Significant Changes In Cardiac Output Research Articles

Myocardial performance index during rapidly changing loading conditions

The myocardial performance index is a non-geometric, heart rate-independent echocardiography-derived index of left ventricular performance combining systolic and diastolic function. There is an ongoing debate whether the myocardial performance index is affected by preload or not. Moreover, a systematic evaluation of the effect of changing tidal volume ventilation on the myocardial performance index is still lacking. The aim of our study was to assess whether acute changes in preload and/or different depth of tidal volume ventilation affect the myocardial performance index. In all, 14 anesthetized pigs (35 +/- 2 kg) were studied during changing tidal volumes (VT 5, 10 and 15 mL kg(-1)) at baseline, after removal of 500 cm(3) of blood (haemorrhage) and after retransfusion of shed blood plus additional 500 cm(3) 6% hydroxyethyl starch (fluid loading). Echocardiographic measurements at each experimental stage included myocardial performance index, left ventricular end-diastolic area and fractional area change. Central venous pressure, pulmonary capillary wedge pressure, cardiac output and stroke volume index were obtained by a pulmonary artery catheter. Global end-diastolic volume was obtained by transpulmonary thermodilution. Comparing different loading conditions, we found significant changes in cardiac output, stroke volume index, central venous pressure, pulmonary capillary wedge pressure, global end diastolic volume and left ventricular end-diastolic area, indicating clinically relevant changes in preload. In the haemorrhage group, there was a significant reduction in the myocardial performance index (P < 0.05) independent of tidal volume applied and this was reversed after fluid loading. However, myocardial performance index was significantly impaired (P < 0.05) by high tidal volume ventilation (15 mL kg(-1)), while tidal volumes of 5 and 10 mL kg(-1) had no effect. The myocardial performance index is largely dependent on changes in preload. Moreover, high tidal volume ventilation significantly impaired the myocardial performance index.

Ability of pleth variability index to detect hemodynamic changes induced by passive leg raising in spontaneously breathing volunteers

IntroductionPleth Variability Index (PVI) is a new algorithm that allows continuous and automatic estimation of respiratory variations in the pulse oximeter waveform amplitude. Our aim was to test its ability to detect changes in preload induced by passive leg raising (PLR) in spontaneously breathing volunteers.MethodsWe conducted a prospective observational study. Twenty-five spontaneously breathing volunteers were enrolled. PVI, heart rate and noninvasive arterial pressure were recorded. Cardiac output was assessed using transthoracic echocardiography. Volunteers were studied in three successive positions: baseline (semirecumbent position); after PLR of 45° with the trunk lowered in the supine position; and back in the semirecubent position.ResultsWe observed significant changes in cardiac output and PVI during changes in body position. In particular, PVI decreased significantly from baseline to PLR (from 21.5 ± 8.0% to 18.3 ± 9.4%; P < 0.05) and increased significantly from PLR to the semirecumbent position (from 18.3 ± 9.4% to 25.4 ± 10.6 %; P < 0.05). A threshold PVI value above 19% was a weak but significant predictor of response to PLR (sensitivity 82%, specificity 57%, area under the receiver operating characteristic curve 0.734 ± 0.101).ConclusionPVI can detect haemodynamic changes induced by PLR in spontaneously breathing volunteers. However, we found that PVI was a weak predictor of fluid responsiveness in this setting.

Cardiac function during steep Trendelenburg position and CO2 pneumoperitoneum for robotic‐assisted prostatectomy: a trans‐oesophageal Doppler probe study

Haemodynamic changes associated with pneumoperitoneum and steep Trendelenburg position were investigated in non-obese, ASA I-II males, using general anaesthesia (sevoflurane in air/O2, 40%) undergoing robotic-assisted laparoscopic prostatectomy. A trans-oesophageal echo-Doppler probe (Arrow International) measured cardiovascular changes in heart rate (HR), mean arterial pressure (MAP), cardiac output (CO), systemic vascular resistance (SVR), stroke volume (SV) and aortic diameter (AoD) in 35 of 37 males. Assessments were conducted after induction of general anaesthesia in: the supine position; at 45 degrees Trendelenburg; Trendelenburg + pnuemoperitoneum (intra-abdominal 15 mmHg); and at the end of surgery in the supine position. The Trendelenburg position increased stroke volume. Trendelenburg position + pneumoperitoneum increased MAP and SVR and decreased AoD. Pneumoperitoneum and steep Trendelenburg position significantly increase MAP and SVR. Trendelenburg position increased stroke volume. Pneumoperitoneum decreases aortic diameter. No significant changes in cardiac output or stroke volume were noted.

Pulse Pressure Respiratory Variation as an Early Marker of Cardiac Output Fall in Experimental Hemorrhagic Shock

Pulse pressure (DeltaPp) and systolic pressure (DeltaPs) variations have been recommended as predictors of fluid responsiveness in critically ill patients. We hypothesized that changes in DeltaPp and DeltaPs parallel alterations in stroke volume (SV) and cardiac output (CO) during hemorrhage, shock, and resuscitation. In anesthetized and mechanically ventilated mongrel dogs, a graded hemorrhage (20 mL/min) was induced to a target mean arterial pressure (MAP) of 40 mm Hg, which was maintained for additional 30 min. Total shed-blood volume was then retransfused at a 40 mL/min rate. CO, SV, right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), and continuous mixed venous oxygen saturation (SvO(2)) were assessed. Both DeltaPp and DeltaPs were calculated from direct arterial pressure waveform. Removal of about 9% of estimated blood volume promoted a reduction in SV (14.8 +/- 2.2 to 10.6 +/- 1.3 mL, P < 0.05). At approximately 18% blood volume removal, significant changes in CO (2.4 +/- 0.2 to 1.5 +/- 0.2 mL/min, P < 0.05), DeltaPp (12.6 +/- 1.4 to 15.8 +/- 2.0%, P < 0.05), and SvO(2) (82 +/- 1.4 to 73 +/- 1.7%, P < 0.05) were observed. Alterations in MAP, RAP, PAOP, and DeltaPs could be detected only after each animal had lost over 36% of estimated initial blood volume. There was correlation between blood volume loss and SV, CO, and SvO(2), as well as between blood loss and MAP, DeltaPp, and DeltaPs. Blood volume loss showed no correlation with cardiac filling pressures. DeltaPp is a useful, early marker of SV and CO for the assessment of cardiac preload changes in hemorrhagic shock, while cardiac filling pressures are not.

Acute effects of low and high intravenous doses of furosemide on myocardial function in anuric haemodialysis patients: a tissue Doppler study

In patients with pulmonary oedema and preserved renal function, furosemide has not only a renal, but also a vascular effect, causing a rapid fall in left ventricular filling pressure accompanied by an increase in venous compliance. Previous studies have shown conflicting findings regarding the vascular effects of furosemide in patients with end-stage renal disease (ESRD). The objective of our study was to investigate whether furosemide induces changes in central cardiac haemodynamics in anuric ESRD patients, using conventional echocardiography and colour tissue Doppler velocity imaging (TVI), a new quantitative and sensitive method. Repeated low doses (40 mg followed by an additional dose of 40 mg after 30 min) of i.v. furosemide were administered to 12 (61.6 +/- 16 years, 7 men) and a high dose (250 mg) of i.v. furosemide to 6 (64.1 +/- 3.6 years, 5 men) clinically stable anuric haemodialysis (HD) patients. Conventional two-dimensional echocardiography and colour TVI images were recorded immediately before (0 min) the furosemide infusion in both groups, and in the group receiving the repeated low-dose infusion (at 0 and 30 min), 10, 20, 30, 40, 50 and 70 min after the administration of the first infusion. In the group receiving the single high dose of furosemide the ultrasound investigation was repeated 10, 20, 30 and 40 min after the infusion. The myocardial tissue velocities (v; cm/s) for isovolumetric contraction (IVC), peak systole (PS), early (E') and late (A') myocardial diastolic filling velocities were measured in the left ventricle (LV) at six sites (infero-septal, antero-lateral, inferior, anterior, infero-lateral and antero-septal walls) at the basal region. IVC time (IVCT), IV relaxation time (IVRT), PS time (PSt), RR interval, mitral annulus motion (MAM), strain rate (SR), left ventricular filling pressure (E/E') and cardiac output were also measured. The average of the different walls was used to evaluate global function. Right ventricle (RV) dynamics was evaluated from measurements of IVC velocity (IVCv), peak systolic velocity (PSv), E' and A' from the RV free wall. No significant changes in cardiac output, IVCv, PSv, SR, MAM, E', A', E'/A', IVRT and LV filling pressure were observed, indicating that neither 40 mg (plus additional 40 mg after 30 min) nor 250 mg of furosemide had any measurable effects on LV filling pressure and LV and RV systolic and diastolic function. In anuric HD patients, low and high doses of furosemide had no significant effects on central cardiac haemodynamics. Therefore, the use of furosemide infusion in anuric ESRD patients with acute pulmonary oedema is not supported by the results of this study.

Lithium dilution cardiac output measurement in the critically ill patient: determination of precision of the technique

Background: Lithium dilution cardiac output by LiDCO TMplus (LiDCO, Cambridge, UK) is a validated methodology for measuring cardiac output. It is used to calibrate a pulse pressure analysis algorithm (PulseCO) for the continuous measurement of subsequent changes in this variable. The variability of measurements, or precision, within patients of lithium dilution cardiac output has not previously been described. Material and methods: Thirty-five hemodynamically stable patients in intensive care, with no significant variability in heart rate, mean arterial pressure or central venous pressure, were recruited. Fifty-three determinations of cardiac output were made, each using four lithium dilution measurement curves performed consecutively within a maximum period of 10 min. The coefficient of variation of the measurements was determined and used to derive the least significant change in cardiac output that this technique could reliably detect. Results: For a single measurement, the coefficient of variation was 8%. This equates to the technique being able to detect a change (least significant change) between two measurements of 24%. Averaging two lithium dilution measurements improved the coefficient of variation to 6% with a least significant change of 17%. Using the average of three curves reduced the coefficient of variation to 5% with a least significant change of 14%. Conclusions: To achieve a good precision with this technique, three lithium dilution measurements should be averaged. This will allow changes in cardiac output of more than 14% to be reliably detected. The understanding of the precision of this technique allows the user to know when a real change has happened to their patient.

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (E(max)) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, E(max), and PRSW. In contrast, after HF was induced, CO, E(max), and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, E(max) and PRSW did not change. In addition, MMR activation caused no significant change in CO, E(max), or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF.

Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy

Patients with multiple system atrophy (MSA) often have clinically significant postprandial hypotension (PPH). To elucidate the cause of insufficient cardiac preload augmentation that underlies PPH, we recorded calf venous capacitance (CVC) by strain-gauge plethysmography, in 17 MSA patients and eight healthy controls before and after oral glucose ingestion. Among 17 MSA patients, nine who showed a decrease in systolic blood pressure exceeding 20 mmHg and were diagnosed with PPH. MSA patients without PPH showed a significant decrease in CVC and a significant increase in cardiac output after oral glucose ingestion, as did controls; those with MSA exhibiting PPH showed a significant increase in CVC and no significant change in cardiac output. The change in CVC correlated positively with the decrease in systolic and diastolic blood pressure after glucose ingestion, and also correlated negatively with the increase in cardiac output. Physiologically, PPH is prevented by a decrease in venous capacitance, which increases circulating blood volume and cardiac output. In some MSA patients, failure of venous capacitance to decrease may induce PPH.

Hemodynamic Changes During Discontinuation of Mechanical Ventilation in Medical Intensive Care Unit Patients

Cardiac dysfunction can prevent successful discontinuation of mechanical ventilation. Critically ill patients may have undetected cardiac disease, and cardiac dysfunction can be produced or exacerbated by underlying pathophysiology. To describe and compare hemodynamic function and cardiac rhythm during baseline mechanical ventilation with function and rhythm during a trial of continuous positive airway pressure in medical intensive care patients. A convenience sample of 43 patients (53% men; mean age 51.1 years) who required mechanical ventilation were recruited for this pilot study. Cardiac output, stroke volume, arterial blood pressure, heart rate, cardiac rhythm, and plasma catecholamine levels were measured during mechanical ventilation and during a trial of continuous positive airway pressure. One third of the patients had difficulty discontinuing mechanical ventilation. Successful patients had significantly increased cardiac output and stroke volume without changes in heart rate or arterial pressure during the trial of continuous positive airway pressure. Unsuccessful patients had no significant changes in cardiac output, stroke volume, or heart rate but had a significant increase in mean arterial pressure. The 2 groups of patients also had different patterns in ectopy. Concurrently, catecholamine concentrations decreased in the successful patients and significantly increased in the unsuccessful patients during the trial. Patterns of cardiac function and plasma catecholamine levels differed between patients who did or did not achieve spontaneous ventilation with a trial of continuous positive airway pressure. Cardiac function must be systematically considered before and during the return to spontaneous ventilation to optimize the likelihood of success.

Prevention of cardiovascular effects of endotoxaemia by monoclonal antibodies specific for core endotoxin.

Passive immunization with antibody to the core region of endotoxin (core lipopolysaccharide (LPS)) has been reported to reduce mortality in severe sepsis. A rat model of endotoxaemia that reproduces the hyperdynamic cardiovascular state seen in early sepsis was developed to test monoclonal antibodies specific for core LPS. A thermodilution technique of measuring cardiac output was adapted for use in rats. Twenty-five animals were anaesthetized and mechanically ventilated with monitoring of central venous pressure and mean arterial pressure. Fluid replacement was adjusted to maintain the central venous pressure. Controls (n = 10) and antibody-treated animals (n = 5) showed no significant change in cardiac output. Animals given 0.1 mg kg-1 R2 endotoxin over 1 h (n = 5) showed a significant rise in cardiac output of 65 per cent (P < 0.01). This was abolished in rats given both antibody and endotoxin (n = 5). This study provides evidence that a monoclonal antibody against core LPS abolishes the hyperdynamic state induced by endotoxin infusion.

Tricuspid Valve Replacement After Cardiac Transplantation

Tricuspid valve insufficiency (TI) is common after orthotopic heart transplantation. However, tricuspid valve replacement or repair (TVR) is rare. The aim of this study is to evaluate our experience with TVR in cardiac transplant recipients. The Utah Transplantation Affiliated Hospitals (UTAH) Cardiac Transplant Program database was queried for TVR in all adult and pediatric heart transplant recipients. Pre-operative parameters and cardiac hemodynamics were compared with post-operative findings. Since 1985, we identified in our database 17 patients who had 16 TVR, and 2 tricuspid valve repair procedures. Thirty-four heart transplant recipients from the same period were used as controls. The indication for TVR was symptomatic right heart failure (RHF) in 89% of cases, and there was no significant difference between the control group and the surgery group in the average number of biopsies. A flail leaflet was found in 16 cases (89%). One patient died post-operatively due to cardiogenic shock, and 1 patient died 8 months after TVR due to progressive RHF. Improvement in heart failure symptoms was seen in 12 cases. The central venous pressure (CVP) decreased from 17.8 +/- 4.1 mm Hg to 11.0 +/- 7.3 mm Hg (p = 0.013). There was no significant change in cardiac output or renal function. However, the furosemide dose decreased significantly from 47.69 +/- 56.44 mg/day to 26.54 +/- 46.43 mg/day (p = 0.009). After orthotopic heart transplantation, TVR is a safe and effective procedure to alleviate RHF symptoms. Flail leaflets are the most common operative finding, suggesting that biopsy-induced trauma is the likely cause of severe TI in these patients.

Relaxin Increases Cardiac Output and Reduces Systemic Arterial Load in Hypertensive Rats

Chronic administration of recombinant human relaxin (rhRLX) to conscious, normotensive rats (male and female) increases cardiac output (CO) and global arterial compliance (ACg) and reduces systemic vascular resistance (SVR) with no change in mean arterial pressure (MAP). Effects (magnitude and temporal pattern) of relaxin on systemic hemodynamics and arterial properties in hypertensive animal models are not known. Accordingly, the major goal of the present study was to determine the cardiovascular effects of rhRLX in hypertensive rats using 2 models: Long-Evans rats chronically administered angiotensin II (AII) and spontaneously hypertensive rats (SHR). CO and systemic arterial load, as quantified by SVR and ACg, were obtained using methods reported previously by us. In rats with AII-induced hypertension, acute rhRLX administration (up to 6 hours) significantly increased CO and ACg (24.9+/-3.9 and 34.3+/-12.6% above baseline, respectively) and significantly decreased SVR (17.2+/-3.5%) without changing MAP. In contrast, acute rhRLX administration to SHR and normotensive rats for up to 6 hours failed to produce any significant changes in CO, ACg, SVR, or MAP. However, chronic rhRLX administration (1 to 7 days) to SHR yielded significant changes (24.0+/-8.1 and 22.3+/-6.6% increases in CO and ACg, respectively, and a 13.3+/-5.3% decrease in SVR, with no change in MAP). In conclusion, rhRLX increases CO and reduces arterial load in hypertensive rats without reducing MAP. However, the time course of response to rhRLX treatment is dependent on the model of hypertension such that rats characterized by AII-mediated hypertension responded more rapidly to rhRLX administration than SHR.

The effects of water ingestion on orthostatic hypotension in two groups of chronic autonomic failure: multiple system atrophy and pure autonomic failure

Background: Oral ingestion of water increases seated blood pressure in patients with chronic autonomic failure by mechanisms that remain unclear. As orthostatic hypotension is common in chronic autonomic failure, and...

Staphylococcus aureus bacteremia after median sternotomy: clinical utility of blood culture results in the identification of postoperative mediastinitis

The hemodynamic and electrophysiologic effects of rilmenidine were examined after single oral administration to hypertensive patients.In 8 untreated hypertensive patients, cardiac output, pulmonary pressure and blood pressure were measured before and for 10 hours after the administration of 25 μg/kg of rilmenidine (1.3 to 2.4 mg, mean 1.88). In addition, electrophysiologic investigations were performed before and 2 hours after administration.Hemodynamics were repeated in 8 other hypertensive patients receiving 50 μg/kg rilmenidine (3.0 to 4.8 mg, mean 3.85 mg).The electrophysiologic study was repeated in 8 other hypertensive patients receiving 50 μg/kg of rilmenidine (3.2 to 4.4 mg, mean 3.90).In contrast to the results obtained at the dose of 50 μg/kg, there was no significant variation in pulmonary arterial pressure, cardiac index or stroke index after administration of 25 μg/kg. No significant variation was observed in heart rate, sinus function, conduction parameters or atrial, nodal and ventricular refractory periods after adminstration of 25 and 50 μg/kg.Rilmenidine, after single oral administration at the 25 μg/kg dose, led to a significant reduction in blood pressure and peripheral resistance without any significant change in cardiac output; the 25-and 50-μg/kg doses led to no alteration in heart rate and cardiac electrophysiology.

Regional blood flows are affected differently by PEEP when the abdomen is open or closed: an experimental rabbit model.

The study of induced circulatory changes requires simultaneous assessment of multiple regional circulations because of interactions and compensatory mechanisms. Positive end expiratory pressure mechanical ventilation (PEEP) is known to cause marked, and potentially deleterious, cardiovascular changes. Our aim was to use a comprehensive approach to assess PEEP-induced circulatory changes in open vs closed abdomen animals. In the anesthetized rabbit, we used implantable Doppler micro-probes to measure blood flow simultaneously in the ascending aorta, inferior vena cava, portal vein, hepatic artery, common carotid artery, and renal artery. We studied spontaneously breathing animals (Group A), and open (Group B) and closed abdomen (Group C) animals mechanically ventilated at 0 (ZEEP) and 12 cm H(2)O PEEP. In Group A, all biological and hemodynamic variables remained unchanged for three hours at the end of the surgical procedure. In Groups B and C, ZEEP produced no significant hemodynamic change. PEEP induced a decrease in carotid, hepatic, and renal artery blood flow in Groups B and C, a decrease in heart rate and mean arterial blood pressure in Group B, and a decrease in aorta blood flow in Group C. These experimental results demonstrate the usefulness of the comprehensive approach of circulatory changes, and confirm that PEEP may have deleterious effects on regional blood flow, even without significant change in cardiac output, especially when the abdomen is open.

Cardiovascular effects of SL65.0472, a 5-HT receptor antagonist

In this study, we describe the cardiovascular effects of SL65.0472 (7-fluoro-2-oxo-4-[2-[4-(thieno[3,2- c] pyridin-4-yl) piperazin-l-yl] ethyl]-1, 2-dihydroquinoline-1-acetamide), a novel 5-hydroxytryptamine (5-HT) receptor antagonist developed for the treatment of cardiovascular disease, in several in vivo models. The haemodynamic profile of SL65.0472 was evaluated in anaesthetised dogs. Following i.v. bolus doses of 0.03 mg/kg i.v. and 0.3 mg/kg, no significant changes in cardiac output, contractility or rate, systemic and pulmonary pressures, regional blood flows and vascular resistances or electrocardiogram were noted. After 1 mg/kg i.v. SL65.0472 significantly reduced arterial blood pressure. In conscious spontaneously hypertensive rats administration of SL65.0472 0.5 mg/kg p.o. had no effect on mean arterial blood pressure or heart rate. Vasoconstriction produced by 5-HT results primarily from the stimulation of two receptor subtypes, 5-HT 1B and 5-HT 2A receptors. In anaesthetised dogs SL65.0472 antagonised sumatriptan-induced decreases in saphenous vein diameter (5-HT 1B-receptor mediated) with an ID 50 of 10.1 μg/kg i.v. (95% c.l. 8.3–12.4). In anaesthetised pithed rats SL65.0472 inhibited 5-HT pressor responses (5HT 2A-receptor mediated) with ID 50 values of 1.38 μg/kg i.v. (95% c.l. 1.15–1.64) and 31.1 μg/kg p.o. (95% c.l. 22.6–42.6). The duration of the 5-HT 2A-receptor antagonist effect of SL65.0472 following oral administration was evaluated in conscious rats. SL65.0472 (0.1 mg/kg p.o.) markedly inhibited 5-HT pressor responses 1 and 6 h after administration. Therefore, in vivo, SL65.0472 potently antagonises vasoconstriction mediated by 5-HT 1B and 5-HT 2A receptors but has minimal direct haemodynamic effects.

Age-related changes in pumping mechanical behavior of rat ventricle in terms of systolic elastance and resistance.

Both the maximal systolic elastance (Emax) and the theoretical maximal flow (Qmax) can quantify the systolic mechanical behavior of the ventricular pump. Physically, Emax can reflect the intrinsic contractility of the myocardium as an intact heart. The quantity in (Qmax is inversely related to the internal resistance of the left ventricle. How great the effects of age are on these Emax and Qmax has never been examined, however. This study was to determine the ventricular pumping mechanics in terms of the systolic elastance and resistance in male Fischer rats at 6, 12, 18, and 24 months of age. We measured left ventricular (LV) pressure and ascending aortic flow waves using a high-fidelity pressure sensor and an electromagnetic flow probe, respectively. Those two parameters that characterize the systolic pumping mechanics of the left ventricle are obtained by making use of an elastance-resistance model. The basic hemodynamic condition in those animals with different ages is characterized by (i) no significant change in cardiac output and (ii) a decrease in basal heart rate, LV end-systolic pressure, as well as effective arterial volume elastance. Changes that take place in the left ventricle with age include a decline in Emax and an increase in Qmax especially at 24 months. These results demonstrate that the impaired intrinsic contractility of an aging heart may be compensated to some extent by the diminished ventricular internal resistance. Such compensation in aging rats may maintain normal blood flow essential for the metabolic needs of tissues and/or organs before heart dysfunction and failure occur.

Effects of cardiotrophin-1 on hemodynamics and endocrine function of the heart.

Cardiotrophin-1 (CT-1), a member of the interleukin-6 superfamily of cytokines, possesses hypertrophic actions and atrial natriuretic peptide (ANP)-producing activity in vitro. The goal of our study is to elucidate whether CT-1 affects the cardiovascular system in vivo. Intravenous injection of CT-1 (4-100 microg/kg) in conscious rats evoked significant declines in blood pressure and reflex increases in heart rate (HR) in a dose-dependent manner. CT-1 induced no significant change in cardiac output (from 260.7 +/- 11.0 to 264.7 +/- 26.6 ml. min(-1). kg(-1), P = not significant), which was compatible with the results from isolated perfused rat hearts; HR, change in pressure over time, left ventricular developed pressure, and perfusion pressure were unaffected. Northern blot and RT-PCR analyses revealed that CT-1 increased expression of inducible nitric oxide synthase (iNOS) in lung and aorta but not in heart or liver. Pretreatment with aminoguanidine, a specific iNOS inhibitor, inhibited both iNOS mRNA production and the depressor effect of CT-1. Interestingly, CT-1 increased ventricular expression of ANP and brain natriuretic peptide (BNP). The data demonstrate that CT-1 elicits its hypotensive effect via a nitric oxide-dependent mechanism and that CT-1 induces ANP and BNP mRNA expression in vivo.

Reproducibility of impedance cardiography hemodynamic measures in clinically stable heart failure patients.

BACKGROUND AND AIMS. One of the greatest challenges confronting physicians who are managing the care of patients with heart failure is to acquire objective data that signals treatment effectiveness and/or disease progression. The aim of this study was twofold: 1) to determine the extent to which (real time) impedance cardiography measurements obtained with a specific medical device (the BioZ) were reproducible in outpatients with clinically stable heart failure; and 2) to establish "normal" ranges of one week hemodynamic variability in this population of patients. Information of this nature would help clinical cardiologists and primary care practitioners to evaluate the implications of their patient's visit-to-visit hemodynamic variability. METHODS. A one group, prospective, time series design was used. The sample consisted of 62 patients who had clinically stable heart failure and who were being treated in an outpatient heart failure clinic at a university medical center. BioZ hemodynamic measures of cardiac output, contractility, and after load were obtained at five points in time: two, 10, and 60 minutes resting following a 40-50 foot walk on the first day and at two and 10 minutes resting following a 40-50 foot walk on the second day, one week later. RESULTS. Small but significant changes in cardiac output and cardiac index (mainly due to changes in heart rate) were seen during the 60-minute period on week one. Stroke index did not change during this period. In general, reproducibility between measurements taken on the same day and between days was quite good. Establishment of 95% confidence intervals helped define boundaries of variability in this population. Further clinical evaluation of the four patients whose values exceeded the 95% confidence intervals revealed unexpected, potentially relevant changes that could have accounted for their interday variability. Conclusion. The BioZ impedance cardiography measurements are responsive to hemodynamic activity-rest changes and are reproducible at a one week interval in clinically stable heart failure patients being treated in an outpatient clinic. Stroke index is a better measure of patient status than cardiac output or cardiac index. (c)2000 by CHF, Inc.

Effects of food restriction on mechanical properties of arterial system in adult and middle-aged rats.

The effects of food restriction on the mechanical properties of the vasculature were determined in Long-Evans male rats with different ages. Rats that began food restriction at the ages of 6 months and 12 months were fed on alternate days for 6 months. Rats at the ages of 12 and 18 months were referred to as adult and middle-aged rats and were anesthetized and thoracotomized. The exponentially tapered T-tube model was employed to relate pulsatile pressure and flow signals measured in the ascending aorta. In each age group, food restriction elicited a decrease in body weight as well as basal heart rate but showed no significant change in cardiac output. Arterial blood pressure, total peripheral resistance, and aortic characteristic impedance were not affected by food restriction in middle-aged rats. However, adult food-restricted rats exhibited lower mean arterial blood pressure (99.1 +/- 3.1 mmHg) than did adult ad libitum-fed rats (110.7 +/- 3.0 mmHg). Total peripheral resistance was reduced from 0.645 +/- 0.045 mmHg-min-kg/ml in adult ad libitum-fed rats to 0.492 +/- 0.030 mmHg-min-kg/ml in adult food-restricted rats. Moreover, aortic characteristic impedance of adult food-restricted rats (0.014 +/- 0.001 mmHg-min-kg/ml) was lower than that of adult ad libitum-fed rats (0.024 +/- 0.002 mmHg-min-kg/ml). Neither age nor diet exerted effects on wave transit time and produced no changes in aortic distensibility. In conclusion, food restriction may elicit significant changes in the mechanical properties of both Windkessel vessels and resistance arterioles in adult rats, but not in middle-aged rats.