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Biomedical subjects

C Vigorito

Publications and source records attributed to C Vigorito.

At least 55 records · Page 3Linked to original sources
PubMed1985

Carotid sinus reflex control of coronary blood flow in human subjects.

Systemic and coronary hemodynamics were assessed before and during a reduction in carotid transmural pressure. This reduction was induced by means of a pneumatic neck chamber in 15 normal subjects and 15 hypertensive patients with a normal coronary arteriogram. A reduced baroreflex responsiveness was demonstrated in hypertensive patients as compared with normal subjects by evaluating both the reflex bradycardia evoked by intravenous administration of phenylephrine and the reflex increase in blood pressure during carotid sinus hypotension. In normal subjects, the reduction in carotid transmural pressure induced a significant increase in mean blood pressure, total peripheral resistance, cardiac output, heart rate, coronary vascular resistance, coronary blood flow assessed by the continuous thermodilution method and myocardial oxygen consumption. In hypertensive patients, the same stimulus significantly increased mean blood pressure, cardiac output, heart rate and coronary blood flow while no significant change was detected in coronary vascular resistance and myocardial oxygen consumption. The increase in mean blood pressure, total peripheral resistance and cardiac output was significantly higher in normal subjects than in hypertensive patients. These results suggest that in normal subjects carotid sinus hypotension evokes reflex coronary vasoconstriction, whereas this response is blunted in hypertensive patients with reduced baroreflex sensitivity.

Adult↗
PubMed1985

Ketone body metabolism in normal and diabetic human skeletal muscle.

Although the liver is considered the major source of ketone bodies (KB) in humans, these compounds may also be formed by nonhepatic tissues. To study this aspect further, 3-[14C]hydroxybutyrate (BOH) or [3-14C]acetoacetate (AcAc) were constantly infused after a priming dose and contemporaneous arterial and venous samples were taken at splanchnic, heart, kidney, and leg sites in eight normal subjects (N) undergoing diagnostic catheterization and at the forearm site in five normal and six ketotic diabetic (D) subjects. After 70 min of infusion, tracer and tracee levels of AcAc and BOH reached a steady state in the artery and vein in both normal and diabetic subjects. The venous-arterial (V-A) difference at the forearm step for cold KB was negligible both in normal and diabetic subjects, whereas for labeled KB it was approximately 10-fold higher in diabetic subjects (V-A AcAc, -31 +/- 7 and -270 +/- 34 dpm/ml in N and D, respectively; V-A BOH, -38 +/- 6 and -344 +/- 126 dpm/ml in N and D, respectively). We assumed that the V-A difference in tracer concentration was consistent with dilution of the tracer by newly synthesized tracee inside the muscle and calculated that the forearm muscle produces KB at a rate of 16.2 +/- 3.3 mumol/min in D and 0.9 +/- 0.9 mumol/min in N. These findings can be accounted for by the hypothesis that the disappearance flux of KB from circulation was replaced by an equivalent flux of KB entering the vein at the muscle step in D but not in N. Moreover, in N KB were not only produced but also utilized by the splanchnic area (39 +/- 9 mumol/min).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1985

Histamine and human heart.

Heart fragments obtained from human right atrium contain 1.5 +/- 0.2 micrograms of histamine per gram of wet tissue. Human heart spontaneously synthesizes significant amounts of PGI2, PGF2 alpha, PGE2 and TxA2. The Ca2+ ionophore A 23187 (0.5-3 micrograms/ml) dose-dependently induces histamine release and prostanoid production. Histamine (0.5-1 micrograms/kg/min) infusion in 10 normal donors produced an increase in heart rate and a significant depression of the ST segment. Selective H1 receptor stimulation in patients undergoing cardiac catheterization resulted in a decrease of the mean aortic pressure and of coronary vascular resistance.

Basophils↗
PubMed1984

Influence of heart rate on exercise-induced R-wave amplitude changes in coronary patients and normal subjects.

In order to study whether different heart rates achieved at peak exercise by normal subjects and patients with coronary artery disease (CAD) affect the results of analysis of R-wave amplitude changes (delta R), we evaluated delta R at progressively increasing heart rate (HR) steps in 60 normal subjects with negative exercise tests (ET), in 130 patients with CAD, in 88 patients with true positive and 42 with false negative ET, and in 43 patients with no CAD and false positive ET. We found that the sensitivity and specificity of delta R were HR dependent, the former decreasing and the latter increasing with progressively increasing HR steps. Mean values of delta R did not discriminate among the four groups for HRs up to 150 bpm; significant differences were found between normal subjects and CAD patients, both with true positive and false negative stress tests, at HR greater than 150 bpm. False positive patients had mean delta R similar to those found in normal subjects. We hypothesize that quantitative delta R analysis could be useful in ECG diagnosis of false negative and false positive patients at HR greater than 150 bpm.

Coronary Disease↗
PubMed1984

Differential roles of splanchnic and peripheral tissues in the pathogenesis of impaired glucose tolerance.

To identify the mechanism(s) of the altered glucoregulatory response to a glucose load in subjects with impaired glucose tolerance, we selectively quantitated the components of net splanchnic glucose balance, i.e., splanchnic glucose uptake and hepatic glucose output, as well as peripheral glucose uptake, by combining [3-3H]glucose infusion with hepatic vein catheterization. After intravenous glucose infusion (6 mg X kg-1 X min-1 for 90 min), blood glucose rose to 172 +/- 7 mg/dl in controls and 232 +/- 13 mg/dl in subjects with impaired glucose tolerance (P less than 0.01). The response of plasma insulin did not differ significantly between the two groups (29 +/- 4 vs. 40 +/- 10 microU/ml at 90 min in control and in glucose intolerant subjects, respectively; P = NS). In both groups, glucose infusion caused the net splanchnic glucose balance to switch from the net output of the basal state to a net glucose uptake. However, this effect was more marked in subjects with impaired glucose tolerance than in control subjects (at 90 min: 2.83 +/- 0.53 vs. 1.60 +/- 0.18 mg X kg-1 X min-1, respectively: P less than 0.05). The different pattern of splanchnic glucose balance was entirely accounted for by a greater rise in splanchnic glucose uptake in the group of glucose intolerants , as the suppression of endogenous glucose output by the glucose load was practically complete in both groups. In contrast, glucose uptake by peripheral tissues increased considerably less in subjects with impaired glucose tolerance than in controls (2.2-2.6 vs 3.6-4.1 mg X kg-1 X min-1, respectively, between 60 and 90 min; P less than 0.01-0.001). Furthermore, a net splanchnic lactate uptake was present in the basal state, which was inhibited by the glucose load and switched to a comparable net lactate output in both groups. These results indicate that the mechanism responsible for the altered glucoregulation in subjects with impaired glucose tolerance resides entirely in the peripheral tissues whose ability to dispose of a glucose load is drastically reduced. On the other hand, no defect is detectable in any of the explored mechanisms regulating splanchnic glucose metabolism during the disposal of an exogenous glucose load.

Blood Glucose↗
PubMed1984

Direct assessment of splanchnic uptake and metabolic effects of human and porcine insulin.

The hepatic vein catheterization technique was used to quantitate the splanchnic uptake and the metabolic effects of biosynthetic human insulin (BHI) and porcine insulin (PI) in normal man. BHI and PI were infused into a peripheral vein (0.9-1.3 mU kg-1 min-1) for 60 min together with SRIH (0.6 mg/h) to inhibit endogenous insulin secretion and glucose to induce moderate hyperglycemia (9-10 mmol/liter). During the infusion period, arterial-hepatic venous difference of plasma C-peptide as well as splanchnic C-peptide output fell by more than 98% indicating virtually complete cessation of endogenous insulin release. Under these conditions, the arterial-hepatic venous differences in plasma insulin concentrations represent a valid and direct measurement of splanchnic insulin uptake. During BHI infusion, arterial insulin levels rose to 82 +/- 11 (SE) microU/ml (range: 33-105 microU/ml). Splanchnic insulin uptake paralleled the rise of arterial insulin, reaching 430 +/- 72 microU kg-1 min-1 at 60 min. No appreciable difference between BHI and PI was demonstrable. A highly significant correlation between arterial insulin concentrations and splanchnic insulin uptake was found (r = 0.816; P less than 0.001). Accordingly, both fractional splanchnic insulin extraction and splanchnic insulin clearance remained unchanged throughout insulin infusion and averaged 70 +/- 4% and 5.3 +/- 2 ml kg-1 min-1, respectively. With BHI infusion, splanchnic glucose balance (-8.5 +/- 0.9 mumol kg-1 min-1, basal) became positive (7.3 +/- 1 mumol kg-1 min-1). In contrast, basal splanchnic lactate uptake was inhibited by BHI and there was lactate production (from 3.4 +/- 0.9 to -1.7 +/- 1.4 mumol kg-1 min-1). Similar changes in splanchnic glucose and lactate metabolism occurred during PI infusion. These studies indicate that: 1) A considerable amount of insulin (70 +/- 4%) is extracted by the splanchnic bed on a single passage, after exogenous administration of either human insulin or PI; 2) over a physiological range of insulin concentrations (33-105 microU/ml) a linear relationship exists between arterial insulin concentrations and splanchnic insulin removal; and 3) BHI and PI do not differ appreciably with respect to their uptake and metabolic effects at the splanchnic level.

Adult↗
PubMed1984

Quantitative and qualitative analysis of the relationship between exercise-induced R wave amplitude changes and severity of coronary artery disease.

The correlation between R wave voltage variations (delta R) and the angiographic severity of coronary artery disease (CAD) at progressively increasing heart rate (HR) steps was evaluated in 51 patients (pts) without CAD (OV), in 42 pts with single (SVD), in 43 with double (DVD) and in 59 pts with triple vessel disease (TVD). At the end of stress the sensitivity of delta R was higher in DVD and TVD pts than in SVD pts. There was no clear correlation between exercise-induced R wave changes and the angiographic severity of CAD, since the qualitative and quantitative delta R evaluation during effort showed similar changes in delta R for a wide range of HR's in the entire study population. Since different degrees of exercise tolerance were found in pts with SVD, DVD and TVD, we hypothesize that the correlation between delta R and the severity of CAD at the end of stress testing may be artifactual.

Analysis of Variance↗
PubMed1983

Protective role of collaterals in patients with coronary artery occlusion.

We reviewed the clinical, hemodynamic and angiographic data of 105 patients with right coronary artery occlusion and 82 patients with left anterior descending coronary artery occlusion, subdivided into 3 groups by the presence and quality of collaterals to the occluded coronary (absent, poor or good collaterals). We found that patients with right coronary artery occlusion and good collaterals had a lower frequency of diaphragmatic myocardial infarction (60%) than patients with absent collaterals (100%) (P less than 0.01). In addition, in patients with old diaphragmatic myocardial infarction, both poor and good collaterals were associated with a lower frequency of severe asynergy of the diaphragmatic left ventricular segments at left ventriculography (54% and 14%, respectively), compared to patients with no collaterals to the right coronary artery (92%, P less than 0.02 vs. poor collaterals, P less than 0.001 vs. good collaterals). In contrast, in patients with left anterior descending coronary artery occlusion, the presence of either poor or good collaterals to the left anterior descending coronary artery was not associated with a lower frequency of old anterior myocardial infarction, or, in patients with old anterior myocardial infarction, with a less severe asynergy of the anterior left ventricular segments. Our results suggest that collaterals are effective in protecting the diaphragmatic left ventricular wall in patients with right coronary artery occlusion, but not the anterior left ventricular wall in patients with left anterior descending coronary artery occlusion.

Collateral Circulation↗
PubMed1983

Role of gluconeogenesis in epinephrine-stimulated hepatic glucose production in humans.

To evaluate the contribution of gluconeogenesis to epinephrine-stimulated glucose production, we infused epinephrine (0.06 micrograms X kg-1 X min-1) for 90 min into normal humans during combined hepatic vein catheterization and [U-14C]alanine infusion. Epinephrine infusion produced a rise in blood glucose (50-60%) and plasma insulin (30-40%), whereas glucagon levels increased only at 30 min (19%, P less than 0.05). Net splanchnic glucose output transiently increased by 150% and then returned to base line by 60 min. In contrast, the conversion of labeled alanine and lactate into glucose increased fourfold and remained elevated throughout the epinephrine infusion. Similarly, epinephrine produced a sustained increase in the net splanchnic uptake of cold lactate (four- to fivefold) and alanine (50-80%) although the fractional extraction of both substrates by splanchnic tissues was unchanged. We conclude that a) epinephrine is a potent stimulator of gluconeogenesis in humans, and b) this effect is primarily mediated by mobilization of lactate and alanine from extrasplanchnic tissues. Our data suggest that the initial epinephrine-induced rise in glucose production is largely due to activation of glycogenolysis. Thereafter, the effect of epinephrine on glycogenolysis (but not gluconeogenesis) wanes, and epinephrine-stimulated gluconeogenesis becomes the major factor maintaining hepatic glucose production.

Adult↗
PubMed1983

Valsalva maneuver in the assessment of baroreflex responsiveness in borderline hypertensives.

Baroreceptor function was assessed by (1) the reflex response during Valsalva maneuver, (2) phenylephrine injection, and (3) increase in neck tissue pressure by a neck-chamber in 15 borderline hypertensives (B) and in 15 age-matched normotensives (N). B responded to the fall in blood pressure, occurring in phase II of Valsalva maneuver, with an increase in blood pressure and a decrease in the R-R interval of comparable extent to those observed in normals. On the contrary, in phase IV B showed a depressed heart rate reflex response whether evaluated by the slope of the regression line obtained by plotting the R-R interval versus the systolic blood pressure (slope: B = 6.1 +/- 3.3; N = 35.6 +/- 7, p less than 0.005) or by the change in R-R interval (delta R-R interval: B = 67.5 +/- 37 ms; N = 319 +/- 55 ms, p less than 0.005). On the other hand, both phenylephrine injection and neck-chamber procedure showed an impaired baroreflex responsiveness in B. A linear positive correlation was found between the individual values of the slopes obtained during phase IV of Valsalva maneuver and after phenylephrine injection both in N (r = 0.944, p less than 0.001) and in B (r = 0.84, p less than 0.001). Finally, a linear positive correlation was found between the individual values of the slopes obtained by the phenylephrine technique and the corresponding maximum percent change in R-R interval during phase IV of the Valsalva maneuver both in normals and in hypertensives. In conclusion, overshoot bradycardia during Valsalva maneuver seems to show enough specificity in the evaluation of baroreflex responsiveness to be employed in epidemiological studies in this area.

Adolescent↗
PubMed1983

Two-dimensional echocardiography in idiopathic enlargement of the right atrium. Reliability and limitations.

A 36-year-old woman was admitted to our hospital with exertional dyspnea, palpitation and cardiac enlargement on standard chest X-ray. Physical examination did not reveal any significant abnormality and routine laboratory tests were normal. ECG showed atrial fibrillation and negative T waves in lead III and a VF, with a stiffened ST segment. M-mode echocardiography showed absence of pericardial effusion and normal size of both ventricular chambers. Two-dimensional echocardiography showed a large saccular dilation of the right atrium without significant enlargement of other cardiac chambers. A slight displacement of tricuspid valve leaflets was also present. Cardiac catheterization was effective in the diagnosis of idiopathic enlargement of the right atrium. Although two-dimensional echocardiography has some limitations in the diagnosis of this unusual malformation, it may prove useful in the noninvasive follow-up of these patients, in order to monitor the eventual increase of atrial size and to promptly detect late complications.

Adult↗
PubMed1983

Intropic effects of several antiarrhythmic drugs.

The effects of intravenous administration of several quinidine-like antiarrhythmic drugs (bunaftine, monochloroacetyl ajmaline, lidocaine, mexiletine, disopyramide, aprindine, diphenylhydantoin, procainamide) on left ventricular performance, evaluated by systolic time intervals (STI), were studied in 100 patients with atherosclerotic heart disease. The STI were measured: the pre-ejection period (PEP), the isometric contraction time (ICT), the left ventricular ejection time (LVET), corrected LVET (LVETc), and the PEP/LVET ratio. The degree of impairment of left ventricular performance was maximal after aprindine and disopyramide administration. This was demonstrated by significant increases in the PEP, ICT, and PEP/LVET and by significant decreases in LVET and LVETc, in patients in both III-IV and I-II NYHA classes. Bunaftine, monochloroacetyl ajmaline, and lidocaine induced a less marked impairment of myocardial performance, since the PEP, ICT, and PEP/LVET increases were not significant compared to controls in patients in NYHA class I-II, and since no variation of LVET and LVETc were observed. Mexiletine effects on myocardial performance appear to be intermediate between these groups of drugs. Diphenylhydantoin and procainamide, considered separately because of their effects on heart rate and blood pressure which are not possessed by the other drugs, induced significant increases of PEP in NYHA class III-IV patients. However, the effects of these 2 drugs on myocardial performance may have been underestimated, due to the concomitant hemodynamic effect of these drugs.

Ajmaline↗
PubMed1983

Exercise induced ventricular arrhythmias. Angiographic correlation with the severity of coronary artery disease.

We correlated the incidence and degree of exercise induced ventricular arrhythmias (EIVA) with the angiographic severity of coronary artery disease (CAD) in 162 patients with a history of stable effort angina, all showing a positive exercise stress test for myocardial ischemia and a greater than or equal to 70% stenosis of a major coronary artery. Patients were grouped according to the following criteria: presence of electrocardiographic evidence of old transmural myocardial infarction (MI), number of significant coronary stenoses and number of left ventricular (LV) areas showing abnormal segmental wall motion (ASWM). The incidence of EIVA in patients with multivessel CAD was higher than in patients with single vessel CAD, but this difference was not statistically significant. The number of LV areas with ASWM was better correlated with the frequency of EIVA, which was 20.0% in patients with normal LV wall motion, 31.2% in patients with 1 area of ASWM, 54.0% in patients with 2 areas of ASWM (p less than 0.005 vs normal LV wall motion), 74.1% in patients with 3 or more areas of ASWM (p less than 0.001 vs normal LV wall motion and 1 area of ASWM), and 81.8% in patients with LV aneurysm (p less than 0.001 vs normal LV wall motion and 1 area of ASWM, p less than 0.005 vs 2 areas of ASWM). Patients with old MI showed a significantly higher incidence of EIVA than those without MI (p less than 0.001), but this difference was due to the more severe LV asynergy in the MI group. In conclusion, our results show that, in a selected population of patients with CAD, the incidence of EIVA correlates better with the extent of LV segmental wall motion abnormalities than with the number of diseased coronary arteries or the presence of an old transmural MI.

Adult↗
PubMed1982

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↗