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Biomedical subjects

C Fiorentini

Publications and source records attributed to C Fiorentini.

At least 145 records · Page 8Linked to original sources
PubMed1987

The lesser circulation in patients with systemic hypertension.

The elevated blood pressure and vascular resistance in patients with systemic hypertension are paralleled by a proportional rise in pressure and resistance in the lesser circulation. We evaluated the hypothesis that the increased systemic reaction to adrenergic stimulation is shared by the pulmonary vessels. For this purpose we investigated nine normotensive subjects and 24 patients with moderate primary hypertension during mental arithmetic and the cold pressor test. Both groups responded to both stimuli, with a pressure reaction that during arithmetic was mediated through an increase of cardiac output, and a reaction during the cold pressor test mediated through a predominant rise in systemic vascular resistance. The pressure changes were emphasized in the hypertensive population. Pressure in the pulmonary artery in normotensive subjects was not affected by cold and was slightly raised (systolic) during arithmetic. In hypertensive patients, on the other hand, systolic and diastolic pressures were consistently augmented by both tests, and pulmonary arteriolar resistance rose by 42% and 29% of control during the cold pressor test and arithmetic, respectively. Changes in resistance reflected neurally mediated vasoconstriction and not variations in the passive relationship between pressure and flow, since during arithmetic, for a similar rise in flow the driving pressure across the lungs was steady in normotensive subjects and rose significantly in hypertensive patients. In these same patients pressure was augmented by cold in the absence of substantial changes in flow. At baseline and during tests pulmonary wedge pressure, pleural pressure, arterial blood gases, and pH were similar in the two populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Hypersensitivity of lung vessels to catecholamines in systemic hypertension.

Among patients with primary systemic hypertension pressure and arteriolar resistance in the pulmonary circulation exceed normal values and are hyper-reactive to sympathetic stimulation. A study was therefore carried out in 16 patients with uncomplicated essential hypertension and nine healthy subjects to compare the pulmonary vascular reactivity to exogenous catecholamines. In the normotensive group the dose response relation to adrenaline (microgram: dyn) was 1 = -4, 2 = -9, 3 = -9, and 4 = -10 and to noradrenaline 2 = +3, 4 = /8, 6 = +4, and 8 = +3. The relations in the hypertensive subjects were 1 = +18, 2 = +42, 3 = +59, and 4 = +77 and 2 = +39, 4 = +54, 6 = +76, and 8 = +100, respectively. Group differences were highly significant. Cardiac output (blood flow through the lungs) was raised by adrenaline and reduced by noradrenaline. In either case the driving pressure across the lungs was significantly augmented in the hypertensive patients but not in the normotensive group. Both catecholamines had a vasoconstrictor effect on the pulmonary circulation as a result of vascular over-reactivity. The opposite changes in resistance between normal and hypertensive subjects produced by adrenaline suggest that a constrictor vascular hypersensitivity occurs in the pulmonary circulation with the development of systemic high blood pressure.

Adult↗
PubMed1986

Morphometric characterization of NK cell subset expressing the Leu-11 antigen in comparison to Leu-7 positive, 11 negative cells.

Three subpopulations of human natural killer (NK) cells were identified by immunoelectron microscopy, using combinations of anti-Leu-7 and anti-Leu-11 monoclonal antibodies. For each subpopulation the nuclear area/cellular area ratio (An/Ac) and the perimeter/equivalent circumference ratio were evaluated employing an interactive image analyzer. Leu-11+ cells showed a larger area, a smaller An/Ac and a higher "villousity degree" in comparison to Leu-7+, 11- cells. These differences were proved to be significant using the Kolmogorov-Smirnov two sample test. Previous studies described the existence of distinct cytotoxic capability, recombinant interleukin 2-mediated activation, and ultrastructural features of Leu-11+ in comparison to Leu-7+, 11- cells. This is the first report in which morphometric differences within NK cell subsets are exactly determined.

Antibodies, Monoclonal↗
PubMed1986

Pulmonary vascular supersensitivity to catecholamines in systemic high blood pressure.

Pulmonary pressure and arteriolar resistance are elevated in uncomplicated primary systemic hypertension. This study was carried out in 16 men with this form of hypertension and in 9 healthy men to compare 1) their pulmonary vascular reactivity to endogenous catecholamines released during mental arithmetic and cold pressor tests, and 2) the dose-response relation to exogenous epinephrine and norepinephrine. Arithmetic and cold pressor tests were associated, respectively, with a predominant increase in plasma epinephrine and norepinephrine concentration; changes were significantly greater in hypertensive men. During the two tests, pulmonary arteriolar resistance in the normotensive group was reduced by 13% and augmented by 7% of baseline, respectively, whereas it was raised by 31 and 70%, respectively, in the hypertensive group. In normal subjects, the dose (microgram)-response (delta dynes) relation to epinephrine was 1 = -4, 2 = -9, 3 = -9 and 4 = -10; to norepinephrine it was 2 = +3, 4 = +6, 6 = +7 and 8 = +7. In hypertensive patients, the respective relations were 1 = +18, 2 = +44, 3 = +59 and 4 = +77; and 2 = +39, 4 = +54, 6 = +76 and 8 = +98. Group differences were highly significant. In each of these circumstances, the driving pressure across the lungs was significantly augmented in the hypertensive but not the normotensive group. Both epinephrine and norepinephrine have a vasoconstrictor influence on the lesser circulation as a consequence of vascular overreactivity. The opposite changes in resistance between normotensive and hypertensive subjects produced by epinephrine suggest that a constrictor vascular supersensitivity becomes active in the pulmonary circuit with the development of systemic high blood pressure.

Blood Pressure↗
PubMed1986

Calcium channel blockade with nifedipine reduces the systemic and the pulmonary vascular reactivity to adrenergic activation in hypertension.

In hypertension the systemic and the pulmonary circulation show exaggerated vascular tone and responsiveness to adrenergic stimuli. In 22 hypertensive men we tested whether the regulation of the two vascular beds is improved by calcium entry blockade with nifedipine. Mental arithmetic raised epinephrine plasma concentration (by 80%), cardiac output (CO) and blood pressure in both circuits, and caused systemic vasodilatation and pulmonary vasoconstriction. After the drug the epinephrine reaction was diminished (+20%), variations in CO and systemic blood pressure were almost unchanged and pulmonary vasoconstriction was abolished. A cold pressor test increased norepinephrine plasma concentration (by 24%), systemic and pulmonary pressure and resistance and did not alter CO. The norepinephrine response to cold was enhanced (+35%) by nifedipine, while systemic and pulmonary resistance rises were importantly attenuated (from +24% to +7% and from +41% to +1%, respectively), and greatly diminished the pressure reactivity. A sympatho-adrenal modulation by calcium blockade, per se, might have restrained the vasomotion during arithmetic. The impressive attenuation of the constrictor responses to cold, which was possibly associated with a potentiated sympathetic drive, prospects that the two circuits share a vascular contractile disorder in which calcium ions are involved.

Adult↗
PubMed1985

Intrarenal beta-receptor and renal baroreceptor interaction in the control of the renin response to transient reduction of the renal perfusion pressure in man.

We have examined the mechanisms mediating the release of renin elicited in man by reduction of renal perfusion pressure. Fifteen patients with essential hypertension and six normotensive subjects were investigated during diagnostic renal arteriography. Renal neural receptors were inhibited by propranolol (10 mg i.v.) and activated by a standard cold pressor test. Vascular receptors were stimulated by unilateral reduction of renal perfusion pressure by 50%, using a balloon-tipped catheter. The stimulus caused release of renin. In hypertensives, arterial plasma renin increased by 44, 69 and 73% of control at 5, 15 and 30 min, respectively. Adrenergic activation by cold raised the arterial and the renal venous renin by approximately 50% of control and caused a fourfold rise when it was combined with the arterial obstruction. Following propranolol the renin response to reduction of the renal perfusion pressure was delayed and reduced, and cold stimulation, both alone and in combination with arterial obstruction, failed to stimulate renin release. Findings were qualitatively and quantitatively similar in the normotensive group. This study supports the hypothesis that the renin response to reduction of renal perfusion pressure in man results from an interaction of adrenergic and vascular receptors. It cannot be stated whether the former are synergistic or supplementary to the latter, even though adrenergic activation by cold stimulation provides evidence that a synergism between the two may exist.

Adult↗
PubMed1985

Limits of antifungal prophylaxis by ketoconazole in leukemic patients.

Serum ketoconazole levels in leukemic patients, subjected to ketoconazole prophylaxis, were determined by an agar diffusion assay. High individual variability of drug concentration was noted. In addition, the highest drug concentration observed was less than 1 microgram/ml in 5 out of 6 patients studied. The reliability of prophylaxis of airborne opportunistic fungal infections by ketoconazole seems, therefore, to be hampered, at least in leukemics, by the too low serum concentrations of the drug. The bioassay proved to be highly reproducible and accurate as well as easy and safe to perform.

Adult↗
PubMed1982

Circulatory response to prenalterol in normal subjects and in patients with primary congestive cardiomyopathy.

Experimental pharmacology indicates that prenalterol is a selective beta 1-adrenoceptor activator. In 5 normal individuals, 15 minutes after the drug (infused at a dose of 15 micrograms/kg over 5 min) the following circulatory changes were seen: a) increase of cardiac index (+31%), heart rate, stroke index, systolic aortic pressure, left and right ventricular mean rate of ejection and mean rate of the pressure rise in either ventricle during the pre-ejection phase; b) reduction of systemic vascular resistance (-18%), appearance, built-up and disappearance times in the left ventricular dye dilution curves. Pulmonary systolic, diastolic and wedge pressures and vascular resistance did not vary consistently. The circulatory effects persisted almost unchanged 30 minutes after the infusion. In a group of 5 patients with heart failure due to primary congestive cardiomyopathy, refractory to conventional therapy, the haemodynamic response to prenalterol (infused at a dose of 30 micrograms/kg over 5 min) was qualitatively similar to that of normal subjects in 3 cases. In 2 other patients cardiac performance deteriorated. The reasons for this paradoxical effect were not identified. These preliminary results suggest that prenalterol is a potent selective inotropic agent in man, that may assist in the therapeutic management of refractory heart failure due to congestive cardiomyopathy. However, careful haemodynamic monitoring is advisable for its use in this dysfunction until broader clinical experience can be accumulated.

Adrenergic beta-Agonists↗
PubMed1982

Evidence of a shared mechanism of vasoconstriction in pulmonary and systemic circulation in hypertension: a possible role of intracellular calcium.

We investigated the hemodynamics of the greater and lesser circulation in 35 patients with primary hypertension, as well as the effects of calcium-channel blockade, to test whether a common factor may account for the excessive vascular resistance in the two circuits and whether intracellular calcium concentration ([Ca++]i) may be involved. We proved that (1) elevated pulmonary arteriolar resistance (PAR) is not related to pulmonary blood flow and volume, pleural pressure, arterial oxygen or carbon dioxide tension and pH, left ventricular filling pressure and function; (2) systemic vascular resistance (SVR) significantly correlates with PAR; (3) calcium-channel blockade with nifedipine reduces systemic and pulmonary arterial pressures toward normal and significantly lowers both SVR and PAR; (4) the percent decrease in vascular resistance after nifedipine is related to the baseline level of resistance in both the greater and the lesser circulations. Failure of the mechanisms currently indicated as responsible for pulmonary vasoconstriction to explain convincingly the increased PAR, the correlation between SVR and PAR, as well as the qualitatively similar response to calcium-channel blockade suggest that a common factor produces vasoconstriction in the two circuits. A pathogenetic role of a primary disorder in [Ca++]i cannot be excluded, but remains to be proved.

Blood Pressure↗
PubMed1981

Circulatory and renin responses in man to unilateral reduction of the renal perfusion pressure.

This study is concerned with the mechanisms of human renovascular hypertension. Unilateral partial occlusion of a renal artery was accomplished using a balloon-tipped catheter for occlusive angiography in seven normotensive and 17 primary hypertensive subjects. The renin and circulatory responses were studied during a 60 min reduction of the renal perfusion pressure (RPP) by 50% of control. This stimulus was considered to be safe and strong enough to produce a three to four-fold rise in plasma renin activity. It was observed that: a) systemic (arterial) renin was significantly raised at 5 min, reached a peak at 15 min and continued to be significantly higher than the baseline until the occlusion was removed; b) venous renin and venous arterial difference on the occluded side became elevated after the stimulus and remained so for the duration of the occlusion; c) renin release from the contralateral kidney became partially inhibited; d) in no case did systemic arterial pressure, heart rate or cardiac output change during the studies; e) renin and circulatory patterns were similar in normotensive and hypertensive subjects. It is concluded that in humans unilateral RPP reduction duplicates the renin pattern of the Goldblatt kidney, but does not duplicate the circulatory response. This evidence applies to a 1 h renal artery occlusion and does not exclude the possibility that renin may have a role in a rise in blood pressure following renal artery stenosis of longer duration.

Blood Pressure↗