Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEMODYNAMICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed2003

Particle-hemodynamics modeling of the distal end-to-side femoral bypass: effects of graft caliber and graft-end cut.

Late-stage occlusions of peripheral synthetic bypass grafts are frequently due to intimal hyperplasia and/or thrombosis at the distal anastomosis, resulting in unacceptably high failure rates. It has been widely established that hemodynamic and blood particle interactions with the vascular surface as well as surgical injury and compliance mismatch are inciting mechanisms capable of eliciting various cellular level responses associated with distal anastomotic intimal hyperplasia (IH) formation. Primary geometric factors influencing anastomotic hemodynamics include the graft-to-artery diameter ratio and graft-hood shape, which are determined by the graft caliber and initial graft-end cut selected by the vascular surgeon. In this study, the particle-hemodynamic effects of graft-end cuts (straight, curved, and S-shaped) and graft-to-artery diameter ratios (2:1 vs. 1.5:1) have been numerically assessed in four common unexpanded anastomotic configurations with respect to vortical flow patterns, wall shear stress based parameters, and platelet interactions with the vascular surface. Sites of significant platelet-wall interactions have been identified by a novel near-wall residence time (NWRT) model, which includes shear stress based factors for platelet activation and endothelial cell expression of anti-thrombogenic compounds. Of the configurations evaluated, straight and curved graft-end cuts with a graft-to-artery diameter ratio of 1.5:1 were found to reduce the particle-hemodynamic potential for IH development at locations critical to flow delivery. Nevertheless, the potential for significant IH occurrence via platelet and/or endothelial response pathways was highly evident in all conventional anastomoses considered, such that a decisively superior configuration was not determined. These results illustrate the need for alternative anastomotic designs with the intent of reducing critical hemodynamic wall parameters and mitigating regions of significant particle-wall interactions.

Anastomosis, Surgical↗
PubMed2000

Limits of corrected flow time to monitor hemodynamic status in children.

OBJECTIVE: Doppler corrected flow time (i.e., corrected left ventricular ejection time) as a noninvasive tool for assessing hemodynamic changes has been previously reported for adult patients. Its use in paediatrics seems to be worthwhile but no data concerning its accuracy are presently available in this population. The purpose of this work was to study the relationships between corrected flow time (FT) and indices of systemic vascular resistance (SVR) and of myocardial contractility in healthy children. METHODS: Twenty healthy children performed a graded maximal bicycle exercise in order to induce physiological hemodynamic alterations. Hemodynamic parameters were measured with an echocardiography-Doppler at rest and within a few minutes of post exercise. Cycle time (RR), mean aortic flow velocity, mean systolic velocity (MSV), FT, peak velocity (PV), and stroke distance were measured on the Doppler aortic velocity waveform. Cardiac index (CI) and SVR were calculated from the classical volumetric equation. Corrected FT was calculated by using Bazett's formula (FTb = FT/square root(RR)) and a simplified formula FTc = FTmeasured + [1.29 x (HR - 60)]. RESULTS: Post exercise, SVR, RR, FT, decreased, while CI, PV and MSV increased and stroke distance remained unchanged. After multiple regression analysis no significant correlation between SVR and FTb and SVR or FTc was noted. A significant correlation appeared between FTb and, respectively, PV (r = -0.83; p < 0.001), stroke distance (r = 0.78; p < 0.001) and RR (r = -0.52; p = 0.0016). A significant correlation was also shown between FTc and, respectively, PV (r = -0.71; p < 0.001) and stroke distance (r = 0.63; p < 0.001) but not with RR. CONCLUSIONS: These results show that the use of Bazett's formula correct FT could lead to hemodynamic misinterpretations, because it does not rule out all the heart rate effect. Moreover, in healthy children corrected FT appears as an inaccurate index to monitor physiological afterload alterations, because of the involvment of other hemodynamic factors such as contractility in its variation.

Adolescent↗
PubMed2003

Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased immunologic activation of donor kidneys.

BACKGROUND: Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death-induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. METHODS: In Wistar rats, short-term (1 hour) or long-term (6 hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1 hour and 6 hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the immunologic status of the kidney. RESULTS: Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. CONCLUSION: Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.

Animals↗
PubMed2001

In situ hemodynamics of perforating veins in chronic venous insufficiency.

PURPOSE: The prevalence of incompetent perforators increases linearly with the clinical severity of chronic venous insufficiency (CVI) and the presence of deep vein incompetence. Putative transmission of deep vein pressure to skin may cause dermal hypoxia and ulceration. Despite extensive prospective interest in the contribution of perforators toward CVI, their hemodynamic role remains controversial. The aim of this prospective study was to determine the in situ hemodynamic performance of incompetent perforating veins across the clinical spectrum of CVI, by means of duplex ultrasonography. METHODS: A total of 265 perforating veins of 90 legs that had clinical signs and symptoms consistent with CVI in 67 patients referred consecutively to the blood flow laboratory were studied. The clinical distribution of the examined limbs was CEAP(0), 10 limbs; CEAP(1-2), 39 limbs; CEAP(3-4), 21 limbs; and CEAP(5-6), 20 limbs. With the use of gated-Doppler ultrasonography on real-time B-mode imaging, the flow velocity waveforms were obtained from the lumen of perforators on release of manual distal leg compression in the sitting position and analyzed for peak and mean velocities, time to peak velocity, volume flow, venous volume displaced outward, and flow pulsatility. The diameter and duration of outward flow (abnormal reflux > 0.5 seconds) were also measured. RESULTS: Incompetent perforators had bigger diameters, higher peak and mean velocities and volume flow, longer time to peak velocity, and bigger venous volume displaced outward (VV(outward)) than competent perforators (all, P <.0001). The diameter of incompetent perforators did not change significantly with CEAP class (all, P >.1). Incompetent thigh and lower-third calf perforators had a significantly bigger diameter than perforators in the upper and middle calf combined (both, P <.05), in incompetent perforators: reflux duration was unaffected by CEAP class or site (P >.3); peak velocity was higher in those in CEAP(3-4) than those in CEAP(1-2) (P =.024); mean velocity in those in CEAP(3-6) during the first second of reflux was twice that of those in CEAP(1-2) (P <.0001); both higher volume flow and VV(outward) were found in the thigh perforators than those in the upper and middle calf thirds (P <.03); CEAP(3-6) volume flow and VV(outward), both in the first second, were twice that in those in CEAP(1-2) (P <.002); flow pulsatility in those in CEAP(5-6) was lower than in those in CEAP(1-2) (P =.014); in deep vein incompetence, higher peak velocity, volume flow, VV(outward), and diameter occurred than in its absence (P <.01). CEAP designation correlated significantly with mean velocity and flow pulsatility, both in the first second (r = 0.3, P <.01). The flow direction pattern in perforator incompetence was uniform across the CVI spectrum: inward on distal manual limb compression, and outward on its release; competent perforators had a smaller percentage of outward flow on limb compression (P <.01). CONCLUSION: In addition to an increase in diameter, perforator incompetence is characterized by significantly higher mean and peak flow velocities, volume flow, and venous volume displaced outward, and a lower flow pulsatility. Differences in early reflux enable a better hemodynamic stratification of incompetent perforators in CVI classes. In the presence of deep reflux, incompetent perforators sustain further hemodynamic impairment. In situ hemodynamics enable quantification of the function of perforators and can be used in the identification of the clinically relevant perforators and the impact of surgery.

Adolescent↗
PubMed1993

Renal hemodynamics and cardiovascular reactivity in the prehypertensive stage.

To examine whether sympathetic nervous activation has an impact on renal circulation in subjects at risk for high blood pressure, we assessed renal hemodynamics and cardiovascular response to mental stress in 40 healthy young white males, 12 normotensive subjects without and 14 with familial hypertension, and 14 with borderline hypertension. The response of systolic and diastolic blood pressure to mental stress was assessed while each patient performed a mental arithmetic task; this was taken as the parameter for the activation of the sympathetic nervous system. Renal plasma flow was measured by para-aminohippuric acid clearance under steady-state conditions. In parallel, glomerular filtration rate as a parameter for functional impairment of the kidneys was determined by creatinine clearance, and filtration fraction was also calculated. Patients with borderline hypertension were characterized by a reduced renal blood flow and increased filtration fraction in comparison with both normotensive groups. The increase in systolic blood pressure during mental stress was more pronounced in borderline hypertensives. We observed no significant difference in renal hemodynamics and cardiovascular response to mental stress between normotensives with and without a family history of hypertension. In the total population, cardiovascular response to mental stress was correlated with renal hemodynamics: The greater the increase in systolic blood pressure during mental stress, the lower was the renal plasma flow and the greater the filtration fraction. Thus, renal plasma flow was found to be already reduced and filtration fraction increased before sustained hypertension developed. Because this pattern in renal hemodynamics was related to cardiovascular response to mental stress, our data suggest that sympathetic activation already appeared to affect renal hemodynamics at the onset of essential hypertension.

Adult↗
PubMed2001

Right heart assist ensures hemodynamic stability during beating heart coronary surgery on marginal arteries. An animal experimental porcine study.

OBJECTIVES: In many heart centers myocardial revascularization using beating heart coronary surgery has partly replaced conventional coronary artery bypass grafting (cCABG) using cardiopulmonary bypass. However, access to the marginal arteries is problematic and hampered by space limitations, which might compromise the quality of the anastomoses and it entails a significant risk of hemodynamic instability subsequent to the manipulations of the heart. Hemodynamic impairment may be caused by dislocation of the low-pressure right atrium and ventricle. Therefore, it was hypothesized that the use of Right Heart Assist (RHA) may be able to ensure hemodynamic stability when tilting and manipulating the heart. DESIGN: In an animal experimental model RHA was implemented in order to study the hemodynamic impact of dislocating the heart in a standardized fashion. RESULTS: Dislocation of the unassisted heart to expose the first and second marginal branches caused a decline in arterial blood pressure, cardiac output and venous saturation of 38-48%. Supported by RHA this decrease was minimized to 0-17%. CONCLUSION: RHA for beating heart procedures indicates several advantages: ample time and safety while making the anastomoses at the marginal branches, less space limitations and enhanced control of hemodynamic stability compared with no RHA. This operation technique is challenging current practice and indications, and may potentially replace cCABG for the majority of patients.

Animals↗
PubMed1993

Fenoldopam improves renal hemodynamics impaired by positive end-expiratory pressure.

BACKGROUND: Mechanical ventilation with positive end-expiratory pressure (PEEP) can impair renal hemodynamics. Fenoldopam, a dopamine receptor agonist, has been shown, in animal experiments, to improve renal perfusion. The purpose of the current study was to examine the effects of this agent on altered renal hemodynamics secondary to positive pressure ventilation. METHODS: Twelve patients requiring mechanical ventilation of their lungs and PEEP for the treatment of hypoxemia after multiple trauma or visceral surgery were studied. Hemodynamic variables, renal vascular resistance, urine flow, creatinine, inulin and PAH clearance, and excretion of sodium and potassium (NaE and KE) were measured before and after introduction of a level of PEEP high enough to decrease urine flow rate by 25% or more, and after administration of intravenous fenoldopam. RESULTS: No hemodynamic effect resulted from 0.1 microgram.kg-1.min-1, but 0.2 micrograms.kg-1.min-1 fenoldopam decreased both diastolic and mean arterial blood pressure from 66 +/- 37 (mean +/- SEM) to 57 +/- 21 mmHg, and from 83 +/- 3 to 74 +/- 4 mmHg, respectively. Renal vascular resistance was reduced from 54 +/- 12 to 19 +/- 5 dynes.s.cm-5 at 0.2 micrograms.kg-1.min-1. Fenoldopam produced a dose-related increase in renal blood flow and PAH clearance. With 0.2 micrograms.kg-1.min-1 fenoldopam, urine flow increased from 81 +/- 25 to 116 +/- 29 ml/h, NaE from 28 +/- 7 to 85 +/- 70 microM/min, and KE from 65 +/- 12 to 109 +/- 16 microM/min. CONCLUSIONS: The results of the current study indicate that intravenous fenoldopam at a dose of 0.2 micrograms.kg-1.min-1 improves renal hemodynamics and increases Na and K excretion in patients requiring mechanical ventilation of their lungs and PEEP. These effects are probably caused by an increased kidney perfusion secondary to renal artery vasodilation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1998

The pharmacodynamic interaction between propofol and fentanyl with respect to the suppression of somatic or hemodynamic responses to skin incision, peritoneum incision, and abdominal wall retraction.

BACKGROUND: Sufficient propofol or fentanyl doses necessary to prevent the response to skin incision do not necessarily attenuate hemodynamic responses during surgery. The goal of this study was to characterize the pharmacodynamic interaction between propofol and fentanyl with respect to the suppression of somatic or hemodynamic responses after three stimuli: skin incision, peritoneum incision, and abdominal wall retraction. METHODS: Propofol and fentanyl were administered via computer-assisted continuous infusion to provide equilibration between plasma-blood and biophase concentrations. Patients were randomized to nine groups that received predetermined concentrations of fentanyl (from 0 to 9 ng/ml). Each patient was administered different target concentrations of propofol. Somatic and hemodynamic responses were measured before and after each of three different stimulations: skin incision (si), peritoneum incision (pi), and abdominal wall retraction (ret). The propofol plasma concentrations at which 50% of the patients did not respond to each type of stimulation (Cp50si, Cp50pi, and Cp50ret) were calculated by fitting the Loewe synergistic model. RESULTS: For propofol alone, Cp50si, Cp50pi, and Cp50ret were 12.9, 17.1, and 19.4 microg/ml, respectively. Increasing the fentanyl concentration markedly reduced propofol Cp50si, Cp50pi, and Cp50ret for somatic response, indicating the potential synergistic interaction of both drugs. During the prestimulation period, fentanyl did not decrease systolic blood pressure; however, propofol specifically decreased systolic blood pressure. Both drugs had a synergistic drug interaction on the systolic blood pressure increase after various surgical stimulations. Fentanyl and propofol concentrations that suppressed both the 50% probability of somatic response and the 50% probability of moderate hemodynamic change defined by the 15% systolic blood pressure increase over the prestimulation value were 3.6 ng/ml and 2.5 microg/ml for skin incision, 8.4 ng/ml and 1.6 microg/ml for peritoneum incision, and 5.9 ng/ml and 5.1 microg/ml for wall retraction, respectively. CONCLUSIONS: The anesthesia requirements for stimuli that are more intense than skin incision should be considered during abdominal surgery. Somatic and hemodynamic responses varied depending on the type of surgical stimuli.

Abdominal Muscles↗
PubMed1992

Control of renal hemodynamics during intrarenal and systemic blockade of nitric oxide synthesis in conscious dogs.

Systemic blockade of nitric oxide (NO) synthesis results in marked increases in the renal vascular resistance (RVR) and decreases in the glomerular filtration rate (GFR) and renal plasma flow (RPF). The renal hemodynamic effect of systemic NO blockade is most likely due to an integration of direct and indirect renal actions. The quantitative importance of local intrarenal blockade of NO synthesis on renal hemodynamics has not been fully elucidated. Therefore, the purpose of this study was to compare the renal hemodynamic effects of intrarenal vs. systemic NO synthesis blockade on renal hemodynamics. Nitro-L-arginine methyl ester (L-NAME) was infused intrarenally at a rate of 3 micrograms/kg/min for 180 min in conscious chronically instrumented dogs (n = 7). Intrarenal infusion of L-NAME for 180 min resulted in a 12% decrease in RPF, 14% increase in RVR, and no effect on mean arterial pressure (MAP) or GFR. In contrast, infusion of L-NAME intravenously at a rate of 10 micrograms/kg/min for 180 min increased the RVR by 124% and decreased the RPF by 55% and GFR by 45%. The MAP and heart rate both increased in response to intravenous administration of L-NAME. The results of this study suggest that the renal hemodynamic effects of systemic administration of L-NAME may, in large part, be secondary to extrarenal effects of NO synthesis blockade, possibly via activation of the sympathetic nervous system.

Animals↗
PubMed1995

Exploratory study of the effects of single doses of isomazole on hemodynamics and heart rate variability parameters in chronic heart failure.

Ventricular arrhythmias and disturbed autonomic control, as reflected by abnormal heart rate variability (HRV), are related to hemodynamic impairment in chronic heart failure (CHF). We investigated the effects of orally (p.o.) administered isomazole, a new phosphodiesterase (PDE) inhibitor with calcium-sensitizing properties, on hemodynamics, ventricular arrhythmias, and HRV and examined a possible interaction between these parameters. Hemodynamic measurements and ambulatory ECG monitoring were performed in 12 patients with stable CHF class III-IV after single doses of isomazole 5-30 mg. Pulmonary wedge pressure decreased after 5, 10, 20, and 30 mg, but cardiac output, (CO) increased only after the higher doses [20 mg, + 20% (p = 0.031)] of isomazole. HR did not change. Mean arterial and pulmonary artery pressure, (MAP, PAP) decreased significantly in the 10- and 20-mg groups [10 mg, -6% (p = 0.035) and -14% (p < 0.001) respectively; 20 mg, -13% (p = 0.047) and -31% (p = 0.006), respectively]. Isomazole did not exert a significant effect on ventricular arrhythmias in the subsequent 24 h after acute dosing. Analysis of HRV showed that rMSSD and pNN50 (parameters of vagal tone) tended to increase after isomazole administration. Normalized high-frequency power during the day increased from 17.4 to 22.3 nu (p < 0.05), whereas low frequency tended to decrease from 52.7 to 48.2 nu (p = 0.06). Acute isomazole administration improves hemodynamics but has no effect on ventricular arrhythmias. The HRV variability data suggest development of an increase in vagal control of HR, parallel to the acute hemodynamic improvement after isomazole. Withdrawal of vagal control of HR in CHF may be a reversible process.

Administration, Oral↗
PubMed2003

Hypoxic hepatitis: clinical and hemodynamic study in 142 consecutive cases.

The centrilobular liver cell necrosis observed in hypoxic hepatitis is generally attributed to failure of hepatic blood perfusion. Accordingly, this injury of the liver is commonly recognized under the terms "shock liver" or "ischemic hepatitis." During a 10-year period, 142 episodes of hypoxic hepatitis were consecutively identified in the intensive care unit of a general hospital, and the clinical, biological, and hemodynamic parameters were prospectively collected on individual files. We conducted the current study to assess retrospectively the role of the hemodynamic mechanisms of tissue hypoxia: ischemia, passive venous congestion, and hypoxemia. Among the 142 episodes of hypoxic hepatitis, 138 were separated in 4 main groups based on clinical features: decompensated congestive heart failure (80 cases), acute cardiac failure (20 cases), exacerbated chronic respiratory failure (19 cases), and toxic/septic shock (19 cases). An elementary hemodynamic evaluation, including blood pressure, central venous pressure, and arterial blood gas analysis, was carried out in every episode and a more complete hemodynamic assessment through pulmonary artery catheterization was performed in 61 episodes. The hemodynamic mechanisms responsible for hypoxic hepatitis were different in the 4 groups. In congestive heart failure and acute heart failure, the hypoxia of the liver resulted from decreased hepatic blood flow (ischemia) due to left-sided heart failure and from venous congestion secondary to right-sided heart failure. In chronic respiratory failure, liver hypoxia was mainly due to profound hypoxemia. In toxic/septic shock, oxygen delivery to the liver was not decreased but oxygen needs were increased, while the liver was unable to use oxygen properly. In all conditions underlying hypoxic hepatitis, except toxic/septic shock, a shock state was observed in only about 50% of the cases. Therefore, the expressions "shock liver" or "ischemic hepatitis" are misleading and should be replaced by the more general term "hypoxic hepatitis."

Adolescent↗
PubMed2004

Identification of hemodynamic compromise by cerebrovascular reserve and oxygen extraction fraction in occlusive vascular disease.

Cerebrovascular reserve (CVR) and oxygen extraction fraction (OEF) are used to identify hemodynamic compromise in symptomatic patients with carotid occlusive vascular disease, but evidence suggests that they are not equivalent. The authors studied the relationship between CVR and OEF to evaluate their equivalence and stages of hemodynamic compromise. Symptomatic patients (N = 12) with carotid occlusion were studied by stable xenon-computed tomography CBF after intravenous acetazolamide administration for CVR, followed within 24 hours by positron emission tomography (PET) for OEF. Middle cerebral artery territories were analyzed by hemisphere and level. Hemispheric subcortical white matter infarctions were graded with magnetic resonance imaging. Both hemispheric and level analysis of CVR and OEF showed a significant (P = 0.001), negative linear relationship [CVR (%) = -1.5 (OEF) + 83.4, (r = -0.57, P = 0.001, n = 24]. However, 37.5% of the hemispheres showed compromised CVR but normal OEF and were associated (P = 0.019) with subcortical white matter infarction. CMRO2 was elevated in stage II hemodynamic compromise (CVR < 10%, OEF > 50%). CVR and OEF showed a significant negative linear relationship in stage II hemodynamic compromise but revealed hemispheres in hemodynamic compromise by CVR but normal OEF that were associated with subcortical white matter infarction.

Aged↗
PubMed2006

Perioperative biventricular pacing leads to improvement of hemodynamics in patients with reduced left-ventricular function--interim results.

BACKGROUND: Cardiac resynchronization therapy (CRT) has been introduced as a new therapeutic modality in patients with chronic heart failure. However, most studies have investigated the hemodynamic effects in congestive, but not postoperative heart failure. OBJECTIVE: The following study investigates hemodynamic effects of perioperative temporary biventricular pacing in patients undergoing open heart surgery. In 54 patients one left and one right ventricular epicardial wire was placed during open heart operations. Hemodynamic parameters were measured immediately after the operation and 6 as well as 24 hours postoperatively. Transesophageal echocardiography was performed 1 hour postoperatively. RESULTS: Of the 54 patients (59.2%), 32 responded to biventricular pacing with an increase in cardiac output; in these patients synchronized ventricular contraction could be verified echocardiographically. This hemodynamic benefit persisted 6 hours and 24 hours postoperatively. The remaining 22 patients did not show any hemodynamic improvement from biventricular stimulation. CONCLUSION: Biventricular pacing leads to significant rise in cardiac output in approximately 59% of patients with severely reduced left ventricular function and widened QRS complexes. Further studies are necessary to define clearly the clinical characteristics of patients who show remodeling by CRT.

Aged↗
PubMed1999

Stress Echocardiography in Aortic Stenosis: Insights into Valve Mechanics and Hemodynamics.

Stress interventions have been classically combined with cardiac catheterization recordings to understand the hemodynamic principles of valvular stenosis. Indices of aortic stenosis such as pressure gradient and valve area were based on simple hydraulic principles and have proved to be clinically useful for patient management during a number of decades. With the advent of Doppler echocardiography, these hemodynamic indices can be readily obtained noninvasively. Abundant evidence obtained using exercise and pharmacological stress echocardiography has demonstrated that the assumptions of classic hemodynamic models of aortic stenosis were wrong. Consequently, it is recognized that conventional indices may be misleading indicators of aortic stenosis significance in particular clinical situations. To improve diagnostic accuracy, several alternative hemodynamic models have been developed in the past few years, including valve resistance and left ventricular stroke work loss, among others. Nevertheless, these more-accurate indices should be obtainable noninvasively and need to demonstrate greater diagnostic and prognostic power than conventional indices; preliminary data suggest such superiority. Stress echocardiography is well established as the tool of choice for testing hypothesis and physical models of cardiac valve function. Although the final role of alternative indices is not yet well established, the new insights into valvular hemodynamics provided by this technique may change the clinical assessment of aortic stenosis.

Journal Article↗
PubMed2004

Effects of anesthetics on systemic hemodynamics in mice.

The aim of this study was to compare the systemic hemodynamic effects of four commonly used anesthetic regimens in mice that were chronically instrumented for direct and continuous measurements of cardiac output (CO). Mice (CD-1, Swiss, and C57BL6 strains) were instrumented with a transit-time flow probe placed around the ascending aorta for CO measurement. An arterial catheter was inserted into the aorta 4 or 5 days later for blood pressure measurements. After full recovery, hemodynamic parameters including stroke volume, heart rate, CO, mean arterial pressure (MAP), and total peripheral resistance were measured with animals in the conscious state. General anesthesia was then induced in these mice using isoflurane (Iso), urethane, pentobarbital sodium, or ketamine-xylazine (K-X). The doses and routes of administration of these agents were given as required for general surgical procedures in these animals. Compared with the values obtained for animals in the conscious resting state, MAP and CO decreased during all anesthetic interventions, and hemodynamic effects were smallest for Iso (MAP, -24 +/- 3%; CO, -5 +/- 7%; n = 15 mice) and greatest for K-X (MAP, -51 +/- 6%; CO, -37 +/- 9%; n = 8 mice), respectively. The hemodynamic effects of K-X were fully antagonized by administration of the alpha(2)-receptor antagonist atipamezole (n = 8 mice). These results indicate that the anesthetic Iso has fewer systemic hemodynamic effects in mice than the nonvolatile anesthetics.

Adjuvants, Anesthesia↗
PubMed2000

Role of neuronal nitric oxide synthase (NOS1) in the pathogenesis of renal hemodynamic changes in diabetes.

Nitric oxide (NO) has been implicated in the pathogenesis of renal hemodynamic changes in diabetes mellitus. However, the contribution of nitric oxide synthase (NOS) isoforms to intrarenal production of NO in diabetes remains unknown. To explore the role of NOS1 in the control of renal hemodynamics in diabetes, we assessed renal responses to inhibition of NOS1 with S-methyl-L-thiocitrulline (SMTC; administered into the abdominal aorta) in moderately hyperglycemic streptozotocin-diabetic rats (D) and their nondiabetic (C) and normoglycemic diabetic counterparts. The contribution of other NOS isoforms was also evaluated by assessing the responses to nonspecific NOS inhibition [N(G)-nitro-L-arginine methyl ester (L-NAME)] in SMTC-treated diabetic rats. The number of NOS1-positive cells in macula densa of D and C kidneys was also evaluated by immunohistochemistry. D rats demonstrated elevated glomerular filtration rate (GFR) compared with C. SMTC (0.05 mg/kg) normalized GFR in D but had no effect in C. SMTC-induced reduction of renal plasma flow (RPF) was similar in C and D. Normoglycemic diabetic rats demonstrated blunted renal hemodynamic responses to NOS1 inhibition compared with hyperglycemic animals. Mean arterial pressure was stable in all groups. L-NAME induced a further decrease in RPF, but not in GFR, in D rats treated with SMTC. Immunohistochemistry revealed increased numbers of NOS1-positive cells in D. These observations suggest that NOS1-derived NO plays a major role in the pathogenesis of renal hemodynamic changes early in the course of diabetes. NOS1 appears to be the most important isoform in the generation of hemodynamically active NO in this condition.

Animals↗
PubMed2005

Hemodynamic and autonomic changes induced by Ironman: prediction of competition time by blood pressure variability.

We hypothesized that the extreme endurance exercise of an Ironman competition would lead to long-standing hemodynamic and autonomic changes. We investigated also the possibility of predicting competition performance from baseline hemodynamic and autonomic parameters. We have investigated 27 male athletes before competition, 1 h after, and then for the following week after the competition. The Task Force monitor was used to measure beat-to-beat hemodynamic and autonomic parameters during supine rest and active standing. Heart rate (P < 0.001) was increased, and stroke index (P = 0.011), systolic blood pressure (P = 0.004), diastolic blood pressure (P < 0.001), total peripheral resistance index (P < 0.001), and baroreceptor reflex sensitivity (P < 0.001) were decreased after the competition. The 0.05- to 0.17-Hz band of heart rate and blood pressure variability was increased (P < 0.001 and P < 0.001, respectively), the 0.17- to 0.40-Hz band of heart rate interval variability was decreased after the competition (P < 0.001). All parameters returned to baseline values 3 days after the competition. After the competition, the autonomic response to orthostasis was significantly impaired. The 0.05- to 0.17-Hz band of diastolic blood pressure variability before competition and weekly net exercise training, but not the other hemodynamic and autonomic parameters, were related to competition time in multivariate regression analysis (multiple r = 0.70, P < 0.001). The marked hemodynamic and autonomic changes after an ultraendurance race, which are compatible with myocardial depression in the face of sympathetic activation and reduction of afterload, return to baseline after only 1-3 days. Because the 0.05- to 0.17-Hz band of diastolic blood pressure variability contributes to the prediction of competition time, the analysis of blood pressure variability in the frequency domain deserves further study for the prediction of endurance capacity.

Adaptation, Physiological↗
PubMed2006

Obesity and renal hemodynamics.

Obesity is a risk factor for renal damage in native kidney disease and in renal transplant recipients. Obesity is associated with several renal risk factors such as hypertension and diabetes that may convey renal risk, but obesity is also associated with an unfavorable renal hemodynamic profile independent of these factors, and that may exert effects on renal damage as well. In animal models of obesity-associated renal damage, micro-puncture studies showed glomerular hypertension and hyperfiltration. In humans an elevated glomerular filtration rate has been demonstrated in several studies, sometimes associated with hyperperfusion as well, independent of blood pressure or the presence of diabetes. An elevated filtration fraction was found in several studies, consistent with glomerular hypertension. This renal hemodynamic profile resembles the hyperfiltration pattern in diabetes and is therefore assumed to be a pathogenetic factor in renal damage. Of note, the association between body mass index and renal hemodynamics is not limited to overt obesity or overweight, but is also present across the normal range, without a particular threshold. Multiple factors are assumed to contribute to these renal hemodynamic alterations, such as insulin resistance, the renin-angiotensin system and the tubulo-glomerular responses to increased proximal sodium reabsorption, and possibly also inappropriate activity of the sympathetic nervous system and increased leptin levels. Obesity has a high world-wide prevalence. On a population-basis, therefore, its contribution to long-term renal risk may be considerable, especially as it is usually clustered with risk factors like hypertension and insulin resistance. In short-term studies the renal hemodynamic alterations in obesity and the associated proteinuria were reversible by weight loss, and renin-angiotensin system-blockade, respectively. These interventions are therefore likely to have the potential to limit the renal risks of obesity.

Animals↗