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PubMed1995

The hemodynamic and arterial blood gas response to asphyxiation: a canine model of pulseless electrical activity.

OBJECTIVE: Asphyxiation is a time-honored animal model for producing pulseless electrical activity cardiac arrest. To date, there has not been a detailed description of the hemodynamic and arterial blood gas response to asphyxiation in a large number of animals. Our objective was to describe a single laboratory's experience with a standardized canine model of asphyxial pulseless electrical activity arrest. METHOD: Design--Data from 4 separate research protocols using a standardized asphyxial model were retrospectively reviewed. Setting--Resuscitation research laboratory. Participants--169 mixed-breed dogs. Interventions--Each animal was anesthetized and instrumented for hemodynamic monitoring. The endotracheal tube was clamped and hemodynamic data was monitored. Following loss of aortic fluctuations by thoracic aortic catheter, animals remained in pulseless electrical activity for up to 20 min. Hemodynamic data was measured continuously and arterial blood gases were sampled intermittently. RESULTS: Following endotracheal tube clamping, there was a characteristic increase in heart rate and systolic blood pressure. The heart rate peaked at 2-3 min following clamping, while the systolic blood pressure peaked at 7 min. Both heart rate and systolic blood pressure then steadily decreased until loss of aortic fluctuations. Loss of aortic fluctuations occurred 11.4 +/- 2.4 min following clamping. Following loss of aortic fluctuations, the heart rate steadily decreased. Arterial blood gases during asphyxiation and pulseless electrical activity arrest showed profound hypoxemia with hypercarbia (pH 7.03 +/- 0.07; Pco2 93 +/- 19; Po2 12 +/- 7 at loss of aortic fluctuation). CONCLUSIONS: In this canine asphyxial model of pulseless electrical activity, a characteristic hemodynamic pattern of mild tachycardia-hypertension-bradycardia-hypotension was produced. Arterial blood gases reflect a profound hypoxemia and respiratory acidosis.

Animals↗
PubMed1986

Protein-mediated elevations in renal hemodynamics: existence of a hepato-renal axis?

Unlike the intestinal hyperemia which occurs following ingestion of a mixed meal, postprandial renal hemodynamic responses to food appear to be specific to protein-rich meals. Several observations have led to the proposal that following ingestion of protein (meat), a blood-borne factor(s) is released into the systemic circulation which elicits the increases in renal hemodynamics. Glucagon was initially considered as a prime hormonal candidate since the polypeptide is preferentially secreted by the endocrine pancreas in response to protein-rich meals and because glucagon elevates renal hemodynamics by selectively dilating renal afferent arterioles. However, recent data indicate that at postprandial blood levels, glucagon fails to directly mediate protein-induced renal hyperemia and hyperfiltration thus questioning the physiologic importance of glucagon on the renal vasculature. Data have accumulated indicating the importance of the liver and hepatic metabolism during protein-mediated elevations in renal hemodynamics. A hypothesis is advanced suggesting the existence and physiologic importance of a "hepato-renal axis" in mediating the postprandial increases in renal hemodynamics following ingestion of protein-rich meals. The blood-borne factor(s) mediating this response remains to be further clarified and defined.

Amino Acids↗
PubMed1990

Doppler echocardiographic quantitation of cross-sectional area under various hemodynamic conditions: an experimental validation in a canine model of supravalvular aortic stenosis.

The hemodynamic effects on cross-sectional area calculated with the continuity equation were assessed in canine experiments. In 13 open chest dogs, 46 supravalvular aortic stenoses were created by aortic root banding. The cross-sectional area of the stenosis was calculated by Doppler echocardiography with application of the continuity equation before and after the following hemodynamic interventions: protocol 1, atrial pacing at 90, 120, 150 and 180 beats/min after sinus node crush; protocol 2, preload reduction by mild and severe clamping of the inferior vena cava; and protocol 3, afterload augmentation by mild and severe clamping of the descending aorta. In each observation, a dimension of the stenosis was directly measured by two-dimensional echocardiography, and the cross-sectional area was determined as a reference standard. As a result of the hemodynamic interventions, significant changes were observed in stroke volume and pressure gradient (protocol 1), in cardiac output, stroke volume and pressure gradient (protocol 2) and in heart rate, cardiac output and pressure gradient (protocol 3). Despite these changes in hemodynamic variables, the Doppler-derived cross-sectional area showed no significant change for a given stenosis. In addition, areas calculated with the continuity equation (x) agreed well with those determined by two-dimensional echocardiography (y) (r = 0.96, p less than 0.001, y = 0.97x + 0.02, SEE = +/- 0.06 cm2). Thus, it is concluded that Doppler echocardiography with application of the continuity equation accurately predicts the stenotic cross-sectional area over a wide range of hemodynamic conditions in supravalvular aortic stenosis.

Animals↗
PubMed1992

Flosequinan, a new vasodilator: systemic and coronary hemodynamics and neuroendocrine effects in congestive heart failure.

OBJECTIVES: The aim of this study was to evaluate the immediate and long-term systemic and coronary hemodynamic, metabolic and neurohormonal effects of flosequinan in patients with congestive heart failure. BACKGROUND: Preliminary studies have shown that this new long-acting oral systemic vasodilator may have beneficial effects in patients with heart failure. METHODS: Thirteen patients with congestive heart failure were studied. Systemic and coronary hemodynamic, metabolic and neurohormonal effects of flosequinan were assessed acutely with repeat systemic hemodynamic studies after 6 weeks of treatment. RESULTS: The administration of flosequinan acutely and after long-term treatment, resulted in a significant increase in cardiac index, stroke work index and stroke volume index with a reduction in systemic and pulmonary vascular resistances. The improvement in ventricular function was associated with an improvement in left ventricular efficiency without a change in myocardial oxygen consumption or coronary sinus blood flow. Myocardial oxygen extraction and net myocardial lactate extraction also did not change significantly with flosequinan therapy. Systemic catecholamine levels and myocardial catecholamine balance did not change. Plasma arterial and coronary sinus atrial natriuretic factor concentrations were elevated at baseline; the latter concentrations at the level of the great cardiac vein were significantly higher than those of arterial concentrations, indicating increased left ventricular release of atrial natriuretic factor in congestive heart failure. Both arterial and coronary sinus atrial natriuretic factor levels were significantly reduced with the administration of flosequinan at peak effect in association with an improvement in systemic hemodynamics. CONCLUSIONS: Flosequinan therapy in patients with congestive heart failure results in a sustained beneficial hemodynamic action and improved cardiac performance without an increase in metabolic demand or activation of the sympathetic nervous system.

Aged↗
PubMed1994

Improved hemodynamic function and mechanical efficiency in congestive heart failure with sodium dichloroacetate.

OBJECTIVES: The purpose of this study was to determine whether sodium dichloroacetate improves hemodynamic performance and mechanical efficiency in congestive heart failure. BACKGROUND: Congestive heart failure is associated with impaired hemodynamic performance and reduced mechanical efficiency. Dichloroacetate stimulates pyruvate dehydrogenase activity by inhibition of pyruvate dehydrogenase kinase, which results in inhibition of free fatty acid metabolism and stimulation of high respiratory quotient glucose and lactate consumption by the heart. Facilitation of glucose and lactate consumption with dichloroacetate should improve mechanical efficiency of the failing ventricle. METHODS: Ten patients with New York Heart Association functional class III to IV congestive heart failure were studied. Dichloroacetate (50 mg/kg body weight) was administered intravenously for 30 min, with measurements of hemodynamic variables, coronary sinus blood flow and blood gas, glucose and lactate levels for 2 h. The same patients were also given dobutamine (5 to 12.5 micrograms/kg per min) for comparison. RESULTS: Therapeutic levels of dichloroacetate were achieved (100 to 160 micrograms/liter of plasma). Myocardial consumption of lactate was stimulated from 29% to 37.4%. Forward stroke volumes increased (+5.3 ml/beat, p < 0.02), as did left ventricular stroke work (+1.8 g-m/m2 per beat, p < 0.02) and left ventricular minute work (from 1.38 to 1.55 kg-m/m2 per min, p < 0.01). Myocardial oxygen consumption decreased (from 19.3 to 16.5 ml/min, p = 0.06) as left ventricular minute work increased. Left ventricular mechanical efficiency thus improved from 15.2% to 20.6% (p = 0.03). Dobutamine administration resulted in the opposite trend with respect to myocardial lactate extraction (from 34% to 15.3%, p < 0.02). Stroke volume increased (+7.4 ml/beat, p = NS vs. dichloroacetate), as did left ventricular minute work (from 1.29 to 1.59 g-m/m2 per min, p < 0.01 vs. dichloroacetate) and myocardial oxygen consumption (from 18.6 to 21.0 ml/min, p = 0.06 vs. dichloroacetate). Left ventricular mechanical efficiency did not change with dobutamine administration (from 16.4% to 15.8%, p = NS). CONCLUSIONS: Dichloroacetate administration stimulates myocardial lactate consumption and improves left ventricular mechanical efficiency. Forward stroke volume and left ventricular minute work increase significantly, with a simultaneous reduction in myocardial oxygen consumption. Dobutamine administration results in similar hemodynamic improvements but with no change in left ventricular mechanical efficiency and with opposite effects on lactate metabolism. The opposing metabolic actions, yet similar hemodynamic responses, of dichloroacetate and dobutamine suggest that these agents may be complementary in the treatment of congestive heart failure.

Dichloroacetic Acid↗
PubMed1994

High dose oral amiodarone loading exerts important hemodynamic actions in patients with congestive heart failure.

OBJECTIVES: The purpose of this study was to use invasive monitoring to analyze the hemodynamic effects of both a large single dose and a 48-h loading regimen of amiodarone in patients with severe heart failure. BACKGROUND: Amiodarone is frequently used as an antiarrhythmic agent in patients with congestive heart failure, but the impact of this agent on cardiac function remains controversial. Recent successful experience with a rapid oral load of amiodarone makes invasive testing of the hemodynamic effects of oral amiodarone in such patients now feasible. METHODS: After baseline hemodynamic assessment (using balloon-tipped pulmonary artery catheters) and electrocardiographic measurements, 16 patients received 12.5 mg/kg body weight of amiodarone orally. Hemodynamic measurements were obtained hourly for 4 h. Patients then received this dose an additional seven times over the next 2 days. Hemodynamic variables and QRS, QT and PR intervals were measured after 48 h of treatment. RESULTS: Vasodilation was seen between 1 and 3 h after drug administration. Systemic vascular resistance decreased 326 +/- 135 dynes.s.cm-5, cardiac index increased 0.24 +/- 0.08 liters/min per m2 and mean arterial pressure decreased 6 +/- 3 mm Hg (mean +/- SEM, all p < 0.05). After 48 h of amiodarone administration, heart rate decreased 23 +/- 3 beats/min (p < 0.005), stroke volume increased 9 +/- 3 ml (p < 0.005), cardiac index decreased 0.23 +/- 0.09 ml/min per m2 (p < 0.05), pulmonary capillary wedge pressure increased 4 +/- 1 mm Hg (p < 0.01), right atrial pressure increased 3 +/- 1 mm Hg (p < 0.005) and QT and PR intervals were markedly prolonged (p < 0.01). CONCLUSIONS: Although the first dose caused vasodilation, a complete loading regimen of amiodarone produced a decreased heart rate with elevated filling pressures and decreased cardiac index.

Administration, Oral↗
PubMed1995

The efficacy of guanfacine in reducing perioperative hemodynamic changes and volatile anesthetic requirement.

STUDY OBJECTIVE: To evaluate the efficacy of guanfacine, an alpha 2-adrenergic agonist, for attenuating hemodynamic changes associated with tracheal intubation or extubation, providing intraoperative hemodynamic stability, and reducing inhalation anesthetic requirement in patients undergoing gynecologic surgery. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Inpatient gynecology at a university hospital. PATIENTS: 45 women (ASA I) undergoing elective abdominal hysterectomy. INTERVENTIONS: Guanfacine and placebo supplementation. Oral guanfacine at 0.5 or 1 mg or a placebo (control) 3 hours before induction of anesthesia. Anesthesia was induced with thiamylal 5 mg/kg and vecuronium 0.2 mg/kg, and maintained with isoflurane and 50% nitrous oxide (N2O) in oxygen. The inspired isoflurane concentration was maintained at 1% during the first 5 minutes following induction of anesthesia and titrated to the concentration required to maintain hemodynamic stability [defined as +/- 10% of systolic blood pressure (SBP)]. The end-tidal concentration of isoflurane was monitored throughout anesthesia. On completion of surgery, N2O and isoflurane were discontinued. Following confirmation of recovery from anesthesia and muscle relaxation, the endotracheal tube was removed. MEASUREMENTS AND MAIN RESULTS: Patients in the control group showed significant increases in SBP and diastolic blood pressure (DBP) and heart rate (HR) associated with tracheal intubation 50 +/- 5, 57 +/- 6.3, and 45 +/- 4.6 (%, mean +/- SEM, p < 0.05 for any variables), respectively. Plasma norepinephrine and epinephrine concentrations increased to 382 +/- 40 pg/ml and 49 +/- 4.2 pg/ml, respectively (p < 0.05 compared with basal values). These changes were attenuated in patients receiving 1 mg of guanfacine (29 +/- 4.2, 33 +/- 4.5, 25 +/- 3.2, 210 +/- 32, and 22 +/- 3.5, respectively (p < 0.05 for any variables compared with placebo group). Higher inspired concentrations of isoflurane (%) were required in the control and 0.5 mg guanfacine-treated groups (1.2 +/- 0.05 and 1.0 +/- 0.04, respectively) than in the 1 mg guanfacine-treated group (0.62 +/- 0.03) for hemodynamic stability (p < 0.05). Coefficient of variation in HR changes during surgery was 17.2, 13.9, and 8.8 in the placebo, guanfacine 0.5 mg, and guanfacine 1 mg treated groups, respectively. Compared with placebo, guanfacine 1 mg reduced the maximum changes (mean +/- SEM) in SBP (7 +/- 1.2 vs. 18 +/- 2.2) and in HR (23 +/- 2.1 vs. 44 +/- 3.6) occurring during tracheal extubation. The incidence of perioperative complications was similar among the three groups. CONCLUSION: Guanfacine 1 mg administered orally proved to be an effective premedicant for providing intraoperative hemodynamic stability, attenuating the increase in BP and HR associated with tracheal intubation and extubation, and reducing anesthetic requirements without increasing the incidence of perioperative complications.

Adult↗
PubMed1996

Effect of oral clonidine premedication on anesthetic requirement, hormonal response, hemodynamics, and recovery in coronary artery bypass graft surgery patients.

STUDY OBJECTIVE: To examine how premedication with clonidine affects opioid use, hemodynamic effects, hormonal responses, and recovery effects. DESIGN: Double blind, placebo-controlled study. SETTING: Operating room and surgical intensive care unit of a university medical center. PATIENTS: 54 patients undergoing elective coronary artery bypass graft (CABG) surgery. INTERVENTIONS: Patients received approximately 5 micrograms/kg of oral clonidine or a placebo together with 40 micrograms/kg lorazepam 90 minutes prior to titrated sufentanil induction of anesthesia. Thirty minutes prior to cardiopulmonary bypass, a second dose of either approximately 5 micrograms/kg clonidine or placebo was given as a slurry via a nasogastric tube. MEASUREMENTS AND MAIN RESULTS: Opioid use, hemodynamic effects, hormonal responses, and recovery effects were recorded. Values for ten hemodynamic variables were compiled on the evening prior to surgery, prior to induction, and during seven additional events and compared. Catecholamines and beta-endorphins were measured prior to induction, after intubation, and after sternotomy. The amount of sufentanil used for induction, maintenance, and total opioid were compared. The times to awakening and response to verbal commands were compared. The two groups exhibited similar patient demographics, cardiopulmonary bypass time, and duration of surgery. Patients receiving clonidine required significantly (p < 0.04) less sufentanil for induction (clonidine: 2.19 +/- 0.95 micrograms/kg vs. placebo: 2.93 +/- 1.07 micrograms/kg) and total amount of sufentanil (clonidine: 9.1 +/- 3.9 micrograms/kg vs. placebo: 11.7 +/- 4.6 micrograms/kg). Patients receiving clonidine required significantly (p < 0.01) less isoflurane (9.7 +/- 6.8 MAC min vs. 19.7 +/- 9.9 MAC min) to maintain heart rate (HR) and mean arterial pressure (MAP) to within 15% of baseline without significant differences in other vasoactive drugs. Catecholamine concentrations were significantly (p < 0.02) lower in patients receiving clonidine without any difference in beta-endorphin concentrations. Patients receiving clonidine had significantly (p < 0.02) lower HR, systolic arterial pressure, MAP, and systemic vascular resistance prior to induction than patients receiving placebo without differences in other hemodynamic variables. CONCLUSION: Clonidine decreases opioid use and lowers hormonal response while maintaining stable hemodynamics in patients undergoing CABG with sufentanil anesthesia.

Adrenergic alpha-Agonists↗
PubMed2005

Comparison of hemodynamics between Norwood procedure and systemic-to-pulmonary artery shunt for single right ventricle patients.

OBJECTIVE: Despite that surgical outcomes of patients with hypoplastic left heart syndrome have improved, one of the problems remaining is the high interstage mortality after a stage I Norwood procedure. The purpose of this study was to determine the hemodynamic characteristics of hypoplastic left heart syndrome after a Norwood procedure. We examined the perioperative hemodynamic differences of the staged operation between the first stage of the Norwood procedure and systemic pulmonary shunt for single right ventricle patients. METHODS: Data from 39 patients who underwent a Norwood procedure (right ventricle to pulmonary artery conduit: 19, Blalock-Taussig shunt, 20) were analyzed. There were nine early and seven interstage deaths. Bidirectional cavopulmonary shunt was performed in 15 patients and the Fontan procedure in 9 (group H). We defined the control group as 26 patients who underwent the first stage of a systemic pulmonary shunt for a single ventricle. Bidirectional cavopulmonary shunt was performed in 14 patients and the Fontan procedure in 8 (group C). We compared the perioperative hemodynamics of the staged operation between the two groups. RESULTS: Cardiothoracic ratio and single ventricular diastolic dimension before bidirectional cavopulmonary shunt were acutely increased in group H (P=0.02, <0.001). There was no significant difference between the two different types of Norwood procedures. The pulmonary artery index for the right heart bypass operation was lower in group H than in group C (P<0.001). Oxygen saturation before bidirectional cavopulmonary shunt in group H decreased (P<0.001) and thus was lower than that in group C (P=0.003). Mortality and the postoperative clinical parameters of the right heart bypass operation were not different between the two groups. CONCLUSIONS: Patients with hypoplastic left heart syndrome showed hemodynamic instability of acutely increased cardiothoracic ratio, and single ventricular diastolic dimension despite decreased oxygen saturation interstage after stage I of a Norwood procedure. This suggests that this hemodynamic characteristics in hypoplastic left heart syndrome correlates with the higher mortality before second stage palliation than in found with single right ventricle patients.

Fontan Procedure↗
PubMed2006

Optimal pulmonary to systemic blood flow ratio for best hemodynamic status and outcome early after Norwood operation.

OBJECTIVE: Imbalances of pulmonary to systemic blood flow ratio (Q(p)/Q(s)) compounded with inadequate systemic oxygen delivery correlate with mortality after first-stage Norwood palliation of hypoplastic left heart syndrome. Mathematical models suggest that maximal systemic oxygen delivery occurs with Q(p)/Q(s) of less than 1. Whether this applies to clinical practice is unclear. This study evaluates the level of Q(p)/Q(s) that correlates with best hemodynamic status in the first 48 postoperative hours. METHODS: Hemodynamic data of 25 consecutive patients who underwent Norwood procedure from October 2002 to January 2005 were retrospectively analyzed. Data included, in particular, systemic venous and arterial oxygen saturation (SvO(2) and SaO(2), respectively), Q(p)/Q(s), lactate levels, and doses of required inotropes. Parameters were recorded 3 hourly. Data were assigned to three groups according to their corresponding Q(p)/Q(s): Groups 1, 2, and 3 for Q(p)/Q(s)< or =1, Q(p)/Q(s) between 1 and 2, and Q(p)/Q(s)> or =2, respectively. Thereafter, independent t-test or Fisher's exact test was used to reveal significant differences. Q(p)/Q(s) ratios and lactate levels were compared in hospital survivors and non-survivors. RESULTS: Out of 343 samples, 110, 184, and 49 were assigned to groups 1, 2, and 3, respectively. Group 1 (Q(p)/Q(s)< or =1) was characterized by lower SaO(2) (p<0.001) with similar SvO(2) (p=0.3 and p=0.5) and, therefore, higher systemic oxygen delivery (arteriovenous oxygen saturation difference, p<0.001; oxygen excess factor, p<0.001) compared to groups 2 and 3. However, lower mean arterial pressure (p=0.07 and p<0.001), higher lactate levels (p=0.009 and p=0.01), and norepinephrine doses (p=0.006 and p<0.001) highlighted worse hemodynamics. The best hemodynamic status corresponded to group 2. Q(p)/Q(s) remained above 1 in 21 survivors and was, most of the times, below 1 in four patients who died. Lactate levels were almost always above 4 mmol/l or increasing in non-survivors. CONCLUSIONS: Maximum oxygen delivery after Norwood operation occurs at Q(p)/Q(s) of less than 1. However, optimal hemodynamic status and end-organ function and higher survival correlates with Q(p)/Q(s) between 1 and 2. Thus, Q(p)/Q(s) should be targeted at 1.5 for improved course early after first-stage Norwood palliation.

Hemodynamics↗
PubMed2004

A state-space model of the hemodynamic approach: nonlinear filtering of BOLD signals.

In this paper, a new procedure is presented which allows the estimation of the states and parameters of the hemodynamic approach from blood oxygenation level dependent (BOLD) responses. The proposed method constitutes an alternative to the recently proposed Friston [Neuroimage 16 (2002) 513] method and has some advantages over it. The procedure is based on recent groundbreaking time series analysis techniques that have been, in this case, adopted to characterize hemodynamic responses in functional magnetic resonance imaging (fMRI). This work represents a fundamental improvement over existing approaches to system identification using nonlinear hemodynamic models and is important for three reasons. First, our model includes physiological noise. Previous models have been based upon ordinary differential equations that only allow for noise or error to enter at the level of observation. Secondly, by using the innovation method and the local linearization filter, not only the parameters, but also the underlying states of the system generating responses can be estimated. These states can include things like a flow-inducing signal triggered by neuronal activation, de-oxyhemoglobine, cerebral blood flow and volume. Finally, radial basis functions have been introduced as a parametric model to represent arbitrary temporal input sequences in the hemodynamic approach, which could be essential to understanding those brain areas indirectly related to the stimulus. Hence, thirdly, by inferring about the radial basis parameters, we are able to perform a blind deconvolution, which permits both the reconstruction of the dynamics of the most likely hemodynamic states and also, to implicitly reconstruct the underlying synaptic dynamics, induced experimentally, which caused these states variations. From this study, we conclude that in spite of the utility of the standard discrete convolution approach used in statistical parametric maps (SPM), nonlinear BOLD phenomena and unspecific input temporal sequences must be included in the fMRI analysis.

Adult↗
PubMed2004

fMRI analysis with the general linear model: removal of latency-induced amplitude bias by incorporation of hemodynamic derivative terms.

Functional magnetic resonance imaging (fMRI) data are often analyzed using the general linear model employing a hypothesized neural model convolved with a hemodynamic response function. Mismatches between this hemodynamic model and the data can be induced by spatially varying delays or slice-timing differences. It is common practice to desensitize the analysis to such delays by incorporation of the hemodynamic model plus its temporal derivative. The rationale often used is that additional variance will be captured and regressed out from the data. Though this is true, it ignores the potential for amplitude bias induced by small model mismatches due to, for example, variable hemodynamic delays and is not helpful for "random effects" analyses which typically do not account for the first level variance at all. Amplitude bias is due to the use of only the nonderivative portion of the model in the final test for significant amplitudes. We propose instead testing an amplitude value that is a function of both the nonderivative and the derivative terms of the model. Using simulations, we show that the proposed amplitude test does not suffer from delay-induced bias and that a model incorporating temporal derivatives is a more natural test for amplitude differences. The proposed test is applied in a random-effects analysis of 100 subjects. It reveals increased amplitudes in areas consistent with the task, with the largest increases in regions with greater hemodynamic delays.

Acoustic Stimulation↗
PubMed2006

The neural basis of the hemodynamic response nonlinearity in human primary visual cortex: Implications for neurovascular coupling mechanism.

It has been well recognized that the nonlinear hemodynamic responses of the blood oxygenation level-dependent (BOLD) functional MRI (fMRI) are important and ubiquitous in a series of experimental paradigms, especially for the event-related fMRI. Although this phenomenon has been intensively studied and it has been found that the post-capillary venous expansion is an intrinsically nonlinear mechanical process, the existence of an additional neural basis for the nonlinearity has not been clearly shown. In this paper, we assessed the correlation between the electric and vascular indices by performing simultaneous electroencephalography (EEG) and fMRI recordings in humans during a series of visual stimulation (i.e., radial checkerboard). With changes of the visual stimulation frequencies (from 0.5 to 16 Hz) and contrasts (from 1% to 100%), both the event related potentials (ERPs) and hemodynamic responses show nonlinear behaviors. In particular, the mean power of the brain electric sources and the neuronal efficacies (as originally defined in the hemodynamics model [Friston et al. Neuroimage, 12, 466-477, 2000], here represent the vascular inputs) in primary visual cortex consistently show a linear correlation for all subjects. This indicates that the hemodynamic response nonlinearity found in this paper primarily reflects the nonlinearity of underlying neural activity. Most importantly, this finding underpins a nonlinear neurovascular coupling. Specifically, it is shown that the transferring function of the neurovascular coupling is likely a power transducer, which integrates the fast dynamics of neural activity into the vascular input of slow hemodynamics.

Adult↗
PubMed2005

Effects of alcohol on hemodynamic and cardiovascular reaction in different genotypes.

This study assessed hemodynamic changes associated with alcohol intake in people who have different sensitivities to alcohol due to an inactive form of mitochondrial aldehyde dehydrogenase (ALDH). People with ALDH2*1/*2 are more sensitive to alcohol than people with ALDH2*1/*1. Six ALDH2*1/*1 subjects and four ALDH2*1/*2 subjects participated in this study. The subjects drank whisky with water (0.4 ml/kg of ethanol). Optical topography (Hitachi Medical Corporation: ETG-100) was used to measure hemodynamic changes in an occipital region during visual stimulation. Hemodynamic changes, heart rate, mean blood pressure, and reaction time were measured 20 min before, immediately after, and 20, 40, and 60 min after alcohol intake. Breath-alcohol concentration was measured at each of the assessment points. After alcohol intake, the hemodynamic peak value, peak time, reaction time, and heart rate of the ALDH2*1/*2 subjects differed from those of the ALDH2*1/*1 subjects. The hemodynamic peak value and reaction time gradually increased 60 min after alcohol exposure, and the peak time was shortest 20 min after alcohol intake. These results might reflect different acetaldehyde levels causing changes in the reactivity of the vascular smooth muscle and cerebral activity in the visual cortex.

Aldehyde Dehydrogenase↗
PubMed2005

Sildenafil improves hemodynamic parameters in COPD--an investigation of six patients.

Pulmonary hypertension (PH) is an important predictor of mortality in chronic obstructive pulmonary disease (COPD). The phosphodiesterase 5 inhibitor sildenafil has been demonstrated to reduce pulmonary arterial pressure (PAP) in different diseases. We wanted to investigate the effect of sildenafil on hemodynamic parameters and the 6-min walk test (6 MWT) in six patients with severe COPD and echocardiographically estimated PH. A 6 MWT was performed and hemodynamic parameters were measured by right heart catheterization before and 1 and 12h after injection of 50mg sildenafil intravenously. A 3-months period of peroral sildenafil therapy 50mg twice daily followed and finally hemodynamic parameters and a 6 MWT were repeated. Intravenously applied sildenafil could be demonstrated to reduce PAP and pulmonary vasculature resistance (PVR) significantly. And after 3 months of oral sildenafil, the mean PAP has decreased from 30.2+/-5.5 mmHg (range: 24-39 mmHg) to 24.6+/-4.2 mmHg (range: 20-30 mmHg) (p=0.01). The PVR has decreased from 401+/-108 dyn s cm(-5) (range: 266-558 dyn s cm(-5)) to 264+/-52 dyn s cm(-5) (range: 204-333 dyn s cm(-5)) (p<0.05). Physical conditions improved: the 6-min walk distance increased from 351+/-49 to 433+/-52 m. In conclusion, in six patients suffering from severe COPD we could demonstrate significantly improved hemodynamic parameters after 50 mg sildenafil intravenous application. And after 3 months of oral sildenafil, walking distance in the 6 MWT increased significantly as well as hemodynamic parameters in the five patients who had accepted a second right heart catheterization.

Administration, Oral↗
PubMed1990

Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias.

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21 +/- 0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8 +/- 4 mm Hg, pulmonary artery wedge pressure was 20 +/- 3 mm Hg, and cardiac index was 3.2 +/- 0.5 L/min/m2. Following acute hemodynamic decompensation, mean right atrial pressure increased to 16 +/- 5 mm Hg and pulmonary artery wedge pressure to 33 +/- 8 mm Hg; cardiac index decreased to 2.1 +/- 0.5 L/min/m2. In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5 +/- 1.1 micrograms/kg/min), there were significant decreases in mean right atrial pressure (11 +/- 3 mm Hg) and pulmonary artery wedge pressure (16 +/- 3 mm Hg), and a significant increase in cardiac index (3.1 +/- 1.1 L/min/m2) (p less than 0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1998

Effects of the 14F hemopump on coronary hemodynamics in patients undergoing high-risk coronary angioplasty.

BACKGROUND: The influence of the 14F Hemopump on coronary hemodynamics in patients with coronary artery disease remains unknown. METHODS: Systemic and coronary hemodynamic measurements were obtained in eight patients among 13 who underwent high-risk coronary angioplasty in our institution with the support of the Hemopump. Coronary blood flow velocity was measured with a 0.014-inch Doppler-tipped guide wire both proximal and distal to the target lesion. RESULTS: Angioplasty decreases the diameter coronary stenosis from 76% +/- 21% to 22% +/- 11%. Hemopump support did not change systemic hemodynamics either before or after angioplasty. During angioplasty Hemopump support decreased the pulmonary capillary wedge pressure from 23.5 +/- 8.5 mm Hg to 18.6 +/- 7 mm Hg (p = 0.013). No changes in either heart rate, mean and systolic aortic pressures, and cardiac index were observed throughout the procedure. After successful angioplasty was performed, the ratio of proximal to distal flow velocity decreased from 2.11 +/- 1 to 1.65 +/- 0.2 (p = 0.05). However, Hemopump did not affect absolute coronary blood flow velocities or the phasic pattern of flow velocities (diastolic systolic velocity ratio, diastolic and systolic velocity integrals) either in proximal or distal locations either before or after angioplasty. CONCLUSIONS: This study shows that although the 14F Hemopump produces unloading of the left ventricle, it does not importantly alter coronary hemodynamics when systemic hemodynamics are stable. Whether the Hemopump would maintain or improve coronary blood flow in compromised patients remains to be determined.

Aged↗
PubMed1999

Short-term and long-term hemodynamic and clinical effects of metoprolol alone and combined with amlodipine in patients with chronic heart failure.

BACKGROUND: Initiation of beta-blocker therapy is often limited by worsening congestive heart failure, which may manifest as worsening hemodynamics. Deleterious hemodynamic effects might be mitigated with the vasodilation of combined calcium channel/beta-blocker therapy. METHODS AND RESULTS: This prospective, randomized study assessed the safety and efficacy of metoprolol alone or combined with amlodipine on hemodynamic parameters at baseline, 2 hours after the first dose of study medication, and after 12 weeks of therapy in patients receiving background triple therapy for mild to severe heart failure. Functional, exercise, and hormonal status were assessed at baseline and end of study. Twenty-nine patients (mean age 50 +/- 12.1 years) were enrolled; 21 completed 12 weeks of treatment. Mean ejection fraction at baseline was 13.4% +/- 5.7%; 79% of patients had heart failure classified as New York Heart Association class III, and 66% had heart failure of idiopathic origin. Heart rate and blood pressure did not change with short-term therapy in either group. The first dose of both regimens produced significant increases in systemic vascular resistance and significant decreases in cardiac output and index and stroke volume and stroke work indexes; combination therapy acutely yielded small but statistically significant increases in pulmonary artery, pulmonary capillary wedge, and right atrial pressures. Long-term therapy with both regimens produced significant decreases in heart rate, systemic vascular resistance, and pulmonary capillary wedge pressure and significant increases in cardiac output and index and stroke volume and stroke work indexes. Combination therapy produced significant long-term decreases in blood pressure. CONCLUSIONS: There was no further measurable benefit with the addition of amlodipine to metoprolol compared with the effects of metoprolol alone. Therapy with metoprolol alone and the combination of metoprolol and amlodipine was well tolerated in patients with mild to severe heart failure, as evidenced by a lack of adverse effects on hemodynamic parameters over the short term and clinical and hemodynamic improvement with long-term treatment.

Adrenergic beta-Antagonists↗