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1.
High-dose atorvastatin enhances impaired cerebral vasomotor reactivity.
Forteza, A, Romano, JG, Campo-Bustillo, I, Campo, N, Haussen, DC, Gutierrez, J, Koch, S
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association. 2012;(6):487-92
Abstract
The influence of statin therapy on cerebral vasomotor function has not been fully characterized. We report the effects of high-dose atorvastatin therapy on cerebral vasomotor reactivity (VMR) in patients with controlled hypertension and dyslipidemia. We prospectively enrolled 36 patients with controlled hypertension and a low-density lipoprotein (LDL) cholesterol concentration >100 mg/dL. Atorvastatin 80 mg was given daily for 6 months and then discontinued. VMR was assessed by hypercapnic and hypocapnic transcranial Doppler challenge in both the right and left middle cerebral artery (MCA) at baseline, and after 3 and 6 months of therapy. Forty-five days after statin cessation, a repeat VMR was performed. VMR impairment was defined as ≤70%. Blood pressure, lipid levels, liver function, and creatine kinase level were monitored. Mean patient age was 60 years, 16 were men, and 13 had a previous history of subcortical infarction. Mean LDL cholesterol level before treatment was 154 ± 30 mg/dL. Atorvastatin lowered LDL by 53% at 3 months and by 46% at 6 months. Baseline VMR was 71% ± 21% in the right MCA and 70% ± 19% in the left MCA. No significant effect of atorvastatin on VMR was seen at 3 months and 6 months in the study population as a whole. In the subgroup of patients with baseline VMR impairment, atorvastatin therapy was associated with significantly improved VMR at both 3 and 6 months. This effect persisted for at least 45 days after discontinuation of therapy. Our findings indicate that high-dose atorvastatin therapy can significantly improve impaired cerebral VMR, and that the effects of atorvastatin on VMR persist for 1.5 months after discontinuation of therapy. We found no benefit of atorvastatin therapy in patients with preserved baseline vasoreactivity.
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2.
Ascorbate improves circulation in postural tachycardia syndrome.
Stewart, JM, Ocon, AJ, Medow, MS
American journal of physiology. Heart and circulatory physiology. 2011;(3):H1033-42
Abstract
Low flow postural tachycardia syndrome (LFP) is associated with vasoconstriction, reduced cardiac output, increased plasma angiotensin II, reduced bioavailable nitric oxide (NO), and oxidative stress. We tested whether ascorbate would improve cutaneous NO and reduce vasoconstriction when delivered systemically. We used local cutaneous heating to 42°C and laser Doppler flowmetry to assess NO-dependent conductance (%CVC(max)) to sodium ascorbate and the systemic hemodynamic response to ascorbic acid in 11 LFP patients and in 8 control subjects (aged 23 ± 2 yr). We perfused intradermal microdialysis catheters with sodium ascorbate (10 mM) or Ringer solution. Predrug heat response was reduced in LFP, particularly the NO-dependent plateau phase (56 ± 6 vs. 88 ± 7%CVC(max)). Ascorbate increased baseline skin flow in LFP and control subjects and increased the LFP plateau response (82 ± 6 vs. 92 ± 6 control). Systemic infusion experiments used Finometer and ModelFlow to estimate relative cardiac index (CI) and forearm and calf venous occlusion plethysmography to estimate blood flows, peripheral arterial and venous resistances, and capacitance before and after infusing ascorbic acid. CI increased 40% after ascorbate as did peripheral flows. Peripheral resistances were increased (nearly double control) and decreased by nearly 50% after ascorbate. Calf capacitance and venous resistance were decreased compared with control but normalized with ascorbate. These data provide experimental support for the concept that oxidative stress and reduced NO possibly contribute to vasoconstriction and venoconstriction of LFP.
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3.
Effects of a mixed meal on hemodynamics and autonomic control of the heart in patients with type 1 diabetes.
Cozzolino, D, Furlan, R, Gruosso, D, Di Maggio, C, Miraglia Del Giudice, E, Torella, R, Giugliano, D
The Journal of clinical endocrinology and metabolism. 2010;(1):194-200
Abstract
CONTEXT Food intake induces relevant cardiovascular changes together with parallel increases in cardiac sympathetic activity and insulin plasma levels in man. OBJECTIVE We evaluated hemodynamics, neurohormones, and cardiac autonomic control after eating in patients with type 1 diabetes, a disease characterized by the absence of basal and stimulated insulin production. DESIGN AND SETTING Fifteen type 1 diabetic patients and 15 healthy controls underwent blood sampling, electrocardiogram, blood pressure and respiration recordings, and heart rate variability analysis while recumbent, during the 70 degrees head-up tilt, and 20 min after a mixed meal; on another occasion, diabetic patients were also studied 20 min after a mixed meal preceded by their scheduled bolus of exogenous insulin. Spectrum analysis of RR interval provided the indices of sympathetic (LF(RR)) and vagal (HF(RR)) modulation of the sinoatrial node. RESULTS At baseline, no significant differences were found between groups, except for metabolic parameters. Compared with baseline, heart rate, plasma catecholamines, and LF(RR) significantly (P < 0.005) increased, whereas HF(RR) significantly (P < 0.0001) decreased during the tilt in all subjects. Compared with baseline, plasma norepinephrine, heart rate, and LF(RR) significantly (P < 0.05) increased, whereas HF(RR) significantly (P < 0.02) decreased after eating in controls but not in diabetic patients (with and without insulin administered before eating). In both controls and diabetic patients, no relationship between postprandial changes of insulin and LF(RR) and HF(RR) was found. CONCLUSIONS Hemodynamic, neurohormonal, and cardiac neural responses to eating are abnormal in type 1 diabetic patients, independently of insulin.
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4.
Influence of venous drainage and hemofiltration on hypercirculatory instability after high volume crystalloid cardioplegia during coronary artery bypass surgery.
Sirbu, H, Busch, T, Buhre, W, Hilgers, RD, Autschbach, R
The Journal of cardiovascular surgery. 2005;(6):539-49
Abstract
AIM: The etiology of hypercirculatory instability following cardiac surgery with cardiopulmonary bypass has not yet been completely investigated and its clinical impact remains unclear. This prospective study was undertaken in order to investigate the impact of the systemic infusion of high volume crystalloid cardioplegia on the incidence of hypercirculatory instability and inflammatory mediator release in patients undergoing coronary artery bypass grafting. METHODS Forty patients with single-atrial cannulation (group A), 40 patients with single-atrial cannulation and intraoperative hemofiltration (group B), and 40 patients with bicaval cannulation and complete removal of the cardioplegic solution from the right atrium (group C) were analyzed for hemodynamic changes and inflammatory mediator release until the postoperative day 2. Myocardial protection was performed using 2,000 mL cold crystalloid cardioplegia. RESULTS A higher incidence of hypercirculatory instability in group A (39.2%) and B (42.8 %) was noted when compared to group C (18%, P = 0.032). Cardiac index was lower in group C when compared with group A (P = 0.001; 95% CI: 4.1, 15.57) and group B (P = 0.02; 95% CI: 1.13, 15.25). Systemic vascular resistance was higher in group C when compared with group A (P = 0.0001; 95% CI: 7108.7, 3131) and group B (P < 0.005; 95% CI 7598.9; 2830.6). High levels of tumor necrosis factor alpha, interleukin-6, interleukin-8, interleukin-10, and intercellular adhesion molecule-1 with no significant differences between the groups were measured early postoperative. CONCLUSIONS High volume crystalloid cardioplegia under use of single-atrial venous cannulation is associated with a higher incidence of hypercirculatory failure. Hemofiltration during cardiopulmonary bypass offers no benefit on the incidence of hypercirculatory instability and to the release of inflammatory mediators.
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5.
Hypertonic glucose-based peritoneal dialysate is associated with higher blood pressure and adverse haemodynamics as compared with icodextrin.
Selby, NM, Fonseca, S, Hulme, L, Fluck, RJ, Taal, MW, McIntyre, CW
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 2005;(9):1848-53
Abstract
BACKGROUND Little is known about the haemodynamic effects of continuous ambulatory peritoneal dialysis (CAPD) despite its widespread use in the management of end-stage renal failure. We undertook a study to delineate the haemodynamic effects of CAPD using glucose-containing fluids (1.36 and 3.86% glucose) and icodextrin. METHODS Eight CAPD patients were recruited for a prospective crossover study. Patients attended for two investigatory days (in random order). CAPD was carried out using 1.36% followed by 3.86% glucose (buffered with lactate/bicarbonate, Physioneal) on one study day and 1.36% glucose followed by 7.5% icodextrin (Extraneal) on the other day. Dwell times were 150 min. Blood pressure (BP) and a full range of haemodynamic variables including pulse (HR), stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were measured non-invasively using continuous arterial pulse wave analysis. RESULTS BP was significantly higher during 3.86% glucose dwells as compared with 1.36% glucose or icodextrin dwells (P<0.0001). TPR during all three dwells was similar; the higher blood pressure was due to an increased HR, SV and, therefore, CO during 3.86% glucose dwells. The higher blood pressure during the 3.86% glucose dwells was present despite the highest ultrafiltration volume and sodium removal. CONCLUSION This study demonstrates large magnitude haemodynamic changes in response to CAPD. In addition to the well-recognized adverse effects on blood glucose and long-term peritoneal membrane viability, CAPD fluids containing high glucose concentrations may also exert undesirable effects on systemic haemodynamics, with potential long-term consequences for patient outcomes.
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6.
Cardiovascular effects of caffeine in men and women.
Hartley, TR, Lovallo, WR, Whitsett, TL
The American journal of cardiology. 2004;(8):1022-6
Abstract
Caffeine increases blood pressure (BP). In men, acute BP elevations after caffeine intake are due to an increase in vascular resistance, with no change in cardiac output. The hemodynamic effects of caffeine have not been studied in women. Accordingly, BP and hemodynamic responses to caffeine were measured in a double-blind trial comparing age-matched men and women at rest and during mental stress. Caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of brewed coffee) or placebo was given to separate groups of women (n = 21 and 21) and men (n = 16 and 19) (mean ages 29 and 27 years, respectively). BP, cardiac output, and vascular resistance were observed at rest, during a stressful public-speaking simulation, reading aloud, and recovery. Caffeine caused nearly identical systolic and diastolic BP elevations in women (4.5 and 3.3 mm Hg, respectively) and men (4.1 and 3.8 mm Hg, respectively). Men given caffeine versus placebo showed the expected elevation in vascular resistance throughout the remainder of the protocol (p <0.001), with no difference in cardiac output. In contrast, women responded to caffeine with increases in stroke volume (p <0.001) and cardiac output (p <0.001), with no difference in vascular resistance from women taking placebo. Men and women have similar BP responses to caffeine, but the BP responses may arise from different hemodynamic mechanisms. Women who consume a dietary dose of caffeine showed an increase in cardiac output, whereas men showed increased vascular resistance.
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7.
Renal, but not systemic, hemodynamic effects of dopamine are influenced by the severity of congestive heart failure.
Ungar, A, Fumagalli, S, Marini, M, Di Serio, C, Tarantini, F, Boncinelli, L, Baldereschi, G, Valoti, P, La Cava, G, Olianti, C, et al
Critical care medicine. 2004;(5):1125-9
Abstract
OBJECTIVE To determine whether the short-term systemic and renal hemodynamic response to dopamine is influenced by clinical severity of congestive heart failure. DESIGN Effects of increasing doses of dopamine were assessed in patients consecutively admitted for acutely decompensated congestive heart failure. SETTING Intensive care unit. PATIENTS We enrolled 16 congestive heart failure patients stratified by clinical severity (New York Heart Association [NYHA] class III, n = 8; NYHA class IV, n = 8) and two additional NYHA class III patients as controls. INTERVENTIONS Measurements were carried out throughout five 20-min experimental periods: baseline, dopamine infusion at 2, 4, and 6 microg x kg(-1) x min(-1), and recovery. Controls received a similar amount of saline. MEASUREMENTS AND MAIN RESULTS Systemic and renal hemodynamics were determined respectively by right cardiac catheterization and radioisotopes (iodine 131-labeled hippuran and iodine 125-labeled iothalamate clearance). The peak increase in heart rate and cardiac index occurred at a dopamine dose of 4-6 microg x kg(-1) x min(-1). The dose-response relation was similar in NYHA classes III and IV. Improvement in effective renal plasma flow and glomerular filtration rate, peaking at 4 microg x kg(-1) x min(-1), was more rapid and marked in NYHA class III than class IV patients, in whom the renal fraction of cardiac output failed to increase. The systemic and renal effects of dopamine were independent of age. No change occurred in controls. CONCLUSIONS The dose of dopamine producing an optimal improvement of systemic and renal hemodynamics in congestive heart failure is higher than usually reported. A greater clinical severity of congestive heart failure impairs the renal effects of dopamine, probably through a selective loss in renal vasodilating capacity.
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8.
Reductions in systemic and skeletal muscle blood flow and oxygen delivery limit maximal aerobic capacity in humans.
González-Alonso, J, Calbet, JA
Circulation. 2003;(6):824-30
Abstract
BACKGROUND A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity (VO2max) in humans. Severe heat stress drastically reduces VO2max, but the mechanisms have never been studied. METHODS AND RESULTS To determine the main contributing factor that limits VO2max with and without heat stress, we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures (+10 degrees C and +1 degrees C). Heat stress reduced VO2max, 2-legged VO2, and time to fatigue by 0.4+/-0.1 L/min (8%), 0.5+/-0.2 L/min (11%), and 2.2+/-0.4 minutes (28%), respectively (all P<0.05), despite heart rate and core temperature reaching similar peak values. However, before exhaustion in both heat stress and normal conditions, cardiac output, leg blood flow, mean arterial pressure, and systemic and leg O2 delivery declined significantly (all 5% to 11%, P<0.05), yet arterial O2 content and leg vascular conductance remained unchanged. Despite increasing leg O2 extraction, leg VO2 declined 5% to 6% before exhaustion in both heat stress and normal conditions, accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis. CONCLUSIONS These results demonstrate that in trained humans, severe heat stress reduces VO2max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O2 delivery, and O2 uptake. Furthermore, the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O2 delivery to locomotive muscle.
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9.
Beneficial effect of sodium nitroprusside after coronary artery bypass surgery: pump function correlates inversely with cardiac release of proinflammatory cytokines.
Freyholdt, T, Massoudy, P, Zahler, S, Henze, R, Barankay, A, Becker, BF, Meisner, H
Journal of cardiovascular pharmacology. 2003;(3):372-8
Abstract
The authors studied the relationship between cardiac cytokine release and pump function and whether low-dose application of sodium nitroprusside (SNP) improves cardiac performance during coronary artery bypass graft (CABG) creation. Cardiac reperfusion and application of nitric oxide have an influence on cytokine release. However, the functional consequences are unclear. Patients with CABGs (n = 30) with severely compromised left ventricular ejection fraction (<40%) were treated with either SNP (0.5 microg/kg/min) or placebo for the first 60 minutes of reperfusion after cardiac arrest. Interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-alpha were determined in blood samples from the radial artery and coronary sinus during reperfusion (5, 35, and 75 minutes). Hemodynamic measurements were performed before and after cardiopulmonary bypass and at the end of surgery. In all patients, the cardiac index at the end of surgery correlated negatively with levels of TNF-alpha at 5 minutes (r = 0.398; P < 0.05), IL-8 at 35 minutes (r = 0.394; P < 0.05), and IL-6 at 75 minutes of reperfusion (r = 0.421; P < 0.025). Sodium nitroprusside improved the cardiac index immediately after reperfusion (4.4 L/min/m2 +/- 0.3 vs. 3.7 L/min/m2 +/- 0.1; P = 0.014) and at the end of surgery (3.8 L/min/m2 +/- 0.3 vs. 3.0 L/min/m2 +/- 0.2; P = 0.023). The negative correlation between cardiac index and transcardiac cytokines suggests that reducing cardiac inflammatory reaction improves postischemic cardiac function. This was achieved by treating CABG patients with the nitric oxide donor SNP at a dosage without vasodilatory action.
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10.
Cerebral hemodynamic responses to betel chewing: a Doppler study.
Lin, SK, Chang, YJ, Ryu, SJ, Chu, NS
Clinical neuropharmacology. 2002;(5):244-50
Abstract
We sought to evaluate cerebral hemodynamic responses to betel chewing. Thirty healthy male volunteers (mean age = 35 years), ten new chewers, ten occasional chewers, and ten chronic chewers were included in this study. We used carotid duplex sonography and transcranial Doppler to measure the flow velocities and flow volume (FV) of the common carotid (CCA), internal carotid (ICA), external carotid (ECA) arteries, and the flow velocity of middle cerebral artery (MCA). Blood pressure (BP) and heart rate (HR) were recorded simultaneously. All subjects were asked to chew fruit-flavored chewing gum for 10 minutes. Blood flows of the above vessels were measured four times at baseline and at the 2nd, 6th, and 12th minute after chewing. A repeated study was followed in the same subject but substituted with betel nut. Chronic chewers had delayed onset time and shortened vanishing time of facial-flushing sensation. Systolic and diastolic BPs were mildly elevated during gum chewing (p = 0.008 and 0.015, respectively), whereas diastolic BP was dropped during betel chewing (p = 0.008). Heart rate increased prominently during betel chewing (p < 0.0001), especially in new and occasional chewers. The peak systolic, end diastolic velocities, and FV in ECA and CCA increased significantly during betel chewing (p < 0.0001). The blood flows in the ICA and MCA had no significant changes during gum or betel chewing. Betel chewing has a central sympathetic effect resulting in accelerated HR, increased blood flows in ECA and CCA, but has a peripheral cholinergic effect resulting in a drop of diastolic BP. Intracranial cerebral hemodynamics is not affected during betel chewing. The inotropic and chronotropic effect to the heart from betel chewing is probably an unfavorable risk for patients with ischemic heart disease.