PubMed Health⌕ Search

Biomedical subjects

B Trimarco

Publications and source records attributed to B Trimarco.

At least 163 records · Page 9Linked to original sources
PubMed1984

Relationships between left ventricular mass and clinical, biohumoral and hemodynamic parameters in human hypertension.

The relationships between left ventricular mass (LVM), assessed by echocardiography, and several biohumoral and hemodynamic parameters were studied in 63 mild or moderate hypertensive patients and in an age-matched group of 23 normotensive subjects. In hypertensive patients, but not in normotensives, LVM index was significantly correlated with beta-adrenoceptor responsiveness, as evaluated by the chronotropic response to isoproterenol ( CD25 ) (r = 0.525, p less than 0.001) and with the 24-hour catecholamine urinary output (r = 0.485, p less than 0.001). Both CD25 and the catecholamine urinary output were significantly higher in the hypertensives as compared with the normotensive subjects. Moreover, left ventricular wall thickness (septum + posterior wall) was significantly correlated with CD25 and urinary catecholamines only in hypertensive patients. No significant correlation was found between LVM or wall thickness and body surface area, age, blood pressure, heart rate, cardiac output, total peripheral resistance and left ventricular systolic wall stress, whereas CD25 was correlated with urinary catecholamines only in hypertensive patients (r = 0.606, p less than 0.001). These results seem to support the hypothesis that an elevated adrenergic tone may exert a permissive role in the development of left ventricular hypertrophy in human hypertension.

Adolescent↗
PubMed1983

Predictability of antihypertensive efficacy of selective beta 1 blockers.

The possibility that hemodynamic and biohumoral factors may help predict the antihypertensive effectiveness of selective beta 1 blockers was investigated. The effects of 3 wk of treatment with two selective beta 1 blockers, metoprolol and atenolol, were observed in 54 patients with mild or moderate essential hypertension. No significant difference between the hemodynamic effects of the two drugs was found. The percent fall in systolic blood pressure induced by the two correlated strongly with the pretreatment values of the chronotropic response to isoproterenol and with the pretreatment values of cardiac output, heart rate, and plasma renin activity (PRA). There was no correlation between the decrease in systolic blood pressure induced and initial 24-hr urinary catecholamine output, total peripheral resistance, and plasma aldosterone. Percent fall in diastolic blood pressure correlated only with the pretreatment levels of PRA. Our results support the view that the hypotensive effect of beta 1 blockers are predictable on the basis of the pretreatment values of chronotropic response to isoproterenol, PRA, heart rate, and cardiac output.

Adult↗
PubMed1983

Haemodynamic and clinical effects of long-term treatment of essential hypertension with captopril.

Captopril, an orally active inhibitor of angiotensin converting enzyme, was administered for 12 months to 20 patients with mild or moderate essential hypertension who initially responded favourably to this pharmacological treatment. Captopril induced a significant reduction in blood pressure which remained unmodified throughout the study. This fall in blood pressure was mainly due to a significant decrease in total peripheral vascular resistance, since no change in cardiac output was observed. Simultaneously, there was no significant change in left ventricular anatomy and performance evaluated by echocardiographic technique.

Adult↗
PubMed1983

Increased cardiac output and lowered peripheral resistance during metoprolol treatment.

Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.

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↗
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↗
PubMed1982

Effects of oral salt loading on beta-adrenergic receptor responsiveness in normal and hypertensive subjects.

The effect of oral salt loading (400 mmol per day of NaCl for 7 days) on cardiac and pancreatic beta-receptor responsiveness has been evaluated in 12 patients with established essential hypertension and in seven age-matched control subjects. Cardiac beta-receptor responsiveness was evaluated by assessing the dose of isoprenaline which increased a stable heart rate by 25% (chronotropic dose 25%, CD 25%). Pancreatic beta-receptor responsiveness was measured by the incremental areas of insulin secretion induced by iv infusion of increasing amounts of isoprenaline. Before salt load, CD 25% was significantly higher in hypertensives compared with controls (7.84 +/- 1.34 micrograms vs 3.9 +/- 0.48 micrograms, P less than 0.05) while there was no difference in the isoprenaline-induced insulin secretion between the two groups of subjects. After salt loading, CD 25% was significantly reduced in hypertensive patients but was not modified in normal subjects. Therefore, the difference in CD 25% was no longer detectable between the two groups (5.5 +/- 1.42 micrograms vs 3.2 +/- 0.48 micrograms in normal subjects and in hypertensives, respectively, NS). Furthermore, salt loading failed to induce any change in isoprenaline-induced insulin secretion in either groups. These results support the existence of a relationship between sodium intake and adrenergic beta-receptor responsiveness in human hypertension.

Adolescent↗
PubMed1982

Renal function in borderline hypertensive first-degree relatives of essential hypertensives. Effects of sodium load.

Renal function in the basal state and after sodium load has been investigated in 21 borderline, hypertensive, first-degree relatives of established hypertensives and in 21 age- and sex-matched, normal subjects with no family history of hypertension. During intravenous infusion of inulin and p-aminohippurate in saline, both groups showed a decrease in plasma aldosterone levels (p less than 0.05) but renal plasma flow (595 +/- 48 vs. 750 +/- 59 ml/min, p less than 0.05), diuresis (1.4 +/- 0.2 vs. 2.2 +/- 0.5 ml/min, p less than 0.05), natriuresis (0.21 +/- 0.02 vs. 0.3 +/- 0.02 mEq/min, p less than 0.05) and sodium clearance (1.05 +/- 0.1 vs. 2.4 +/- 0.4 ml/min, p less than 0.05) in borderline hypertensives were higher than in the control group. After the salt load (NaCl, 1.35% i.v., 5 ml/min for 2 h) there was an increase in blood pressure and a decrease in plasma aldosterone and potassium levels in both groups. However, borderline hypertensives showed higher diuresis, natriuresis, sodium clearance and also kaliuresis compared to normotensives. These results suggest that borderline hypertensives already present the changes in renal function which are characteristics of established hypertensives.

Adolescent↗
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↗
PubMed1981

The glucoregulatory response to intravenous glucose infusion in normal man: roles of insulin and glucose.

In order to differentiate the roles of hyperinsulinemia and hyperglycemia per se in the homeostatic response to i.v. glucose administration, two groups of normal subjects were given either glucose alone (3.5 mg kg-1 min-1) or glucose (3 mg kg-1 min-1) in conjunction with somatostatin (500 microgram hr-1), insulin (0.15 mU kg-1 min-1) and glucagon (1 ng kg-1 min-1). Glucose kinetics were measured by the primed-constant infusion of 3-3H-glucose. During the infusion of glucose alone, plasma glucose stabilized at levels 45--50 mg/dl above the fasting values. Endogenous glucose output was markedly suppressed by 85%--90% while glucose uptake rose to values very close to the infusion rate of exogenous glucose. Glucose clearance remained unchanged. Plasma insulin rose to three-fourfold while plasma glucagon fell by 25%--30%. When glucose was infused with somatostatin, insulin, and glucagon, plasma insulin was maintained at levels 50% above baseline while glucagon remained at preinfusion levels. Under these conditions, the infusion of exogenous glucose resulted in a progressive increase of plasma glucose which did not stabilize until the end of the study period (190 mg/dl at 120 min). Endogenous glucose production was consistently suppressed (52%) but significantly less than observed with the infusion of glucose alone (p less than 0.01). Glucose uptake increased to the same extent as with glucose alone, despite the more pronounced hyperglycemia. Thus, glucose clearance fell significantly below baseline (25%--30%; p less than 0.01). These data demonstrate that hyperglycemia per se (fixed, near basal levels of insulin and glucagon) certainly contributes to the glucoregulatory response to i.v. glucose administration by both inhibiting endogenous glucose output and increasing tissue glucose uptake. However, the extra-insulin evoked by hyperglycemia is necessary for the glucoregulatory system to respond to the glucose load with maximal effectiveness.

Adult↗
PubMed1981

The reflex control of arginine-vasopressin release in essential hypertension.

1. The reflex control of arginine-vasopressin release was studied in 12 essential established hypertensive patients and in 12 age-matched normal subjects by comparing the effects of head-up tilt and a variable-pressure neck-chamber. 2. After 45 min 85 degrees head-up tilt, normal subjects showed an increase in plasma arginine-vasopressin and in plasma renin activity, while plasma volume decreased. In hypertensive patients, plasma arginine-vasopressin showed changes after tilt opposite to those of controls, while the changes in plasma renin activity and plasma volume were similar to those observed in the normal group. In both groups the changes in systolic and diastolic blood pressure were not statistically significant. A reduction in carotid sinus transmural pressure obtained by increasing neck-tissue pressure (+50 mmHg) by means of a neck-chamber, evoked different responses in mean blood pressure in the two groups, but failed to induce any significant change in plasma arginine-vasopressin concentration both in the normal and in the hypertensive subjects. 3. These results seem to suggest that carotid sinus baroreceptors, though active in blood pressure control, do not play a direct role in arginine-vasopressin release and, therefore, the opposite response of arginine-vasopressin observed after tilt in the two groups of subjects should be ascribed to more complex mechanisms.

Adolescent↗
PubMed1981

Glucoregulatory response to intravenous fructose administration in the dog.

This study was designed to evaluate the influence of fructose administration on glucose kinetics and the role of fructose conversion to glucose in the maintenance of glucose homeostasis. Intravenous fructose infusion (4.5 mg/kg min-1) produced a stable plasma fructose concentration of about 20 mg/dl and a small but sustained decrease (10 mg/dl) of plasma glucose levels. The latter effect was entirely attributable to a rapid 30-35% fall in hepatic glucose output which later returned slowly to pre-infusion levels. No significant change in the rate of glucose utilization was observed. The rate of fructose conversion to glucose rose progressively during fructose infusion reaching a plateau of 1.4 mg/kg min-1 which corresponded to about 40% of total glucose production. Furthermore, as much as one third of the infused fructose was converted to circulating glucose. No appreciable changes in plasma insulin and glucagon levels occurred during fructose infusion while plasma alanine concentration increased remarkably. These data indicate that 1) fructose administration induces a transient fall in endogenous glucose production not accompanied by significant changes in glucose utilization; 2) the rapid conversion of the infused fructose to circulating glucose provides for the restoration of normal rates of glucose production; and 3) the glucoregulatory response to the administration of fructose occurs in the absence of detectable changes in plasma pancreatic hormone concentration.

Alanine↗