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C Vigorito

Publications and source records attributed to C Vigorito.

At least 73 records · Page 4Linked to original sources
PubMed1982

Mechanisms of epinephrine-induced glucose intolerance in normal humans.

To evaluate the role of the splanchnic bed in epinephrine-induced glucose intolerance, we selectively assessed the components of net splanchnic glucose balance, i.e., splanchnic glucose uptake and hepatic glucose production, and peripheral glucose uptake by combining infusion of [3-(3)H]glucose with hepatic vein catheterization. Normal humans received a 90-min infusion of either glucose alone (6.5 mg/kg(-1) per min(-1)) or epinephrine plus glucose at two dose levels: (a) in amounts that simulated the hyperglycemia seen with glucose alone (3.0 mg/kg(-1) per min(-1)); and (b) in amounts identical to the control study. During infusion of glucose alone, blood glucose rose twofold, insulin levels and net posthepatic insulin release increased three- to fourfold, and net splanchnic glucose output switched from a net output (1.65+/-0.12 mg/kg(-1) per min(-1)) to a net uptake (1.56+/-0.18). This was due to a 90-95% fall (P < 0.001) in hepatic glucose production and a 100% rise (P < 0.001) in splanchnic glucose uptake (from 0.86+/-0.14 to 1.71+/-0.12 mg/kg(-1) per min(-1)), which in the basal state amounted to 30-35% of total glucose uptake. Peripheral glucose uptake rose by 170-185% (P < 0.001). When epinephrine was combined with the lower glucose dose, blood glucose, insulin release, and hepatic blood flow were no different from values observed with glucose alone. However, hepatic glucose production fell only 40-45% (P < 0.05 vs. glucose alone) and, most importantly, the rise in splanchnic glucose uptake was totally blocked. As a result, splanchnic glucose clearance fell by 50% (P < 0.05), and net splanchnic glucose uptake did not occur. The rise in peripheral glucose uptake was also reduced by 50-60% (P < 0.001). When epinephrine was added to the same dose of glucose used in the control study, blood glucose rose twofold higher (P < 0.001). The initial rise in splanchnic glucose uptake was totally prevented; however, beyond 30 min, splanchnic glucose uptake increased, reaching levels seen in the control study when severe hyperglycemia occurred. Splanchnic glucose clearance, nevertheless, remained suppressed throughout the entire study (40%-50%, P < 0.01). It is concluded that (a) the splanchnic bed accounts for one-third of total body glucose uptake in the basal state in normal humans; (b) epinephrine markedly inhibits the rise in splanchnic glucose uptake induced by infusion of glucose; and (c) this effect does not require a fall in insulin and is modulated by the level of hyperglycemia. Our data indicate that the splanchnic bed is an important site of glucose uptake in post-absorptive humans and that epinephrine impairs glucose tolerance by suppressing glucose uptake by both splanchnic and peripheral tissues, as well as by its well known stimulatory effect on endogenous glucose production.

Adult↗
PubMed1982

Differential effects of insulin on splanchnic and peripheral glucose disposal after an intravenous glucose load in man.

The present study was designed to investigate the mechanisms by which insulin regulates the disposal of an intravenous glucose load in man. A combined tracer-hepatic vein catheter technique was used to quantitate directly the components of net splanchnic glucose balance (NSGB), i.e., splanchnic glucose uptake and hepatic glucose output, and peripheral (extrasplanchnic) glucose uptake. Four different protocols were performed: (a) intravenous infusion of glucose alone (6.5 mg kg(-1) min(-1)) for 90 min (control group); (b) glucose plus somatostatin (0.6 mg/h) and glucagon (0.8 ng kg(-1) min(-1); (c) glucose plus somatostatin, glucagon, and insulin (0.15 mU kg(-1) min(-1)); and (d) glucose plus somatostatin, glucagon, and insulin (0.4 m U kg(-1) min(-1)). In groups 2-4, arterial blood glucose was raised to comparable levels to those of controls ( approximately 170 mg/dl) by a variable glucose infusion. In the control group, plasma insulin levels reached 40 muU/ml at 90 min. NSGB switched from a net output of 1.71+/-0.13 to a net uptake of 1.5-1.6 mg kg(-1) min(-1) due to a 90-95% suppression of hepatic glucose output (P < 0.01) and a 105-130% elevation of splanchnic glucose uptake (from 0.78+/-0.13 to 1.6-1.8 mg kg(-1) min(-1); P < 0.01). Peripheral glucose uptake rose by 150-160% (P < 0.01). In group 2, plasma insulin fell to <5 muU/ml. Net splanchnic glucose output initially rose twofold but later returned to basal values. This response was entirely accounted for by similar changes in hepatic glucose output since splanchnic glucose uptake remained totally unchanged in spite of hyperglycemia. In contrast, peripheral glucose uptake rose consistently by 100% (P < 0.01) despite insulin deficiency. In an additional group of experiments, glucose metabolism by the forearm muscle tissue was quantitated during identical conditions to those of group 2 (hyperglycemia plus insulin deficiency). Both the arterial-deep venous blood glucose difference and forearm glucose uptake increased markedly by 300-400% (P < 0.05 - <0.01). In group 3, plasma insulin was maintained at near-basal, peripheral levels (12-14 muU/ml). Hepatic glucose output decreased slightly by 35-40% (P < 0.05) while splanchnic glucose uptake remained unchanged. Consequently, the net glucose overproduction seen in group 2 was totally prevented although NSGB still remained as a net output. In group 4, peripheral insulin levels were similar to those of the control group (35-40 muU/ml). The suppression of hepatic glucose output was more pronounced (60-65%) and splanchnic glucose uptake rose consistently by 65% (P < 0.01). Consequently, NSGB did not remain as a net output but eventually switched to a small uptake (0.3 mg kg(-1) min(-1)). Peripheral glucose uptake rose to the same extent as in controls. IT IS CONCLUDED THAT: (a) the suppressive effect of hyperglycemia on hepatic glucose output is strictly dependent on the degree of hepatic insulinization; (b) insulin plays an essential role in promoting splanchnic glucose uptake after an intravenous glucose load whereas hyperglycemia per se is totally unable to activate this process; (c) peripheral glucose uptake is markedly stimulated by hyperglycemia even in the face of insulin deficiency. Direct evidence also demonstrates that the skeletal muscle is involved in this response. Our data, thus, indicate that insulin rather than hyperglycemia regulates splanchnic glucose disposal in man. On the other hand, hyperglycemia per se appears to be an important regulator of glucose disposal by peripheral tissues.

Adult↗
PubMed1982

[Influence of myocardial infarct on ventricular arrhythmias during the exercise test. Study in patients with stable angina of effort].

The incidence of ventricular arrhythmias observed during exercise (EVA) was correlated with the presence of previous myocardial infarction (IM) and angiographic severity of coronary artery disease (CAD) in 162 patients (pts.) with stable angina on effort, who had a positive stress test and greater than 70% stenosis of a major coronary artery. Our study population was divided in two groups: the first was composed of 95 pts. with previous MI, the second of 67 pts. without previous MI. Pts. of both groups were subdivided according to severity of CAD and to presence and degree of abnormal segmental wall motion (ASWM). In the MI group only 11.5% of pts. had single vessel disease, and 86.3% had ASWM. In pts. without MI 28.6% had single vessel disease; ASWM was found in 59.7% (p less than 0.001 vs MI pts.). Pts. with MI showed a higher incidence of EVA than pts. without MI (60% vs 32.8%, p less than 0.001). In both groups EVA were more frequent among pts. with double, triple vessel and main left CAD, than in pts with single vessel disease, but the difference was not significant. In general, EVA were found to correlate better with the number of areas with ASWM: in both groups significant differences of EVA frequency were found when pts. with normal left ventricular function were compared to those with more severe ASWM, while no difference was found between pts with and without MI who had the same degree of CAD. The most severe EVA (Tilkian's classification), were found in pts with a previous MI and a high ASWM score. In conclusion, our results show that a previous MI affects the development of EVA in pts. with stable effort angina. However EVA seem to be better correlated with the severity of LV impairment than with the extent of CAD.

Adult↗
PubMed1981

Baroreflex responsiveness in borderline hypertensives: a study with neostigmine.

The baroreflex response to changes in transmural pressure throughout the arterial tree or limited to the carotid sinus was evaluated in ten borderline hypertensives and compared with that observed in ten normal subjects and in ten established hypertensives. 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 increased neck tissue pressure by means of a neck chamber. The heart rate response to phenylephrine (evaluated by the regression of the R-R interval versus the systolic blood pressure) was depressed both in borderline and established hypertensives as compared with controls. Similarly, the heart rate and the pressor response to increased neck tissue pressure were depressed in both groups of hypertensives. In borderline, but not in established hypertensives, neostigmine administration improved consistently the pressor baroreflex response to increased neck tissue pressure and the heart rate reflex response to both the employed stimuli. These findings indicate that a reduced parasympathetic activity is one of the components involved in the altered baroreflex sensitivity in borderline hypertensives.

Adult↗
PubMed1981

Echocardiographic evaluation of acute administration of oxyfedrine in patients with coronary artery disease.

In order to assess the effects of oxyfedrine in ischaemic heart disease, echocardiographic evaluation of left ventricular function was performed 2,5,10,15 and 20 minutes after the intravenous administration of 12 mg oxyfedrine in 15 patients with coronary artery disease without angiographic abnormalities of left ventricular wall motion. The following parameters were measured: heart rate, mean arterial blood pressure, internal dimension in diastole (LVIDd) and in systole (LVIDs) of the left ventricule and the percentage shortening of the LVID (%LVID). There was a significant increase in %LVID (peak 10 minutes after drug administration; p less than 0.001) indicating improved left ventricular function, associated with slight changes in pre-load (LVIDd) and in heart rate, and no variation in mean blood pressure. No abnormalities of contraction were observed after the administration of oxyfedrine. These results suggest that oxyfedrine exerts a direct positive inotropic effect of the myocardium in patients with significant coronary artery stenoses.

Aged↗
PubMed1981

Clinical hemodynamic and angiographic findings in 94 patients with old myocardial infarction. Comparison with 79 patients with coronary artery disease and no myocardial infarction.

Clinical, hemodynamic, coronary arteriographic, and ventriculographic findings of 94 patients (pts) with coronary artery disease (CAD) and old myocardial infarction (MI) have been described and compared with those of 70 pts with CAD and no previous MI. Pts with old MI presented a more compromised functional and hemodynamic status, with a higher incidence of NYHA class III-IV pts (40%), symptoms of left ventricular (LV) failure (31%), cardiomegaly (70%), higher left ventricular end-diastolic pressure (LVEDP) (19.6 +/- 9.6 mmHg, p less than 0.05), compared with 32%, 22%, 54% and 16.0 +/- 6.8 mmHg respectively in CAD pts with no MI. MI pts presented more severe CAD, higher incidences of three vessel disease (56%, p less than .005) and of left anterior descending (LAD) (34%) and right coronary artery (RCA) (36%) occlusions, compared with 34%, 6%, and 9% respectively in pts with no MI. Furthermore, pts with old MI showed more diffused and severe LV segmental wall contraction abnormalities, with higher frequencies of LV aneurysm (31%) and of pts with asynergy of more than 2 LV segments (26%), compared with 1% and 3% respectively in pts with no MI. Within the group with old MI, LVEDP was higher in pts with anterior (A) (22.0 +/- 11 mmHg, p less than .02) and anterior ł diaphragmatic (AłD) (21.5+/- 7.9 mmHg, p less than .05) MI, compared with pts with diaphragmatic (D) MI (16.6 +/- 7.1 mmHg); furthermore, LVEDP increase was significantly correlated with the severity and the extent of LV asynergy. In A and D MI, LAD and RCA stenoses or occlusions were prevalent respectively; pts with AłD MI showed larger numbers of coronary stenosis (3.05) and occlusions (1.05) per patient. The coronary artery supplying the infarcted area showed stenosis (greater than 75%) in 95.6% and was normal in 2.2% of cases. Thus, pts with CAD and old MI, and particularly of AłD and A MI, show a more compromised hemodynamic status and more severe degrees of CAD and of LV segmental wall contraction abnormality, which are responsible for their poor prognosis, compared to pts with CAD but no old MI.

Adult↗
PubMed1981

Clinical study of possible interactions between indoprofen and oral anticoagulants.

Possible interactions between indoprofen (IP) and Warfarin Na (W) were studied in 18 patients under chronic anticoagulant treatment, according to a cross-over, double-blind design, comparing 600 mg daily of IP with placebo (PL). In all subjects the dosage of W was kept constant throughout the study (21 days). No significant differences were found between IP and PL either on coagulation parameters or on platelet count and platelet adhesiveness. Afte IP a significant decrease in platelet aggregation (induced by ADP and adrenaline) was observed. The results suggest that indoprofen can be administered to patients under anticoagulant treatment, although frequent checks of the coagulation parameters are advisable in these cases.

Administration, Oral↗
PubMed1981

[Influence of left ventricular volume changes induced by Valsalva maneuver on R wave amplitude (author's transl)].

Exercise-induced changes of R wave amplitude (delta R) during exercise has been employed to improve the reliability of stress testing in detecting patients with coronary artery disease. Several authors postulated that delta R are related to changes of ventricular volumes. Furthermore Valsalva Maneuver (VM) is able to induce a decrease of left ventricular volumes induced by VM and the variations of R wave. Echocardiographic method was used to determine left ventricular volumes and R wave amplitude changes were evaluated by Frank's lead. Our findings suggest that R wave amplitude changes are not related to variations of cardiac volume. Electrophysiological mechanisms of delta R need further investigation.

Adolescent↗
PubMed1981

[Coronary artery disease (CAD) in females. Coronary arteriographic findings in 34 women and comparison with 184 males with cad].

We studied the clinical, hemodynamic and angiographic findings of 34 women (W) and of 184 men (M) with significant (greater than or equal 50%) CAD. W, compared to M, presented a higher incidence of systemic hypertension (p less than .025), while less frequent were among W smoking habits (p less than .001), history of old myocardial infarction (MI) (p less than .005), and patients in III-IV NYHA class (p less than .025). Left ventricular (LV) dP/dt was higher in W than in M (p less than .005). At coronary arteriography, single vessel disease (SVD) was more frequently found in W than in M (70% vs 23%, respectively, p less than .001); this findings was more evident in patients under 50 years of age (100% vs 30%, respectively, p less than .055). Prevalence of left anterior descending (LAD) over right (RCA) and circumflex (Cx) coronary artery stenoses was more marked in W than in M, especially in patients under 50 years of age (SVD of the LAD in 67% and of RCA in 33% of young W). Poor angiographic run-off of LAD was found in 21% of W, and only in 10% of M. In 2 of the 3 W with poor run-off of LAD operated on, a coronary bypass on the distal LAD was no technically feasible. At left ventriculography, a lower frequency of LV segmental wall motion abnormalities was found in W than in M, especially in patients with no history of MI (p less than .001). In summary, W with significant CAD, compared to age matched M, presented in our experience with a higher frequency of SVD and of LAD stenoses, and with a better LV contractile performance at left ventriculography. Furthermore, in W LAD more frequently showed a poor angiographic run-off. Such findings may bear important implications on the indication and results of coronary surgery in W with CAD.

Adult↗
PubMed1980

[Correlations between angiocardiography and changes of R wave amplitude during effort in patients with coronary heart disease (author's transl)].

The Authors studied correlations between angiocardiography and changes of R wave amplitude (delta R) during effort in 113 patients. They showed coronarographic evidence: 69 with stenosis greater than or equal to 70% of at least one major coronary vessel and 44 with no significant lesions. delta R values greater or equal than 0 were considered as pathologic. delta R appeared greater than or equal to 0 in 8 of 14 patients (57%) with single stenosis, 4 (28%) with abnormal wall motion (AWM). delta R increase or unchanged in 26 of 31 (84%) patients with double stenoses, 25 of them (81%) with AWM. delta R was greater than or equal to 0 in 22 of 24 (92%) with triple stenoses. In subjects with milk coronary artery disease (CAD) R wave increased or unchanged in 47% (19/44). Pathologic changes of R wave are highly frequent in CAD patients, especially in those with severe impairment. These changes, however, are not specific or costant because they appeared enough frequently in subjects with normal doronary vessels, and, moreover, R wave may decrease also in CAD patients with severe impairment. The Authors consider that evidence of delta R values greater than or equal to 0 may not be considered as a sign of CAD, but it must be evaluated with the other data showed by ergometric tests.

Adult↗