Analysis of central cardioarrhythmogenic triggers in experimental epilepsy.

The cardioarrhythmogenic potential of epileptic foci induced at mesencephalic and rhombencephalic levels was analyzed in hemispherectomized rats. Topical application of penicillin-G onto the mesencephalic quadrigeminal lamina or onto the fourth ventricle induced paroxysmal activity at the mesencephalic or bulbar neurone level. At the mesencephalic levels, the paroxysmal activity was characterized by a significant increase in the spontaneous frequency of the neurones, with the appearance of multiunit activity and rhythmical outbursts. The simultaneous recording of myocardial electrical activity and blood pressure showed that the paroxysmal activity triggered short-latency sinus bradyarrhythmias with wandering of the sinus pacemaker, the appearance of biphasic or negative P waves, some premature ventricular contractions and non-significant reduction of systolic and diastolic pressures. When the paroxysmal activity stopped, the cardiac rhythm and blood pressure returned to basal values. At the bulbar level, the paroxysmal activity appeared with longer latency and usually the rhythmical outbursts were not observed. Following bulbar paroxysmal activity only short-lasting episodes of sinus bradyarrhythmias appeared. Midcollicular transection eliminated paroxysmal activity at the bulbar level, and blood pressure and cardiac rhythm resumed basal values. After transection, an additional application of convulsant drug (penicillin-G or pentylenetetrazole) onto the fourth ventricle did not induce the reappearance of paroxysmal activity and the consequent cardiovascular alterations. The results showed the existence of a cardioarrhythmogenic trigger localized at the mesencephalic level which spreads paroxysmal activity upwards. A hypothesis to explain the appearance of fetal haemodynamic modifications and life-threatening arrhythmias has been proposed.

Animals↗
PubMed1990

[Circadian rhythm of spontaneous ventricular arrhythmias in elderly patients with myocardial ischemia at low risk for sudden death].

In 26 patients (65-80 yr) with low risk of sudden death, the circadian rhythm of spontaneous ventricular arrhythmias was analyzed, throughout 72 h, by the Holter monitoring method. The prolonged ECG monitoring is indispensable to evaluate the real necessity of an antiarrhythmic therapy and to establish the therapeutic approach. Premature ventricular complexes (PVC): isolated, couplets and runs of ventricular tachycardia have been considered. The isolated PVC showed uniform distribution throughout 24h, with higher frequency/hour ratio (f/h) in females. Couplets and runs showed circadian diurnal distribution with higher f/h ratio in smokers and males. After analysis of the results, the patients were additionally subdivided into smokers and non-smokers. Since smokers showed a diurnal distribution of all kinds of arrhythmias, antiarrhythmic drugs whose pharmacological peak corresponds to the distribution peaks of arrhythmias were proposed. Non-smokers could be divided into two groups: a) patients with isolated extrasystoles which did not show a circadian rhythm of arrhythmias and who must be treated with retard-drugs, which give protection throughout 24h; b) patients with runs or couplets of PVC showing a circadian rhythm of arrhythmias and who must be treated with drugs whose pharmacological peak corresponds to the distribution peaks of arrhythmias.

Aged↗
PubMed1989

[Carcinoid tumor in Meckel's diverticulum].

The accidental finding of a carcinoid tumour in Meckel's diverticulum, a very uncommon event, triggered a physiopathological and clinical analysis of this very interesting but very rare association. The value of systematic identification and removal of the diverticulum during laparotomy is underlined.

Carcinoid Tumor↗
PubMed1989

[Intraoperative pancreatic echography].

The US intraoperative diagnostic procedure is useful either for the higher sensitivity rate or for the surgical decision making. The Authors' intraoperative diagnostic experience in pancreatic diseases is reported: 23 exocrine and endocrine neoplasms, 3 chronic pancreatitis and 8 acute pancreatitis cases are discussed.

Humans↗
PubMed1989

[Determination of the range of physiologic variation of the electrical axes using P, QRS, and T waves in pregnancy].

Since functional overload in pregnancy frequently induces the appearance of symptoms that could arouse suspicion of myocardiopathy, it is important to analyse and characterize all electrocardiographic modifications during a healthy subject's pregnancy. Variations of the mean electrical axis (A) of P, QRS and T waves were evaluated in 52 healthy volunteers, 17-37 years, during pregnancy. The A values were measured, in the frontal plane, at the end of both I and III quarter of pregnancy, using a method of scalar determination. The As in I and III quarters was compared with those observed in the post-partum (at 5th day) and statistical evaluations were performed (Student t-test for paired observations). In the I quarter the mean A was 40 +/- 3 degrees for P, 40 +/- 16 degrees for QRS and 32.5 +/- 9 degrees for T wave, whereas in the III quarter the mean A changed to 37 +/- 2 degrees for P, 34 +/- 18 degrees for QRS and 31 +/- 9 degrees for T. During pregnancy, all mean As significantly diverted to the left side, AP about 3 degrees, AQRS about 6 degrees and AT about 1.5 degrees. These results were also confirmed by analysis of A frequency distribution histograms. In the post-partum (5th day) the A resumed basal values (I quarter's values). These results show: i) the physiological range of AP, AQRS and AT, during pregnancy; ii) left deviation of all three As at the end of III quarter. It is possible to conclude that variation over this range, particularly for QRS, could give evidence of the onset of cardiopathy.

Adolescent↗
PubMedDate not supplied

[Chronic inflammation and endothelial dysfunction: analysis of a cohort of patients with SLE and UCTD].

OBJECTIVE: Cardiovascular complications, mainly caused by an accelerated atherosclerosis, are one of the leading causes of death and disability in patients with systemic autoimmune diseases. Endothelial dysfunction is considered the earliest and reversible step of atherogenesis. Aim of the present study is to investigate endothelial function (EF) in patients with systemic lupus erythematosus (SLE), undifferentiated connective tissue diseases (UCTD) and correlate the results with clinical and laboratory variables. METHODS: EF was assessed on the peripheral microcirculation by the perfused forearm technique that can estimate both endothelium- dependent and endothelium- independent vasodilatation. The same evaluation has been repeated in two patients after the administration of 20 mg of 6-metilprednisolone. RESULTS: Twenty-three female patients with SLE or UCTD, with a follow up of at least 1 year have been studied and compared with 8 healthy controls matched for epidemiological variables and traditional risk factors for cardiovascular disease. A significant reduction both in endothelium dependent than endothelium independent vasodilatation was observed in both patients groups compared with controls. In addition, UCTD patients demonstrated a significant reduction in the nitric oxide pathway compared with controls and SLE patients. Finally, steroid administration induced an improvement of vascular reactivity. CONCLUSIONS: Despite the well documented side effects of chronic corticosteroid therapy, our data might suggest a role for antinflammatory and immunosuppressive therapy in the prevention of premature atherosclerosis in patients with systemic autoimmune diseases.

Adult↗
PubMedDate not supplied

Endothelial dysfunction in hypertension.

Endothelium can deeply influence vascular tone and structure. The main endothelium derived factor is nitric oxide, which is not only a potent vasodilator but also inhibits platelet aggregation, smooth muscle cell migration and proliferation, monocyte adhesion and adhesion molecule expression, thus protecting the vessel wall against the development of atherosclerosis and thrombosis. In human hypertension, endothelial dysfunction has been documented in peripheral and coronary macro and microcirculation and in renal circulation. Impaired endothelium-dependent vasodilation associated with essential hypertension seems to be a primary phenomenon, since it can be detected in the offspring of essential hypertensive patients, shows no clear correlation with blood pressure value, and is not normalized by the mere reduction of blood pressure. The phenomenon responsible for endothelial alteration in essential hypertensive patients seems to be the activation of an alternative pathway involving cyclooxygenase which reduces NO availability through production of oxidative stress. This alteration in the NO pathway could be the main mechanism through which a dysfunctional endothelium could be a promoter of atherosclerosis and thrombosis in essential hypertension.

Endothelium, Vascular↗
PubMedDate not supplied

Endothelial function in hypertension.

Endothelial dysfunction has been documented both in the forearm and coronary beds of essential hypertensive patients. Impairment in the tonic release of nitric oxide (NO) is secondary to hypertension, while the alteration in agonist-induced endothelium-dependent vasodilation seems to be a primary defect caused both by an alteration of the L-arginine-NO pathway and the production of cyclooxygenase-dependent EDCFs, such as prostanoids or superoxide anions. These latter substances curtail endothelium-dependent vasodilation mainly by inactivating NO production. Although experimental data clearly indicate that the L-arginine-NO pathway participates in the regulation of renal hemodynamics and renal excretory function under basal and stimulated conditions, data in humans are scanty and confounded by methodological approaches. A posteriori interpretation of data obtained with intrarenal infusion of acetylcholine in kidney donors suggests that endothelium dependent vasodilation in the kidney is impaired by aging, a phenomenon well documented in the forearm and coronary circulation. Systemic infusion of L-arginine induced renal vasodilation and natriuresis in normotensive subjects, an effect which seems to be mediated mainly by intrarenal NO production. Moreover the few available data suggest that both renal vasodilation and renal production of NO in response to L-arginine are blunted in patients with essential hypertension and that superoxide anions, may be, at least partially, responsible for this alteration of the L-arginine-NO pathway. In conclusion, endothelial dysfunction has been well documented in the forearm and coronary circulation of patients with essential hypertension. Available data suggest that endothelial, dysfunction is also detectable in the kidney and that a common mechanism, probably superoxide anions, can account for this abnormality.

Arginine↗