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Biomedical subjects

P Mattei

Publications and source records attributed to P Mattei.

At least 37 records · Page 2Linked to original sources
PubMed1996

Cardiovascular characteristics in normotensive subjects with or without family history of hypertension.

The aim of our study was to evaluate whether initial changes of cardiovascular structure and/or function can be detected in young normotensive subjects with (F+) and without (F-) family history of hypertension. Thirty-two subjects (19 F+, 10 males and 9 females, age range 17-32 years; 13 F-, 6 males and 7 females, age range 19-33 years) were studied. In each subject 24 hours ambulatory blood pressure monitoring, a M-mode, 2d guided and pulsed doppler echocardiogram and postischemic forearm strain gauge plethysmography were performed. The two groups of subjects did not differ for causal systolic and diastolic BP and 24 hours systolic and diastolic ambulatory monitored blood pressure. No differences in LV end-diastolic and end-systolic diameters, as well as in LV wall thickness, and in LV mass index were observed. Systolic functional parameters were also similar in the two groups. In F+ subjects peak early filling velocity was reduced in respect to F- (p < 0.01), peak late filling velocity integral was increased (p < 0.05) and the ratio of peak E/peak A integrals was decreased (p < 0.05). No difference was observed for postischemic forearm blood flow and minimal vascular resistance, taken as an index of arteriolar structural changes as well as intima-media thickness of carotid arteries. In conclusion in this study F+ and F- had similar BP values, LV mass and min VR; differences previously observed in LV mass between F+ and F- may have been due to the presence of different basal levels of BP; in F+ LV diastolic filling, although still in the normal range, shifted early toward the pattern of LV filling usually observed in hypertensive patients.

Adult↗
PubMed1995

Effect of insulin on acetylcholine-induced vasodilation in normotensive subjects and patients with essential hypertension.

BACKGROUND: The present study was designed to directly test the vasodilation action of insulin and its relation to endothelium-dependent mechanisms. METHODS AND RESULTS: In 18 normotensive subjects and 27 patients with untreated mild to moderate essential hypertension, we studied the effect of intrabrachial insulin on the changes in forearm blood flow (strain-gauge plethysmography) induced by intrabrachial acetylcholine (at doses of 0.15, 0.45, 1.5, 4.5, and 15 micrograms.min-1.dL-1), an endothelium-dependent vasodilator, or sodium nitroprusside (at doses of 1, 2, and 4 micrograms.min-1.dL-1), and endothelium-independent vasodilator. Local hyperinsulinemia (deep venous plasma insulin, 48 +/- 6 and 51 +/- 5 microU/mL in control subjects and hypertensive patients, respectively) did not affect basal forearm blood flow and stimulated forearm glucose extraction (control subjects, 3 +/- 1% to 11 +/- 2%, P < .001; hypertensive patients, 3 +/- 1% to 6 +/- 1%, P < .001; P < .01 for the between-group difference). In both normotensive and hypertensive subjects, insulin significantly potentiated acetylcholine-induced vasodilation, whereas it did not alter the vasodilatory response to sodium nitroprusside. NG-monomethyl-L-arginine, an inhibitor of endothelial nitric oxide synthesis, blunted insulin-induced facilitation of acetylcholine vasodilation in normotensive but not in hypertensive subjects. In contrast, in hypertensive patients but not in normotensive control subjects, the potentiation of the vascular response to acetylcholine induced by local hyperinsulinemia was abolished by intrabrachial ouabain, an inhibitor of Na(+)-K+ pump. CONCLUSIONS: In healthy humans and essential hypertensive patients alike, local physiological hyperinsulinemia per se does not increase forearm blood flow but potentiates the vasodilation induced by acetylcholine regardless of metabolic insulin resistance. This effect is endothelium-dependent because it is not seen with nitroprusside and is related to the L-arginine-nitric oxide pathway in normotensive subjects and to smooth muscle cell hyperpolarization in essential hypertensive patients.

Acetylcholine↗
PubMed1995

Aging and endothelial function in normotensive subjects and patients with essential hypertension.

BACKGROUND: Experimental data from normotensive and hypertensive animals indicate that aging is associated with impaired endothelium-dependent relaxations to acetylcholine, and this possibility appears to be confirmed in the human coronary artery. In the present study, we evaluated the effect of age on endothelial responsiveness in the forearm vessels of either normotensive control subjects or essential hypertensive patients. METHODS AND RESULTS: Within the normotensive or hypertensive group (n = 53 and n = 57, respectively), subjects were selected with similar blood pressure, plasma cholesterol, and glucose values, and hypercholesterolemic subjects, diabetics, and smokers were excluded. We evaluated forearm blood flow (by strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 micrograms/100 mL per minute), an endothelium-dependent vasodilator, and sodium nitroprusside (1, 2, and 4 micrograms/100 mL per minute), an endothelium-independent vasodilator. Acetylcholine caused a dose-dependent vasodilation that was significantly (P < .01) lower in essential hypertensive patients than in normotensive control subjects. However, a significant negative correlation was observed between acetylcholine-induced vasodilation and patient age in both normotensive (r = -.86, P < .001) and hypertensive (r = -.85, P < .001) patients. In contrast, vasodilation to sodium nitroprusside was similar in normotensive control subjects and essential hypertensive patients with a poorer inverse correlation with patient age (normotensive control subjects, r = -.37; hypertensive patients, r = -.36) compared with acetylcholine. CONCLUSIONS: The present data indicate that there is a blunted response to acetylcholine with advancing age in both normotensive control subjects and essential hypertensive patients, suggesting that aging is associated with reduced endothelium-dependent vasodilation in humans.

Acetylcholine↗
PubMed1995

Humoral and haemodynamic effects of idrapril calcium, the prototype of a new class of ACE-inhibitors, in essential hypertensive patients.

Idrapril is the prototype of a new class of ACE inhibitors, characterised by the presence of a hydroxdmic group. Six untreated in-patients with essential hypertension were given single oral doses of the calcium salt of idrapril, idrapril calcium (200 mg) and placebo according to a double blind, randomised experimental design. Supine and upright blood pressure, heart rate, plasma idrapril serum UCE, active renin and angiotensin II were measured at timed intervals for 24 hours after dosing. Plasma idrapril reached a peak after 2 hours (3.01 microgm x ml(-1)), and by 12 hours the compound had almost disappeared (67 ng x ml(-1)). Derived t1/2 was 1.4-2.2 h. ACE activity was suppressed [from 77.9 to 3.3 after 2 hours and 11.8 after 12 hours nmol(-1) x min(-1) x ml] and angiotensin II production inhibited [from 8.8 to 3.1 (after 1 hour) and 7.5 (after 24 hours) pg x ml(-1)]. Compared to placebo, idrapril calcium significantly lowered both supine blood pressure starting at 4 hours (idrapril calcium 140/93 mmHg; placebo 157/101 mmHg; placebo 147/100 mmHg), and upright blood pressure starting at 3 hours (idrapril calcium 135/95 mmHg; placebo 147/100 mmHg) up to 24 hours (idrapril calcium 132/92 mmHg; placebo 145/100 mmHg). Idrapril calcium appears to be an effective ACE inhibitor in essential hypertension, with a hypotensive action for up to 24 h.

Absorption↗
PubMed1995

Lack of correlation between microalbuminuria and endothelial function in essential hypertensive patients.

OBJECTIVE: To evaluate whether microalbuminuria, defined as urinary albumin excretion between 30 and 300 mg/24 h, is associated with endothelial dysfunction in essential hypertensive patients. DESIGN: We correlated urinary albumin excretion with vasodilatation in response to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) agonists in the forearm vascular bed in essential hypertensive patients with (n = 13) and without (n = 23) microalbuminuria and matched normotensive controls (n = 21). METHOD: We studied forearm vascular responses (strain-gauge plethysmography) to intrabrachial infusion of acetylcholine (0.15, 0.45, 1.5, 4.5 and 15 ng/100 ml forearm tissue/min) and of sodium nitroprusside (1, 2, 4ng/100 ml forearm tissue per min). Minimal forearm vascular resistances (the ratio between mean arterial pressure and maximal forearm vasodilation induced by 13 min of ischaemia + 1 min of exercise) were also evaluated. RESULTS: Responses to acetylcholine, but not to sodium nitroprusside, were significantly blunted and minimal forearm vascular resistances were increased in hypertensive patients compared with controls. However, no correlation was found between urinary albumin excretion and vasodilatation in response to acetylcholine or to sodium nitroprusside or between urinary albumin excretion and minimal forearm vascular resistances. CONCLUSIONS: In hypertensive patients, increased urinary albumin excretion is associated neither with functional nor with structural dysfunction in the forearm vasculature.

Acetylcholine↗
PubMed1995

Angiotensin II and sympathetic activity in sodium-restricted essential hypertension.

Angiotensin II (Ang II) potentiates sympathetic neurotransmission by presynaptic facilitation of norepinephrine release. We investigated whether endogenous Ang II modulates peripheral sympathetic activity in sodium-depleted essential hypertensive patients. We evaluated the effect of intrabrachial infusion of saralasin, an Ang II antagonist (5 micrograms/100 mL forearm tissue per minute), and benazeprilat, an angiotensin-converting enzyme inhibitor (2 micrograms/100 mL forearm tissue per minute), on forearm vasoconstriction (measured by strain-gauge venous plethysmography) induced by the application of lower body negative pressure (-10 mm Hg for 5 minutes). Both saralasin and benazeprilat (n = 6 for each group) blunted the vasoconstrictor action of lower body negative pressure, suggesting that circulating Ang II modulates peripheral sympathetic activity. In addition, since beta-adrenoceptor stimulation can activate the production of vascular Ang II, the effect of saralasin and benazeprilat on lower body negative pressure application was evaluated in the presence of isoproterenol (0.09 microgram/100 mL forearm tissue per minute) and propranolol (10 micrograms/100 mL forearm tissue per minute). In two other groups of hypertensive patients, isoproterenol infusion increased the release of Ang II in the forearm vasculature (arteriovenous values measured by radioimmunoassay). Furthermore, isoproterenol potentiated lower body negative pressure-induced vasoconstriction. This facilitating effect was abolished by either saralasin or benazeprilat (n = 6 for each group). In contrast, in two further groups of patients (n = 6 for each group), in the presence of the beta-blocker propranolol saralasin and benazeprilat did not alter the vasoconstrictor action of the endogenous sympathetic stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Three-dimensional in vivo planum temporale reconstruction.

We describe a new multistep technique for three-dimensional reconstruction and analysis of the in vivo planum temporale (PT) based on the manipulation of magnetic resonance raw data obtained with a special protocol. Measurements of left and right plana confirm previous neuroanatomical descriptions of a larger left planum temporale. This method can be easily adopted, allowing anatomically valid PT measurements.

Adult↗
PubMed1994

Magnetic resonance imaging findings of amygdala-anterior hippocampus shrinkage in male patients with schizophrenia.

Recent magnetic resonance imaging (MRI) studies found abnormalities of medial temporal lobe and basal ganglia structures. We used an inversion recovery (IR) protocol with the assistance of the Talairach atlas to identify neuroanatomical regions of interest in 19 male schizophrenic patients and 14 matched control subjects. The patient group showed smaller amygdala-hippocampus volume as compared with normal control subjects. This finding was more pronounced for the left side, although no diagnosis X side interaction was present. Third ventricle volume was also enlarged in schizophrenic patients. Trends toward an overall reduction of basal ganglia (striatum and lenticular nucleus) and limbic structures and toward an increase in ventricle-brain ratio were also seen. The study confirms previous evidence of mesial temporal lobe shrinkage, more evident on the left side in a group of relapsing noninstitutionalized male schizophrenic patients.

Adult↗
PubMed1994

Vascular renin-angiotensin system and sympathetic nervous system activity in human hypertension.

Experimental data indicate the existence of a vascular tissue renin-angiotensin system in several different vessels from various animal models. Active renin can be locally synthesized into the vessel wall or taken up from circulating plasma to produce vascular angiotensin II. Using the human forearm technique, we produced evidence indicating the release of active and inactive renin and of angiotensin II from the vessels of hypertensive patients. Moreover, the production of vascular angiotensin II seems to be strictly correlated to the circulating renin profile, suggesting the possibility that vascular renin might be at least partially taken up from plasma. To investigate a possible function of the vascular renin-angiotensin system, we studied its interaction with sympathetic neurotransmission in essential hypertensive patients. In line with animal studies, vascular angiotensin II increases the vasoconstriction induced by the stimulation of the sympathetic nervous system through the potentiation of noradrenaline release at a presynaptic level, and this effect seems to be mediated by beta-adrenoceptor activation. This facilitating effect on sympathetic neurotransmission exerted by vascular angiotensin II can be antagonized by both angiotensin II antagonists and angiotensin-converting enzyme inhibitors.

Blood Vessels↗
PubMed1994

Rupture of the right diaphragm following blunt trauma in an infant: case report.

Traumatic diaphragmatic rupture is a rare childhood injury and is often difficult to diagnose. This is particularly true in infants. We present the case of a 3-month-old infant with traumatic rupture of the right diaphragm that became clinically apparent only after extubation. The diagnosis can often be made on the basis of chest radiography and clinical signs. Surgical treatment is required. Some phrenic nerve injuries can be anticipated and late sequelae may result.

Female↗
PubMed1994

Effect of potassium on vasodilation to acetylcholine in essential hypertension.

Patients with essential hypertension show impaired endothelium-dependent vasodilation induced by acetylcholine. Because dietary potassium supplementation increases endothelium-dependent relaxations to acetylcholine in hypertensive rats, we designed the present study to investigate whether potassium increases endothelium-dependent vasodilation in essential hypertensive patients. Therefore, in patients with essential hypertension (n = 13) and in normotensive control subjects (n = 13) we evaluated the effect of intrabrachial potassium chloride (0.2 mmol/min) on forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 micrograms/100 mL forearm tissue per minute). In both groups of patients, potassium chloride infusion augmented local plasma potassium concentrations. Furthermore, in essential hypertensive patients but not in normotensive subjects it increased the vasodilating effect of the first three infusion rates of acetylcholine. In contrast, in seven adjunctive essential hypertensive patients, potassium chloride did not alter intrabrachial sodium nitroprusside-induced forearm vasodilation (1, 2, and 4 micrograms/100 mL forearm tissue per minute). Finally, to evaluate the role of nitric oxide on potassium-dependent facilitation of acetylcholine-induced vasodilation in essential hypertension, we studied the effect of intrabrachial NG-monomethyl L-arginine (100 micrograms/100 mL per minute) in another group of seven hypertensive patients. Vasodilation to acetylcholine was again increased by potassium chloride; NG-monomethyl L-arginine slightly blunted the vasorelaxing effect of acetylcholine but abolished the potentiating effect of potassium.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Information processing strategy to remediate Wisconsin Card Sorting Test performance in schizophrenia: a pilot study.

A modified procedure for administering the Wisconsin Card Sorting Test, focusing on a hypothesized deficit of organizational strategy in information processing, was used to administer the test to 20 schizophrenic patients. By using this procedure, 61.5% of the poor performers (eight of 13) were dramatically transformed into good performers without any task instruction or reinforcement. The results, albeit preliminary, support the hypothesis and the possibility of remediating the task performance of some schizophrenic patients.

Adult↗
PubMed1994

Chronic and recurrent appendicitis are uncommon entities often misdiagnosed.

Those having chronic and recurrent appendicitis represent a small portion of patients with disorders of the appendix. We present a series of nine patients who underwent appendectomy for chronic or recurrent appendicitis at The Johns Hopkins Hospital, Baltimore, Maryland, between July 1984 and October 1992. There were seven women and two men (median age of 30 years, range of 15 to 63 years). All patients presented with pain in the right lower quadrant or lower abdomen of three or more weeks duration (mean of 16.0 +/- 8.4 months, range of three weeks to seven years), had no alternative diagnosis to account for the symptoms, had pathologic evidence of chronic inflammation or fibrosis of the appendix and had complete relief of the symptoms after appendectomy. Although the patients presented herein had clinical and pathologic evidence for recurrent or chronic appendicitis, careful review of the course of each patient before surgical referral revealed at least one episode of acute pain in the abdomen consistent with acute appendicitis managed by nonoperative means. This suggests that, while recurrent acute appendicitis and chronic appendicitis do occur, they can be avoided by the accurate diagnosis and operative management of acute appendicitis. We conclude that acute appendicitis can resolve spontaneously and recur repeatedly in the same individual; in the evaluation of a patient with abdominal pain, a history of prior similar episodes of pain should never dissuade one from considering the diagnosis of acute appendicitis, and recurrent acute appendicitis and chronic appendicitis should be considered in the differential diagnosis of recurrent pain in the lower abdomen.

Acute Disease↗