Hypertension detection, treatment and control: a call to action for cardiovascular specialists.
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Adult↗
Biomedical subjects
F M Fouad-Tarazi
Publications and source records attributed to F M Fouad-Tarazi.
Isoproterenol induced cardiovascular hypersensitiviy in nonpheochromocytoma patients with paroxysmal hyperadrenergic symptoms.
The objective of this study was to determine whether graded isoproterenol infusion test identifies a specific hypersensitivity response of the LV diastolic relaxation properties in nonpheochromocytoma patients with paroxysmal symptoms of hyperadrenergic surges. We hypothesized that patients with hyperadrenergic surges, not due to pheochromocytoma, have hypersensitivity of cardiac beta-adrenergic receptor responses to exogenous catecholamines, resulting in enhancement of LV relaxation. We assessed the physiological beta 1 and beta 2 receptor responsiveness to graded isoproterenol infusion (0.01, 0.02, 0.03 and 0.04 microgram/kg per min) in 32 patients presented with hyperadrenergic surges not due to pheochromocytoma. Two major observations were made. First, systemic hemodynamic evaluation using 99m Technetium first pass method revealed hyperkinetic state only in 21 patients (20 females and 1 male; aged 31 +/- 9 years); the other 11 patients were without hyperkinetic circulatory state (10 females and 1 male; aged 41 +/- 9 years). At baseline, plasma catecholamines were not significantly different between the two groups. The baseline corrected LV peak filling and ejection rates (cPFR and cPER) were significantly higher in hyperkinetic group (cPFR: 10 +/- 2 vs 8 +/- 2 x 10(-2) Hz/ms, P = 0.03; cPER: 11 +/- 2 vs 8 +/- 1 x 10(-2) Hz/ms, P = 0.002) and their baseline HR was faster (85 +/- 16 vs 70 +/- 9 beats/min, P = 0.006). Second, the cardiac and vascular responses to isoproterenol infusion were compared between these two groups. During the graded isoproterenol infusion, the response of HR, systolic, and diastolic BP were not significantly different between the two groups at all doses of isoproterenol, but cPFR and cPER had a more marked response to the lowest dose of 0.01 mg/kg per min in the hyperkinetic group. Thus, the graded isoproterenol infusion test can differentiate between two groups of nonpheochromocytoma patients presenting with paroxysmal symptoms of hyperadrenergic surges. Only patients with baseline hyperkinetic hemodynamic profile had accentuated cardiac hyperresponsiveness to a low dose of isoproterenol. We concluded that cPFR and cPER is a more sensitive index to assess the response to isoproterenol, because of metabolic determinants affecting the rate of change in LV volume.
Adrenergic beta-Agonists↗
Venous dysfunction and the change of blood viscosity during head-up tilt.
The precise stimulus that induces vasovagal syncope is still unclear. We have previously demonstrated that the peripheral distribution of blood volume (venous pooling) is a strong predictor of tilt induced vasovagal reaction. We hypothesized that an increase in venous pooling during tilt accentuates the measured increase in blood viscosity. This hypothesis is based on the previously demonstrated increase in venous pressure and subsequent increase in transcapillary fluid transudation during tilt. The increased blood viscosity, in turn, increases vascular shear rate, which may alter the vasoconstrictive and other cardiovascular responses to decreased preload. We measured blood viscosity (supine and tilt) in 56 patients with a history of orthostatic intolerance (37 with venous pooling [VP] and 19 without venous pooling [non-VP]). VP and non-VP were separated into subgroups based on blood pressure and heart rate response to tilt. There was a positive correlation between blood viscosity and plasma aldosterone in the supine. In the group as a whole, neither supine blood viscosity nor its increase during tilt differed between VP and non-VP. However, the tilt induced increase of blood viscosity was significant only in patients with tilt provoked tachycardia plus normal blood pressure response in VP group. We suggest that the increase of blood viscosity in this group led to the normal blood pressure response. The positive correlation between supine blood viscosity and supine plasma aldosterone indicates that the normal blood pressure response in this group possibly was via stimulation of the renin-angiotensin-aldosterone system.
Adult↗
Usefulness of plasma catecholamines during head-up tilt as a measure of sympathetic activation in vasovagal patients.
Vasovagal syncope is a common clinical disorder which has been traditionally related to a vasovagal reflex precipitated by an initial excess sympathetic stimulation. We hypothesized that the increase in plasma catecholamines during head-up tilt is more accentuated in patients with tilt induced vasovagal syncope. To test this hypothesis, plasma catecholamines were measured in supine posture and during head-up tilt in patients with a history suggestive of vasovagal syncope. Of these, 13 had a normal response to tilt (nonvasovagal group; age 41 +/- 19 [SD]years) and 11 had a vasovagal response to tilt (vasovagal group; 39 +/- 20 years). In the supine posture at rest, plasma epinephrine and norepinephrine were not significantly different between the nonvasovagal and the vasovagal groups (39 +/- 28 ng/L vs 46 +/- 38 ng/L, P = 0.5792, 335 +/- 158 ng/L vs 304 +/- 124 ng/L, P = 0.6007, respectively). Furthermore, the tilt induced changes in plasma epinephrine and norepinephrine were not different between the two groups (20 +/- 20 ng/L vs 35 +/- 55 ng/L, P = 0.3562, 264 +/- 158 ng/L vs 242 +/- 205 ng/L, P = 0.7724, respectively) suggesting that differences in the hemodynamic response to tilt are not predictable by the supine levels of circulating plasma catecholamines, and that the extent of plasma catecholamines increase during tilt does not determine the hemodynamic outcome of the tilt test. Since orthostatic changes of plasma catecholamines could be influenced by volume factors, we assessed plasma renin activity and aldosterone as surrogates of blood volume. Baseline plasma renin activity and aldosterone were not significantly different between the two groups. We conclude that inasmuch as plasma catecholamines reflect the status of sympathetic activity, our data do not support the hypothesis that accentuation of sympathetic activity precedes necessarily the tilt induced vasovagal syncope. However, one should take in consideration that multiple factors may influence catecholamine levels and catecholamines kinetics. A hyperresponsiveness of beta-receptors to catecholamines in patients with vasovagal syncope may be suggested but needs to be tested.
Adolescent↗
The connection between chronic fatigue syndrome and neurally mediated hypotension.
Research from several groups of investigators indicates that some patients with chronic fatigue syndrome have abnormal vasovagal or vasodepressor responses to upright posture. If confirmed, these findings may explain some of the symptoms of chronic fatigue syndrome. There is also speculation that neurally mediated hypotension may be present in fibromyalgia. This article discusses the original research in this area, the results of follow-up studies, and the current approach to treating patients with chronic fatigue syndrome in whom neurally mediated hypotension is suspected.
Fatigue Syndrome, Chronic↗
Paradoxical failure of QT prolongation during cardioinhibitory neurocardiogenic syncope.
QT modulation was explored in 31 patients with cardioinhibitory neurocardiogenic syncope. Despite a marked in increase in RR intervals, the QT interval remained stable.
Adult↗
Hypertension hemodynamics.
The hemodynamic factors in hypertension should be evaluated in terms of early versus late stages, autoregulation versus amplifying mechanisms, and arterial compliance versus arteriolar vasoconstrictive responses. In addition, evaluation of hemodynamic changes in hypertension should include the role of vascular endothelium, genetic factors, volume factors, salt intake, vascular reactivity, presence or absence of left ventricular hypertrophy or left ventricular diastolic dysfunction, and finally the presence of left ventricular systolic failure. Whether therapy directed by knowledge of hemodynamic profiling will be more efficacious or more cost-effective than standard therapy in reducing morbidity and mortality of hypertension needs to be proven.
Animals↗
Plasma volume and its regulatory factors in congestive heart failure after implantation of long-term left ventricular assist devices.
BACKGROUND: Congestive heart failure is associated with blood volume expansion caused by stimulation of the renin-aldosterone system and arginine vasopressin. The use of left ventricular assist devices as bridges to heart transplantation has improved the survival of patients during this critical period. In studying heart failure physiology on support devices, we hypothesized that improvement of cardiac function by a left ventricular assist device is associated with normalization of volume load secondary to normalization of its regulatory substances. METHODS AND RESULTS: We studied 15 patients (13 men, 2 women: age 51 +/- 8 years) with end-stage heart failure who were cardiac transplant candidates eligible for HeartMate implantation. We measured plasma volume and plasma levels of atrial natriuretic peptide, aldosterone, renin, and arginine vasopressin sequentially before HeartMate implantation (baseline), after HeartMate implantation (weeks 4 and 8), and after transplantation. Baseline plasma volume was 123 +/- 20% of normal; it was 122 +/- 22% at week 4 and decreased to 115 +/- 14% at week 8. Atrial natriuretic peptide was 359 +/- 380 pg/mL at baseline, 245 +/- 175 pg/mL at week 4, and 151 +/- 66 pg/mL at week 8. Plasma aldosterone fell from 68 +/- 59 ng/dL at baseline to 17 +/- 16 ng/dL at week 4 (P < .05 versus baseline) and was 32 +/- 50 ng/dL at week 8. Plasma renin activity decreased from 80 +/- 88 ng/dL at baseline to 11 +/- 12 ng/dL at week 4 and was 16 +/- 38 ng/dL at week 8 (both P < .05 versus baseline). Arginine vasopressin fell from 5.0 +/- 4.8 fmol/mL at baseline to 1.1 +/- 0.7 fmol/mL at week 4 and 1.2+/-0.8 fmol/mL at week 8 (both P < .05 versus baseline). CONCLUSIONS: The reduction of plasma renin activity, plasma aldosterone, and arginine vasopressin occurred earlier than the reduction of plasma volume and atrial natriuretic peptide after HeartMate implantation, possibly because of decreased pulmonary congestion and improved renal perfusion. The reduction of atrial natriuretic peptide cannot be responsible for the lack of adequate decrease of plasma volume; its reduction can be taken as a marker of improved cardiac pump function and decreased atrial stretch.
Blood Volume↗
Changes in left ventricular volume during head-up tilt in patients with vasovagal syncope: an echocardiographic study.
We tested the hypothesis that patients who have vasovagal syncope during head-up tilt have a greater decrease in their left ventricular volume in response to tilt than do normal subjects. Measurements were done in the supine position and during graded tilt by using two-dimensional echocardiography. We compared seven patients with vasovagal syncope with nine normal volunteers. The rate of reduction of end-diastolic volume index during tilt was faster in the vasovagal group than in normal subjects. A more significant reduction of stroke index and ejection fraction during tilt was found in the vasovagal group than in normal subjects, possibly because of more peripheral translocation of blood volume in the venous system during tilt and an early vagal effect on ventricular contraction.
Adolescent↗
Alpha sympathomimetic treatment of autonomic insufficiency with orthostatic hypotension.
PURPOSE: In this double-blind study, the authors compared the safety and efficacy of the investigational oral agent midodrine, a specific alpha 1-sympathomimetic agent, with ephedrine, a nonspecific alpha- and beta-adrenergic receptor agonist. Eight patients (4 men and 4 women) with refractory orthostatic hypotension resulting from autonomic failure were studied. This study was based on the notion that neurogenic orthostatic hypotension results from attenuation of adrenergic nerve traffic and not from alpha-adrenergic receptor dysfunction. Although arteriolar vasoconstrictors seem to be appropriate therapeutic agents, their success has been limited, and the search for an ideal drug is ongoing. METHODS: The authors employed a blocked, double-blind, randomized crossover design. The single-blind placebo run-in period was 2 days. The double-blind titration period with either midodrine or ephedrine was 3 to 5 days; the titration end point was to increase standing systolic blood pressure to > or = 80 mm Hg and to maintain a supine pressure below 180/100 mm Hg. The maintenance period was 3 to 5 days. A 4-day placebo washout period was interposed at the crossover point. RESULTS: The ability to stand improved in patients treated with midodrine but not with ephedrine. Midodrine significantly increased both systolic (P < 0.001) and diastolic (P < 0.001) standing blood pressure over placebo (P < 0.001) and ephedrine (P < 0.05). In contrast, ephedrine-induced changes in standing pressures did not significantly differ from placebo (P > 0.05). Midodrine treatment improved the frequency of the ability to stand as compared with ephedrine, and was associated with a significantly higher incidence of standing systolic pressures > 80 mm Hg than was placebo (P < 0.001). Both midodrine and ephedrine significantly increased supine systolic and diastolic blood pressures over placebo (P < 0.001, P < 0.01, P < 0.01, P < 0.01, respectively), but were not significantly different from each other. Ephedrine significantly increased (P < 0.05) the pulse rate as compared with placebo and midodrine, whereas midodrine produced a statistically significant (P < 0.05) but clinically minimal decrease in pulse rate compared with placebo. Neither drug affected clinical laboratory variables. CONCLUSIONS: Midodrine safely and effectively improved orthostatic hypotension caused by autonomic failure. Our data suggest that the ability to stand is improved better by midodrine than by ephedrine.
Adrenergic alpha-Agonists↗
Left ventricular diastolic dysfunction in hypertension.
Abnormalities of left ventricular diastolic function in hypertension are multifactorial in origin. Of importance is the demonstration that abnormalities of left ventricular filling in hypertension may be accompanied by deleterious cardiovascular neurodynamic regulations. However, the left ventricular filling rates can be normalized during medical treatment of hypertension. In particular, regression of left ventricular hypertrophy is almost always associated with or followed by improvement of left ventricular filling. The effects of this normalization on cardiovascular dynamics and the outcome of hypertensive heart disease are yet to be demonstrated.
Antihypertensive Agents↗
Hemodynamic effects of inhibitors of the renin-angiotensin system.
PURPOSE: To review the hemodynamic effects of the various classes of inhibitors of the renin-angiotensin system. DATA PRESENTATION: First, hemodynamic alterations related to inhibition of the renin-angiotensin system were defined. Second, some comparative studies on the various types of inhibitors were examined. RESULTS: Angiotensin converting enzyme (ACE) inhibitors have been well studied in both hypertension and heart failure and have been shown to produce both arteriolar and venous dilation. Renin inhibitors have been shown to achieve equipotent blood pressure reductions to those induced by ACE inhibitors in experimental studies; the mechanism of blood pressure reduction was related to a decrease in systemic resistance, without altering the heart rate or cardiac output. Angiotensin II antagonists are still being studied. CONCLUSIONS: It may be still too early to predict how useful the renin inhibitors and the angiotensin II antagonists will be for the therapy of cardiovascular diseases, compared with ACE inhibitors.
Angiotensin II↗
Neurogenic orthostatic hypotension: a double-blind, placebo-controlled study with midodrine.
PURPOSE: To investigate the efficacy and safety of midodrine for treatment of patients with orthostatic hypotension due to autonomic failure. PATIENTS: Ninety-seven patients with orthostatic hypotension were randomized in a 4-week, double-blinded, placebo-controlled study with a 1-week placebo run-in period. Patients ranged in age from 22 to 86 years (mean: 61 years). METHODS: After a 1-week run-in phase, either placebo or midodrine at a dose of 2.5 mg, 5 mg, or 10 mg was administered three times a day for 4 weeks. Both the placebo group and the 2.5-mg midodrine group received constant doses throughout the double-blind phase. The patients receiving 5 mg or 10 mg of midodrine were given doses that were increased at weekly intervals by 2.5-mg increments until the designated dose was reached. Efficacy evaluations were based on an improvement at 1-hour postdose in standing systolic blood pressure and in symptoms of orthostatic hypotension (syncope, dizziness/lightheadedness, weakness/fatigue, and low energy level). RESULTS: Midodrine (10 mg) increased standing systolic blood pressure by 22 mm Hg (28%, p < 0.001 versus placebo). Midodrine improved (p < 0.05) the following symptoms of orthostatic hypotension compared to placebo: dizziness/lightheadedness, weakness/fatigue, syncope, low energy level, impaired ability to stand, and feelings of depression. The overall side effects were mainly mild to moderate. One or more side effects were reported by 22% of the placebo group compared with 27% of the midodrine-treated group. Scalp pruritus/tingling, which was reported by 10 of 74 (13.5%) of the midodrine-treated patients, was most frequent. Other reported side effects included supine hypertension (8%) and feelings of urinary urgency (4%). CONCLUSION: We conclude that midodrine is an effective and well-tolerated treatment for moderate-to-severe orthostatic hypotension associated with autonomic failure.
Adult↗
Is absolute hypovolemia a risk factor for vasovagal response to head-up tilt?
To test the hypothesis that hypovolemia is associated with an increased incidence of vasovagal syncope during head-up tilt (HUT) 45 patients with history of syncope or presyncope were studied. Blood volume (radio-iodinated serum albumin) was determined, then subjects underwent a graded HUT (from 15 degrees-60 degrees HUT) with cuff blood pressure and ECG monitoring. All patients were kept on their own medications during evaluation. Thirty patients (12 male, 18 female, mean age 50 +/- 19 [SD] years) had hypovolemia, defined as blood volume < 90% of lab normal for corresponding sex, while 15 patients (7 male, 8 female, mean age 52 +/- 21 years) were normovolemic with blood volume ranging from 91%-110% of sex-matched normal subjects. The normovolemic patients served as controls. During HUT, a vasovagal response was elicited in 5 of the 30 hypovolemics and in 4 of the 15 normovolemic (16.7% and 26.7%, respectively, P = NS). In those who developed vasovagal response, the changes of heart rate and blood pressure during HUT were not significantly different between hypovolemics and normovolemics, neither at the endpoint (vasovagal response) nor immediately before the development of the vasovagal response. In patients with nonvasovagal events, four types of hemodynamic responses to tilt were observed: normal blood pressure response associated with normal heart rate increase, normal blood pressure response in association with accentuated increase in heart rate, orthostatic hypotension with normal acceleration of heart rate, and orthostatic hypotension with accelerated increase in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Reduced vascular excitatory responses to cardiopulmonary unloading in hypertensive patients with left ventricular diastolic dysfunction.
Physiological consequences of altered peak left ventricular diastolic filling rate in hypertension have not yet been fully assessed. The hypothesis that altered left ventricular diastolic filling rate interferes with inhibitory cardiopulmonary reflexes was tested. Normalized peak left ventricular diastolic filling rate was calculated from radionuclide ventriculography. Haemodynamic changes during lower body negative pressure (-5 to -40 mmHg) in nine hypertensive patients with slow normalized left ventricular filling rate (Group A) were compared with 16 hypertensive patients with normal normalized peak left ventricular diastolic filling rate and ten normal volunteers of the same age group. Baseline total peripheral resistance was higher in essential hypertension compared to normals but did not differ significantly between the two hypertensive groups. For data analysis, the levels of lower body negative pressure were grouped as low levels of -5 to -10, and -15 to -20 mmHg, an intermediate level of -25 mmHg, and high levels of -30 to -40 mmHg; the change in total peripheral resistance (from baseline) was less prominent in Group A compared to Group B and to normals (-1.4 +/- 1.7 [SE], -0.06 +/- 1.4, 1.1 +/- 1.2 and 4.5 +/- 2 u.M2 in Group A at the four consecutive levels of lower body negative pressure vs. 0.9 +/- 0.7, 3.8 +/- 0.9, 7.2 +/- 1.6, and 8.2 +/- 1.4 in Group B, and 2.0 +/- 0.7, 3.3 +/- 0.8, 4.9 +/- 0.8, and 5.6 +/- 1.0 in normals). The reductions in central venous pressure and in pulmonary wedge pressure were not significantly different among the three groups at the different levels of lower body negative pressure, but the reduction in cardiac output was smaller in patients with reduced dv/dt ratio than in the other two groups. The responses to the cold pressor test were similar in all subjects. We conclude that patients with essential hypertension and diastolic dysfunction have impaired total peripheral resistance responses to lower body negative pressure. This abnormality may reflect an alteration in cardiac baroreflexes secondary to left ventricular diastolic dysfunction, an influence of baseline sympathetic activity on the observed vascular responsiveness to lower body negative pressure, or primary differences among groups in the changes in cardiac output induced by similar levels of lower body negative pressure.
Adult↗
Effect of Buckberg cardioplegia and peripheral cardiopulmonary bypass on infarct size in the closed chest dog.
OBJECTIVES: To simulate a human catheterization laboratory setting of controlled reperfusion during myocardial infarction, regional infusion of commercially available Buckberg cardioplegic solution and peripheral vented bypass were administered in the closed chest dog. BACKGROUND: Studies in open-chest dogs have demonstrated a significant reduction in infarct size and improvement in regional wall motion with a similar controlled reperfusion method using infusion of substrate-enriched (Buckberg) cardioplegic solution during cardiopulmonary bypass coupled with left ventricular venting. METHODS: After 100 or 180 min of balloon occlusion of the proximal left anterior descending artery, controlled reperfusion was performed with cardioplegic infusion and vented bypass. Dogs matched for occlusion time underwent balloon deflation without bypass or cardioplegia (uncontrolled reperfusion groups). Microspheres were used to quantify coronary ischemia during balloon inflation. All four groups (n = 8 to 9 per group) were followed up at 1 week to determine regional wall motion and infarct size. RESULTS: Qualitative echocardiographic analysis demonstrated no significant difference among groups in recovery of regional wall motion at 1 week; however, wall motion improved significantly in all groups between the ischemia and 1-week recovery periods. The histologic infarct size compared with the area at risk for dogs with uncontrolled versus controlled reperfusion, respectively, was 17.9 +/- 10.5% versus 31.9 +/- 8.3% (p < 0.05) for dogs with 100 min of occlusion and 40.1 +/- 11.7% versus 46.2 +/- 8.4% (p = NS) for dogs with 180 min of occlusion. A greater rate-pressure product in the dogs with controlled reperfusion after 100 min of occlusion (p < 0.05) may explain the larger infarct size observed for that group. CONCLUSIONS: These results demonstrate that regional infusion of substrate-enriched cardioplegic solution in combination with peripheral vented bypass does not further reduce infarct size after prolonged ischemia in the closed chest dog (compared with uncontrolled reperfusion).
Animals↗
Differences in left ventricular structural and functional changes between pheochromocytoma and essential hypertension. Role of elevated circulating catecholamines.
Experimental findings suggest that catecholamines increase protein synthesis and play a role in cardiac hypertrophy. We hypothesize that elevated circulating plasma catecholamines in pheochromocytoma influence cardiac structural and functional remodeling. We compared 15 patients with surgically proven pheochromocytoma and 15 with untreated essential hypertension; we matched the patients for age, sex, body surface area, and blood pressure (BP) levels. Left ventricular hypertrophy (LVH) was identified by M-mode echocardiography in six patients with pheochromocytoma and in four with essential hypertension. Among both groups there were no differences in cardiac structure, no correlation between left ventricular mass and BP, no significant differences in mitral E-F slope, no correlation between either plasma norepinephrine or plasma epinephrine levels, and no differences in the left ventricular structural indices measured. In the pheochromocytoma group, left ventricular end systolic stress and end systolic diameter were significantly lower and left ventricular percent fractional shortening was higher. Plasma norepinephrine levels were higher in the pheochromocytoma group, but did not differ among patients of that group with and without LVH. We conclude that in both pheochromocytoma and essential hypertension, only a subset of patients develop evidence of LVH, and that in pheochromocytoma, the elevation of circulating plasma catecholamines is not necessarily associated with LVH. These results indicate that factors other than catecholamines and BP determine the development of LVH in pheochromocytoma.
Adolescent↗
Effects of propranolol on myocardial performance during acute normovolemic hemodilution.
The effects of propranolol and hemodilution on myocardial performance and oxygen delivery were evaluated in 36 anesthetized rats. Oral propranolol treatment consisted of 64 mg/kg/d for 6 weeks prior to the experiments, whereas intravenous (IV) propranolol treatment consisted of 5 micrograms/kg/min for 60 minutes after hemodilution. The hematocrit was reduced to 20% by a hetastarch-for-blood exchange. Animals were divided into six equal groups as follows: (1) no oral drug (water), no hemodilution, no IV drug (saline); (2) oral water, hemodilution, IV saline; (3) oral water, no hemodilution, IV propranolol; (4) oral water, hemodilution, IV propranolol; (5) oral propranolol, no hemodilution, IV saline; and (6) oral propranolol, hemodilution, IV saline. Left ventricular (LV) pressure, maximal dP/dt, ascending aortic blood flow, and response to preload (peak cardiac and stroke volume indices) and afterload (LV-developed pressure) stress were measured. In group 2, hemodilution significantly increased cardiac index, stroke volume index, and dP/dt, and decreased blood pressure, peripheral resistance, and oxygen delivery compared with group 1. Compared with group 2, IV propranolol after hemodilution in group 4 significantly decreased cardiac index, dP/dt, LV-developed pressure, and peak cardiac index, and increased peripheral resistance. Stroke volume index and peak stroke volume index after preload stress remained elevated in group 4, despite the negative inotropic effects of IV propranolol. Oral propranolol in group 6 did not prevent the hemodilution-induced increase in stroke volume index and peak stroke volume index in response to preload stress, although it did decrease cardiac index and dP/dt compared with group 2. Oxygen delivery was reduced in the hemodiluted animals in proportion to the decrease in hemoglobin, regardless of propranolol treatment. It is concluded that reduced myocardial contractility and cardiac performance by nonselective pharmacological beta-adrenoceptor blockade does not interfere with the compensatory increase in stroke volume index after hemodilution.
Administration, Oral↗