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PubMed1994

Anesthetic depth defined using multiple noxious stimuli during isoflurane/oxygen anesthesia. II. Hemodynamic responses.

BACKGROUND: The hemodynamic effects of isoflurane have been studied extensively. However, most data are obtained from volunteers or patients in the absence of surgical stimulation. The hemodynamic responses to various stimulation patterns of different intensity have not been evaluated. METHODS: In 26 patients, the ability of isoflurane to suppress motor and hemodynamic reactions in response to noxious stimulations of variable degree (trapezius squeeze, tetanic stimulation, laryngoscopy, skin incision, and laryngoscopy plus intubation) was evaluated by measuring arterial blood pressure and heart rate before and after stimulation. RESULTS: At concentrations that inhibited motor response to these stimuli in 50% of all patients, systolic blood pressure increased by 9 (trapezius squeeze), 15 (tetanic stimulation), 23 (laryngoscopy), 35 (skin incision) and 49 (intubation) mmHg, and heart rate by 5 (trapezius squeeze), 15 (tetanic stimulation), 17 (laryngoscopy), 36 (skin incision), and 36 (intubation) min-1 compared to the prestimulation values. An analysis using multiple regression showed that blood pressure response was influenced most by the type of stimulation followed by the concomitantly occurring motor reaction, the anesthesia time, and least by the isoflurane concentration per se. A high isoflurane concentration had no influence on the magnitude of blood pressure or heart rate increase to stimulation, but it decreased the prestimulation blood pressure and slightly increased the prestimulation heart rate. Heart rate responses were less consistent than those of blood pressure. CONCLUSIONS: Isoflurane used as a sole agent is unable to suppress hemodynamic reactions (blood pressure and heart rate) to painful stimuli. A "normal" blood pressure following stimulation can be achieved only if prestimulation blood pressure is depressed to levels that may be clinically unacceptable. The lack of motor response is not an accurate predictor of the ability of an agent to depress hemodynamic reaction.

Adult↗
PubMed1994

Hemodynamic response to induction and intubation. Propofol/fentanyl interaction.

BACKGROUND: When given as an intravenous bolus for induction of anesthesia, propofol can decrease postintubation hypertension but can also create moderate to severe postinduction, preintubation hypotension. The addition of fentanyl usually decreases the postintubation hypertension but can increase the propofol-induced preintubation hypotension. The goal of the study was to determine the relation between propofol and fentanyl doses and the hemodynamic changes post-induction, preintubation and postintubation. METHODS: Twelve groups of 10 patients, ASA physical status 1 or 2, first received fentanyl 0, 2, or 4 micrograms.kg-1 and then 5 min later received propofol 2.0, 2.5, 3.0, or 3.5 mg.kg-1 as an intravenous bolus for induction of anesthesia. Arterial blood pressure was continuously monitored. The trachea was intubated 4 min after propofol administration. RESULTS: The mean decrease in systolic blood pressure after propofol was 28 mmHg when no fentanyl was given, 53 mmHg after 2 microgram.kg-1 of fentanyl (P < 0.05 vs. no fentanyl), and 50 mmHg after 4 micrograms.kg-1 (P < 0.05 vs. no fentanyl; no statistically significant difference 4 vs. 2 micrograms.kg-1). There was no statistically significant difference in hemodynamic response to intubation relative to propofol dose. Hemodynamic response to intubation was decreased by the administration of fentanyl; the mean increase of systolic blood pressure after intubation was 65 mmHg from preintubation value without fentanyl, 50 mmHg after 2 micrograms.kg-1, and 37 mmHg after 4 micrograms.kg-1 (P < 0.05 for 2 and 4 micrograms.kg-1 vs. no fentanyl and for 4 vs. 2 micrograms.kg-1). Hemodynamic changes postintubation were not statistically different with increasing doses of propofol. CONCLUSIONS: Hemodynamic changes after induction with propofol or propofol/fentanyl, pre- or postintubation, are not modified when the propofol dose is increased from 2 to 3.5 mg.kg-1. Maximal hypotension preintubation occurs with a fentanyl dose of 2 micrograms.kg-1, whereas the magnitude of postintubation hypertension is significantly decreased with an increase in the fentanyl dose to 4 micrograms.kg-1.

Adult↗
PubMed2000

Plasma concentration of fentanyl with xenon to block somatic and hemodynamic responses to surgical incision.

BACKGROUND: Although anesthesia with xenon has been supplemented with fentanyl, its requirement has not been established. This study was conducted to determine the plasma concentrations of fentanyl necessary to suppress somatic and hemodynamic responses to surgical incision in 50% patients in the presence of 0.7 minimum alveolar concentration (MAC) xenon. METHODS: Twenty-five patients were allocated randomly to predetermined fentanyl concentration between 0.5 and 4.0 ng/ml during 0.7 MAC xenon anesthesia. Fentanyl was administered using a pharmacokinetic model-driven computer-assisted continuous infusion device. At surgical incision each patient was monitored for somatic and hemodynamic responses. A somatic response was defined as any purposeful bodily movement. A positive hemodynamic response was defined as a more than 15% increase in heart rate or mean arterial pressure more than the preincision value. The concentrations of fentanyl to prevent somatic and hemodynamic responses in 50% of patients were calculated using logistic regression. RESULTS: The concentration of fentanyl to prevent a somatic response to skin incision in 50% of patients in the presence of 0.7 MAC xenon was 0.72 +/- 0.07 ng/ml and to prevent a hemodynamic response was 0.94 +/- 0.06 ng/ml. CONCLUSIONS: Comparing these results with previously published results in the presence of 70% nitrous oxide, the fentanyl requirement in xenon anesthesia is smaller than that in the equianesthetic nitrous oxide anesthesia.

Abdomen↗
PubMed2005

Hemodynamic changes after protamine administration: association with mortality after coronary artery bypass surgery.

BACKGROUND: Protamine sulfate is standard therapy to reverse heparin anticoagulation. Hemodynamic responses to protamine are common, ranging from minor perturbations to cardiovascular collapse. Although severe fatal reactions occur, the relation of less extreme responses with postoperative mortality is unknown. Therefore, the authors tested the hypothesis that hemodynamic "protamine reactions" (systemic hypotension and pulmonary hypertension) are associated with mortality after cardiac surgery. METHODS: In a university hospital setting, the authors studied 6,921 coronary bypass patients using automated anesthesia record-keeping data and quality assurance databases. Degree/duration integrals of systemic hypotension (< 100 mmHg) and pulmonary hypertension (> 30 mmHg) for the 30-min after protamine administration were assessed for linear associations with mortality using multiple logistic regression models adjusting for risk factors. RESULTS: Overall mortality was 2%; greater hemodynamic responses were associated with increased mortality by odds ratios of 1.28 (systemic hypotension: 95% confidence interval, 1.14-1.43; P < 0.001) and 1.27 (pulmonary hypertension: 95% confidence interval, 1.06-1.48; P < 0.001) per 150-mmHg . min increment. Proximity of the response to protamine administration strengthened the relation, which persisted after exclusion of major hemodynamic disturbances. Tests for linearity confirmed an association even at the lowest range of values for both pressure effects. CONCLUSIONS: Hemodynamic perturbations after protamine administration are independently related to in-hospital mortality after primary coronary artery bypass surgery; the relation is present even in the lowest observed range of values for both systemic hypotension and pulmonary hypertension. Although randomized trials are necessary to address causality, this evidence suggests that strategies that avoid or attenuate these reactions may improve patient care.

Aged↗
PubMed2000

Effects of brain death and hemodynamic status on function and immunologic activation of the potential donor liver in the rat.

OBJECTIVE: To assess the effect on the function and immunologic status of potential donor livers of the duration of brain death combined with the presence and absence of hemodynamic instability in the donor. SUMMARY BACKGROUND DATA: Brain death, regarded as a given condition in organ transplantation, could have significant effects on the donor organ quality. METHODS: Brain death was induced in Wistar rats. Short or long periods of brain death in the presence or absence of hemodynamic instability were applied. Sham-operated rats served as controls. Organ function was studied by monitoring standard serum parameters. The inflammatory status of the liver was assessed by determining the immediate early gene products, the expression of cell adhesion molecules, and the influx of leukocytes in the liver. RESULTS: Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors. Irrespective of hemodynamic status, a progressive inflammatory activation could be observed in brain-dead rats compared with controls. CONCLUSIONS: Brain death causes progressive liver dysfunction, which is made worse by the coexistence of hemodynamic instability. Further, brain death activates the inflammatory status of the potential donor liver, irrespective of the presence of hypotension. The changes observed may predispose the graft to additional damage from ischemia and reperfusion in the transplant procedure.

Animals↗
PubMed1988

Effects of food ingestion on hemodynamics in chronic congestive heart failure.

This study evaluates the effects of a standardized meal on cardiovascular hemodynamics in 12 patients with New York Heart Association Class III congestive heart failure. This was done as part of a larger study in which an orally active dopaminergic agonist was given on two mornings, once with a standardized breakfast and once fasting, and one morning a placebo was given with the breakfast. The order of days was randomized. Hemodynamic data were obtained over 8 h each day. There were significant changes in several hemodynamic variables after the placebo-food regimen lasting up to 1.5 h: cardiac index rose from 1.8 +/- 0.4 to 2.2 +/- 0.5 L/min.m2 at 30 min (p less than .001) and to 2.0 +/- 0.5 L/min.m2 at one hour (p less than .05); stroke volume index rose from 20 +/- 7 to 24 +/- 7 ml/min at 30 min (p less than .05) and to 23 +/- 7 ml/min at one hour (p less than .05); systemic vascular resistance fell from 1890 +/- 685 to 1534 +/- 497 dyne.sec/cm5 at 30 min (p less than .001) and to 1668 +/- 524 dyne.sec/cm5 at one hour (p less than .05). Mixed venous oxygen saturation was measured continuously in seven patients and rose significantly at one and 1.5 h. We conclude that food ingestion can have a significant effect on cardiovascular hemodynamics and that this effect should be considered when therapeutic effects are to be guided by invasive hemodynamic monitoring in this population.

Adult↗
PubMed1994

Comparison of the hemodynamic and oxygen transport responses to modified fluid gelatin and hetastarch in critically ill patients: a prospective, randomized trial.

OBJECTIVE: To compare the hemodynamic and oxygen transport responses to a rapid (< 10-min) infusion of 500 mL of modified fluid gelatin (group A) or hydroxyethyl starch (group B) in patients suffering from acute hypovolemia. DESIGN: Prospective, randomized, noncrossover study. SETTING: University hospital, general intensive care unit. PATIENTS: Twenty-eight patients with hypovolemia mechanically ventilated for concurrent acute respiratory failure. INTERVENTIONS: Patients were mechanically ventilated. Pulmonary and femoral artery catheters were used for hemodynamic monitoring. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and oxygen transport variables were determined at baseline, 15 mins, and 30 mins after the infusion of each fluid. In both groups pulmonary artery occlusion pressure, stroke volume, and cardiac index significantly increased. In neither group did heart rate decrease. Oxygen delivery increased significantly in group A patients but not in group B patients. This result was due to greater hemodilution in group B patients. CONCLUSIONS: There are no significant differences in the hemodynamic responses to hydroxyethyl starch or modified fluid gelatin. The hemodynamic and oxygen transport effects of artificial colloid solutions may not be entirely predictable and should be monitored in critically ill patients.

Adult↗
PubMed1994

No differences in hemodynamics, ventricular function, and oxygen delivery in septic and nonseptic patients with the adult respiratory distress syndrome.

OBJECTIVE: To determine whether there are differences in hemodynamics, ventricular function, oxygen delivery, and oxygen consumption between septic and nonseptic patients who have the adult respiratory distress syndrome (ARDS). DESIGN: Cohort analytic study. SETTING: Tertiary care medical and surgical intensive care unit, university hospital. PATIENTS: Eighteen septic (survivors, n = 8; nonsurvivors, n = 10) and 14 nonseptic (survivors, n = 7; nonsurvivors, n = 7) patients studied within 24 hrs of the diagnosis of ARDS. INTERVENTIONS: Simultaneous hemodynamic, radionuclide cineangiographic, and oxygen delivery and consumption measurements. MEASUREMENTS AND MAIN RESULTS: Cardiac index, right and left ventricular ejection fractions, end-diastolic volume indices, oxygen delivery, and oxygen consumption were measured. There were no differences in mean systemic and pulmonary arterial pressures, cardiac index, systemic vascular resistance, right and left ventricular ejection fractions, end-diastolic volumes, and oxygen delivery and consumption between septic and nonseptic patients. CONCLUSIONS: Early in the course of ARDS, there were no differences in hemodynamics, ventricular function, and oxygen delivery and consumption between septic and nonseptic patients. Sepsis does not account for the previously reported differences in hemodynamics, ventricular function, and oxygen delivery and oxygen consumption between survivors and non-survivors of ARDS. We speculate that both ARDS and sepsis cause release of mediators which cause similar changes in hemodynamics, ventricular function, and oxygen delivery and consumption.

Adult↗
PubMed1997

Effects of pentoxifylline on hemodynamics and oxygenation in septic and nonseptic patients.

OBJECTIVE: To evaluate the effects of pentoxifylline on hemodynamics and systemic oxygenation in septic and nonseptic critically ill patients. DESIGN: Prospective clinical investigation. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Nineteen critically ill patients were included in the study 1 to 4 days after their admission to the ICU. A systemic inflammatory response syndrome was present in 12 patients, fulfilling at least two of the American College of Chest Physicians/ Society of Critical Care Medicine Consensus Conference criteria. The other seven patients did not fulfill these criteria and were classified as nonseptic. INTERVENTIONS: All patients were mechanically ventilated. The dosage of catecholamines was kept constant during the entire study period and at least during 15 mins before the start of the study. In both study groups, pulmonary and radial artery catheters were inserted and 5 mg/kg of pentoxifylline (diluted in 300 mL of physiologic saline) was intravenously administered over a period of 180 mins at a rate of 100 mL/hr. MEASUREMENTS AND MAIN RESULTS: Hemodynamic variables, oxygen transport (DO2), oxygen uptake (VO2), and oxygen extraction ratio were determined before pentoxifylline, after 2.5 mg/kg of pentoxifylline, after 5 mg/kg of pentoxifylline, and 60 mins after the termination of pentoxifylline. Repeated-measures analysis of variance and Mann-Whitney test were used for statistical analysis. At baseline, there were significant differences between the septic and the nonseptic groups in mean pulmonary arterial pressure (septic: 31 +/- 5 mm Hg; nonseptic: 26 +/- 7 mm Hg, p < .05), and pulmonary vascular resistance index (PVRI) (septic: 344 +/- 121 dyne.sec/ cm5.m2; nonseptic: 233 +/- 100 dyne.sec/cm5.m2, p < .05). In the septic group, significant increases in heart rate and cardiac index were observed. Systemic vascular resistance index and PVRI decreased. No significant changes in hemodynamic variables occurred in the nonseptic group. In both groups, DO2 and VO2 increased significantly, while oxygen extraction ratio remained unchanged. CONCLUSIONS: The administration of pentoxifylline to septic patients results in a significant improvement in hemodynamic performance compared with critically ill nonseptic patients. The better hemodynamic state is accompanied by an increase in DO2 and VO2 with unchanged oxygen extraction ratio.

Adult↗
PubMed1997

Relationship between hemodynamic and vital support measures and pharmacokinetic variability of amikacin in critically ill patients with sepsis.

OBJECTIVE: To examine the relationship between aminoglycoside disposition kinetics and hemodynamic response to sepsis, as well as vital support therapy, in critically ill patients with sepsis. DESIGN: Cross-sectional study of critically ill patients with sepsis undergoing physiologic and aminoglycoside pharmacokinetic monitoring. SETTING: Ten-bed general intensive care unit in a tertiary care center. PATIENTS: Thirty consecutive critically ill patients who had Gram-negative sepsis treated with amikacin and who were undergoing hemodynamic monitoring. INTERVENTIONS: Clinical, hemodynamic, oxygenation, and amikacin pharmacokinetic data were obtained simultaneously in each patient during aminoglycoside therapy. MEASUREMENTS AND MAIN RESULTS: Aminoglycoside pharmacokinetic values were estimated from serum amikacin concentration-time data using a nonlinear least squares regression computer program, assuming a one-compartment infusion pharmacokinetic model. Individual pharmacokinetic values were subjected to statistical analysis to explain their variability. Selection of the subset of variables to be used in the final model was performed by combining principal component analysis and multiple stepwise linear regression. The mean prediction error and the root mean square error, as expressions of bias and precision, were estimated. Mean volume of distribution was 0.47 L/kg, with a coefficient of variation of 35%. Mean serum amikacin clearance was 60.2 mL/min, with a coefficient of variation of 34%. Seventy-six percent of the variability in volume of distribution was explained by three covariates: body weight (p < .0001); oxygen extraction (p < .001); and serum albumin (p < .001). For serum amikacin clearance, 70% of the variability was explained by three covariates: creatinine clearance (p < .001); positive end-expiratory pressure (p < .01); and use of catecholamines as vital support therapy (p < .05). CONCLUSIONS: Factors related to hemodynamic response and vital support measures have a significant influence on the disposition kinetics of amikacin in severely ill patients with sepsis. Consideration of hemodynamic response and vital support measures, in addition to other previously described covariates, can be of great value in the design of initial dosing regimens.

APACHE↗
PubMed2000

Prolonged low-dose dopamine infusion induces a transient improvement in renal function in hemodynamically stable, critically ill patients: a single-blind, prospective, controlled study.

OBJECTIVE: To evaluate the length of the effects of long-term (48 hrs), low-dose dopamine infusion on both renal function and systemic hemodynamic variables in stable nonoliguric critically ill patients. DESIGN: Prospective, single-blind, controlled clinical study. SETTING: University hospital, 19-bed multidisciplinary intensive care unit. PATIENTS: Eight hemodynamically stable, critically ill patients with a mild nonoliguric renal impairment (creatinine clearance between 30 and 80 mL/min). INTERVENTIONS: Each patient consecutively received 4 hrs of placebo, followed by a 3 microg/kg/min dopamine infusion during 48 hrs, then a new 4-hr placebo period. We measured cardiac output and other hemodynamic variables by using a pulmonary artery catheter. The bladder was emptied to determine urine volume and to collect urine samples. Measurements were performed at six times: after the initial control of 4 hrs of placebo (C1); after 4 hrs (H4), 8 hrs (H8), 24 hrs (H24), and 48 hrs (H48) of dopamine infusion; and after the second control of 4 hrs of placebo (C2). MEASUREMENTS AND MAIN RESULTS: We saw no significant change in systemic hemodynamic variables with dopamine at all times of infusion. Diuresis, creatinine clearance, and the fractional excretion of sodium (FENa) at C1 and C2 were not different. Urine flow, creatinine clearance, and FENa increased significantly 4 hrs after starting dopamine (for all these changes, p < .01 vs. C1 and C2). The maximum changes were obtained at H8, with an increase of 50% for diuresis, 37% for creatinine clearance, and 85% for FENa (for all these changes, p < .01 vs. C1 and C2). But these effects waned progressively from H24, and both creatinine clearance and FENa at H48 did not differ from control values. CONCLUSIONS: In stable critically ill patients, preventive low-dose dopamine increased creatinine clearance, diuresis, and the fractional excretion of sodium without concomitant hemodynamic change. These effects reached a maximum during 8 hrs of dopamine infusion. But despite a slight persistent increase in diuresis, improvement in creatinine clearance and FENa disappeared after 48 hrs. According to these data, it is likely that tolerance develops to dopamine-receptor agonists in critically ill patients at risk of developing acute renal failure.

APACHE↗
PubMed2002

Effect of histamine H3 receptor blockade on venous return and splanchnic hemodynamics in experimental bacteremia.

OBJECTIVE: In the heart, histamine H3 receptors may function as inhibitory presynaptic receptors that decrease adrenergic neural norepinephrine release in conditions of enhanced sympathetic tone. In a previous study, we found that H3 receptor blockade improved cardiac contractility and systemic hemodynamics in experimental bacteremia in dogs. Because histamine H3 receptors have been found in the splanchnic circulation in other animal models, it was not clear the extent to which H3 receptor blockade may have altered splanchnic hemodynamics, and variables of venous return, that in turn contributed to the overall improvement in systemic hemodynamics observed in the previous experiment. In the present study, we examined splanchnic hemodynamics in the presence of H3 receptor blockade in a canine model of Escherichia coli bacteremia. DESIGN: Bacteremia was produced by intravenous infusion of live E. coli administered throughout the experiment. Variables of venous return included mean systemic pressure, resistance to venous return, and mean right atrial pressure. Splanchnic measurements included hepatic and portal pressures and flows. Measurements were obtained before and after H3 receptor blockade with thioperamide maleate. The animals were studied while ventilated and anesthetized. RESULTS: H3 receptor blockade caused a decrease in mean right atrial pressure from 5.9 mm Hg pretreatment to 3.5 mm Hg posttreatment (p < .05), although it did not affect mean systemic pressure or resistance to venous return. There were no changes in portal or hepatic flows after H3 receptor blockade. The cardiac function curve after H3 receptor blockade was shifted upward and to the left compared with the pretreatment curve. CONCLUSIONS: The results showed that the primary effect of H3 receptor blockade in experimental bacteremia was attributable to an increase in inotropy. There was no evidence to indicate that H3 receptor activation contributed to altered splanchnic hemodynamics in this model.

Analysis of Variance↗
PubMed1997

Hemodynamic tolerance of intravascular contrast agents for magnetic resonance imaging.

RATIONALE AND OBJECTIVES: Intravascular contrast agents for magnetic resonance imaging (MRI) facilitate the quantification of tissue perfusion. The authors determined the hemodynamic tolerance of these agents. METHODS: Doses of 0.05, 0.15, and 0.45 mmol/kg of the polymeric intravascular contrast agent gadolinium-DTPA-polylysine, and di-nitrobenzyl-gadolinium-DTPA, a non-polymeric intravascular contrast agent with high protein binding, and gadolinium-DTPA dimeglumine, a paramagnetic contrast agent with extracellular distribution, were injected into 18 normal male rats as a peripheral intravenous bolus. Systolic, diastolic, and mean blood pressure, left ventricular end-diastolic and developed pressure, positive rate of pressure change (+dP/dt), dP/dt, the rate-pressure product, and heart rate were recorded during a period of 20 minutes. Hemodynamic effects were established by analysis of variance for repeated measurements. RESULTS: There was a transient increase of all blood pressure parameters and contractility for Gd-DTPA-polylysine at the dose of 0.45 mmol/kg only. Di-nitrobenzyl-Gd-DTPA increased blood pressure parameters at 0.45 mmol/kg only. At doses of 0.05 and 0.15 mmol/kg, no significant hemodynamic effects were observed. CONCLUSIONS: The authors conclude that Gd-DTPA-polylysine is hemodynamically safe at doses to 0.15 mmol/kg and acts like a plasma expander at higher doses after peripheral bolus injection in normal rats. Additional investigations are indicated to elucidate the mechanism of a nonsignificant and satiable transient hemodynamic depression after injection of 0.05 mmol/kg DNB-Gd-DTPA.

Animals↗
PubMed1997

The effect of nitric oxide synthase inhibition on acute platelet accumulation and hemodynamic depression in a rat model of thromboembolic stroke.

The relative importance of hemodynamic factors in the pathogenesis of thrombotic or embolic stroke is unclear. Of particular therapeutic interest are those substances that facilitate vasodilation and the clearance of platelet aggregates in the compromised microvasculature. A likely contributor to these functions is nitric oxide because it is known to inhibit platelet aggregability and promote vascular relaxation. To investigate the involvement of nitric oxide in the hemodynamic changes after experimental ischemia, photochemically induced nonocclusive common carotid artery thrombosis (CCAT) was studied. CCAT is a rat model of unilateral carotid artery stenosis and platelet embolization to the brain. This study characterized the acute hemodynamic consequences of CCAT and the resultant pattern of platelet deposits with and without nitric oxide synthase inhibition by nitro-L-arginine methyl ester (L-NAME). In addition, the subacute local cerebral blood flow changes were studied at 24 hours. Right CCAT was produced in 30 male Wistar rats injected with (111)In-labeled platelets. Between 5 and 15 minutes after thrombosis, rats were treated with either 15 mg/kg of L-NAME (intravenously) or saline vehicle. Hemodynamic changes were studied 30 to 45 minutes after thrombosis using [14C]iodoantipyrine autoradiography. Eight coronal levels were analyzed, and cortical and subcortical regions of interest were defined. Significant increases were observed in total platelets in the ipsilateral hemisphere after L-NAME treatment, and in the distribution of platelets in the anterior frontal and occipital cortices with nitric oxide synthase inhibition, encompassing the anterior and posterior border zone areas of the ipsilateral cortex. Otherwise, foci of labeled platelets were detected throughout the ipsilateral and contralateral hemispheres. Mean local cerebral blood flow images (n = 5) revealed a moderate bilateral global reduction in flow acutely, which normalized in the untreated thrombosed group by 24 hours. In contrast, the L-NAME-treated groups (sham and experimental) had lasting, widespread reductions in flow of approximately 25%. Pairwise comparisons between groups showed that CCAT/L-NAME was significantly different from shams in the corpus callosum and different from L-NAME shams in the internal capsule (P < 0.05) These hemodynamic and platelet accumulation changes may partially account for the aggravation of cognitive and sensorimotor deficits previously reported in this model of thromboembolic stroke.

Animals↗
PubMed2001

Usefulness and limits of distal echo-Doppler velocimetric indices for assessing renal hemodynamics in stenotic and non-stenotic kidneys.

BACKGROUND: Distal echo-Doppler velocimetric indices are widely used for revealing the presence of a renal artery stenosis but there is scarce information as to whether they reflect the renal hemodynamics in stenotic and nonstenotic kidneys. OBJECTIVES AND METHODS: We evaluated the pulsatility and resistive indices (PI and RI), acceleration (A) and acceleration time (At) and correlated their values with those of effective renal plasma flow (ERPF), glomerular filtration rate (GFR), renal vascular resistance (RVR) and filtration fraction (FF) estimated by single kidney scintigraphy in 24 kidneys with 70-95% renal artery stenosis (atherosclerotic n = 17, fibromuscular n = 7) and in 27 non-stenotic kidneys (11 contralateral to renal artery stenosis and 16 of patients with essential hypertension). In patients with stenotic kidneys, these measurements were repeated within 7 days after a successful percutaneous transluminal renal angioplasty (PTRA) (in 11 arteries performed in combination with stent implantation). RESULTS: Prior to dilation we found that the stenotic kidneys had significantly lower values of ERPF, GFR and higher RVR than the non-stenotic kidneys and that these hemodynamic alterations were associated with those, also statistically significant, of the four velocimetric indices. In non-stenotic kidneys, there were highly significant relationships between PI and ERPF, and RVR (r = -0.68 and 0.81 respectively P < 0.01); similar relationships were found for RI (r = -0.67 and 0.78 P < 0.01) whereas no such correlations were found between these two velocimetric indices and GFR and FF; also no correlations were found between A and Atand ERPF, GFR, RVR and FF. In stenotic kidneys no significant correlations were found between any of the velocimetric and the hemodynamic indices. Renal artery dilation induced clear cut increments in ERPF, GFR and reduction in RVR in post-stenotic kidneys, which were associated with normalization of all four velocimetric indices. No relationships were observed between the renal hemodynamic and the velocimetric changes induced by dilation; however in post-stenotic kidneys the relationships between PI and RI, ERPF and RVR were restored as in nonstenotic kidneys. CONCLUSIONS: These data indicate that PI and RI can be used to assess ERPF and RVR both in non-stenotic and post-stenotic kidneys; however, none of the velocimetric indices examined in this study can provide valid informations on the renal hemodynamics of stenotic kidneys and on their changes induced by PTRA.

Adolescent↗
PubMed1987

Central hemodynamic changes of calcium antagonists at rest and during exercise in essential hypertension.

Since the cardinal hemodynamic disorder in essential hypertension is an increased total peripheral resistance, drugs that can lower resistance without reducing blood flow would be particularly useful. The calcium antagonists seem to fulfill this criterion. The purpose of this work was to study the hemodynamic effects at rest and during exercise of three calcium channel blockers, verapamil, nifedipine, and nisoldipine, in patients with mild to moderate essential hypertension. Fifty-four patients aged 20-64 years with pretreatment diastolic blood pressures of between 95 and 120 mm Hg were studied at rest and during exercise on an ergometer bicycle. Blood pressure was recorded intraarterially and cardiac output was measured by Cardiogreen. After the initial study, 10 patients were treated with verapamil (40-80 mg three times daily), 15 with nifedipine (long-acting form, 20-80 mg daily), and 19 with nisoldipine (10-40 mg daily). After 1 year the hemodynamic study was repeated. The immediate response to the first dose was studied in the patients taking nisoldipine and in 10 patients after taking placebo tablets. Placebo induced no significant changes in central hemodynamics during the first 3 h after tablet intake. The calcium antagonists induced a reduction in blood pressure and in total peripheral resistance (in the order of 10-18%) without any reduction in cardiac index. Reflex tachycardia and an increase in cardiac output were seen in the first 2 h after the first dose of nisoldipine, but after 1 year the heart rate was unchanged compared with the pretreatment rate at rest and during exercise. In contrast, heart rate was reduced on verapamil treatment, particularly during exercise (about 10% of patients), but this was compensated for by an increase in the stroke volume. The hemodynamic profiles of the three calcium channel blockers were slightly different, especially with respect to the heart rate response. Total peripheral resistance was reduced, acutely as well as chronically, and no depression in cardiac pump function was seen, either at rest or during exercise.

Adult↗
PubMed1990

The hemodynamics effects of ACE inhibitors in the treatment of congestive heart failure.

To determine the safety and efficacy of single oral doses of quinapril in the treatment of congestive heart failure (CHF), an open-label, hemodynamic trial was conducted in 11 patients with severe CHF [New York Heart Association (NYHA) class III or IV] in whom previous or current therapy with diuretics and digitalis had been inadequate. After participating in this single-dose trial (acute phase), all 11 patients were entered into a 16-week, multiple-dose investigation (chronic phase). In the acute phase of the study, single oral doses of quinapril (2.5, 5, and 10 mg/day) achieved beneficial hemodynamic changes within 1 h after the onset of therapy. Maximal improvements in key hemodynamic variables (i.e., pulmonary capillary wedge pressure, mean arterial blood pressure, cardiac output, and total systemic vascular resistance) were observed within 4 h after dosing. The hemodynamic changes after 16 weeks of chronic quinapril therapy (5, 10, 15, and 30 mg/day) were equivalent or superior to those observed after acute therapy, indicating that quinapril produces a sustained hemodynamic benefit after chronic oral dosing. Quinapril was shown to be safe and effective in the treatment of patients with severe CHF.

Administration, Oral↗
PubMed1994

Systemic and coronary hemodynamic effects of repetitive cocaine administration in conscious dogs.

The cardiovascular actions of cocaine are complex, and previous studies suggest that tachyphylaxis to the positive chronotropic and pressor effects of cocaine may develop after repetitive administration. We examined changes in systemic and coronary hemodynamics when single or multiple doses of intravenous (i.v.) cocaine were administered to conscious dogs. Dogs were chronically instrumented for measurement of aortic blood pressure (BP) and left ventricular pressure (LVP), LV dP/dtmax and dP/dt50, subendocardial segment length (%SS), diastolic coronary blood flow (CBF) velocity, and cardiac output (CO). Myocardial oxygen consumption was estimated by the pressure-work index (PWI). In one series of experiments, a single dose of cocaine (0.1, 0.2, 0.4, 0.8, or 1.6 mg/kg) was administered on 5 consecutive days in random fashion and peak changes in systemic and coronary hemodynamics were recorded. These doses were then randomly repeated in a second group of experiments with a 1-h interval between doses on the same day. Peak and steady-state changes in cardiovascular variables were recorded within and between each dose, respectively. In other experiments, higher doses of cocaine (0.8 or 1.6 mg/kg; separate groups) were administered four times at 1-h intervals in the same dogs and peak and steady-state changes in hemodynamics were determined. Cocaine caused dose-related increases in heart rate (HR), mean arterial pressure (MAP), LV systolic pressure (LVSP) and end-diastolic pressure (LVEDP), PWI, CO, and diastolic coronary vascular resistance and decreases in %SS when administered on different days. Cocaine also caused significant increases in baseline HR, MAP, LVSP, and PWI between doses given on the same day at 1-h intervals, but the absolute value of the peak response to cocaine of these hemodynamic parameters was independent of dosing regimen. These results were confirmed when we administered four doses of 0.8 mg/kg cocaine at 1-h intervals. The results indicate that baseline changes in systemic hemodynamic variables are a predominant feature of repetitive administration of lower doses of cocaine (< or = 0.8 mg/kg), but administration of higher doses of cocaine (> or = 8 mg/kg) at 1-h intervals caused tachyphylaxis to the hypertensive actions and myocardial oxygen consumption effects of cocaine.

Analysis of Variance↗