Changes In Ventricular Pressure Research Articles

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

We tested whether mild and moderate dynamic exercise and muscle metaboreflex activation (MMA) affect dynamic baroreflex control of heart rate (HR) and cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing-induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo-F, 0.04-0.15 Hz; Hi-F, 0.15-0.6 Hz). In N dogs, both workloads significantly decreased the gains for LVSP-HR and LVSP-CO in Hi-F, whereas only moderate exercise also reduced the LVSP-CO gain in Lo-F. MMA during mild exercise further decreased the gains for LVSP-HR in both frequencies and for LVSP-CO in Lo-F. MMA during moderate exercise further reduced LVSP-HR gain in Lo-F. Coherence for HR-CO in Hi-F was decreased by exercise and MMA, whereas that in Lo-F was sustained at a high level (>0.8) in all settings. HF significantly decreased dynamic HR and CO regulation in all situations. In HF, the coherence for HR-CO in Lo-F decreased significantly in all settings; the coherence for SV-CO in Lo-F was significantly higher. We conclude that dynamic exercise and MMA reduces dynamic baroreflex control of HR and CO, and these are substantially impaired in HF. In N conditions, HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes, and fluctuations of SV dominate in CO variations.

Validity of predicting left ventricular end systolic pressure changes following an acute bout of exercise

ObjectivesLeft ventricular end systolic pressure (LV ESP) is important in assessing left ventricular performance and is usually derived from prediction equations. It is unknown whether these equations are accurate at rest or following exercise in a young, healthy population. DesignMeasured LV ESP vs. LV ESP values from the prediction equations were compared at rest, 15min and 30min following peak aerobic exercise in 60 participants. MethodsLV ESP was obtained by applanation tonometry at rest, 15min post and 30min post peak cycle exercise. ResultsMeasured LV ESP was significantly lower (p<0.05) at all time points in comparison to the two calculated values. Measured LV ESP decreased significantly from rest at both the post15 and post30 time points (p<0.05) and changed differently in comparison to the calculated values (significant interaction; p<0.05). The two LV ESP equations were also significantly different from each other (p<0.05) and changed differently over time (significant interaction; p<0.05). ConclusionsThe two commonly used prediction equations did not accurately predict either resting or post exercise LV ESP in a young, healthy population. Thus, LV ESP needs to be individually determined in young, healthy participants. Non-invasive measurement through applanation tonometry appears to allow for a more accurate determination of LV ESP.

Nitric Oxide Synthase Inhibition Weakens Beneficial Effects of Increased Plasma Viscosity on Cardiac Function in Hemodilution Model

This study tested the hypothesis that the inhibition of nitric oxide synthase negatively affects the beneficial effects of high viscogenic plasma expander (HVPE) on cardiac performance in a state of hemodilution. Five anesthetized hamsters were administered with N(G)‐nitro‐L‐arginine methyl ester (L‐NAME), nitric oxide synthase inhibitor, as a tested group whereas other five without L‐NAME infusion were used as a control group. Animals were performed an isovolemic hemodilution by 40% of estimated blood volume with dextran 2000 kDa, HVPE with viscosity 6.34 cP. L‐NAME administration followed by isovolemic hemodilution significantly decreased heart rate from 441±41 bpm at baseline to 355±27 bpm at 60 min after hemodilution. End‐systolic pressure increased 14% after L‐NAME infusion and maintained higher than baseline after hemodilution whereas it gradually decreased in animals without L‐NAME infusion. L‐NAME significantly decreased the maximum rate of ventricular pressure change, stroke volume and cardiac output after hemodilution compared to a control group. Systemic vascular resistance increased to 162% and 135% of baseline after L‐NAME infusion and 60 min after hemodilution which is particularly higher than a control group. These results indicate that nitric oxide induced by HVPE play a major role on cardiac function during an isovolemic hemodilution.

Neuropeptide Y Reverses Chronic Stress-induced Baroreflex Hypersensitivity in Rats

Chronic stress, as a risk factor for cardiovascular diseases, has been reported to result in elevated plasma neuropeptide Y (NPY) and be highly associated with abnormal cardiac autonomic function. This study aimed to explore the effect of NPY on the chronic stress-induced abnormal baroreceptor reflex sensitivity (BRS). Seven types of recognized stressors were used to develop chronic stress rat model. Subcutaneously implanting ALZET mini-osmotic pumps containing NPY were used to evaluate the action of NPY on the stressed male rats. We found that chronic stress showed no influence on baseline systolic blood pressure (SBP) and heart rate (HR), whereas NPY (85 µg for 30 days) could elevate baseline SBP and induce bradycardia in rats intervened by various stimuli. NPY pretreatment could preserve chronic stress-induced decreases in left ventricular systolic pressure (LVSP) and the maximum rate of change in left ventricular pressure in the isovolumic contraction period (+dp/dt_max) but has shown no effect on left ventricular end diastolic pressure (LVEDP) and the maximum rate of change in left ventricular pressure in the isovolumic relaxation period (-dp/dt_max). Notably, chronic stress led to baroreflex oversensitivity indicated by the elevated ratio of Δheart rate (HR)/ Δmean arterial blood pressure (MABP) in rats followed by vasoconstrictor (phenylephrine, PE) or vasodilator (sodium nitroprusside, SNP) administration, which was almost completely reversed by NPY pretreatment. The expressions of substance P (SP) and gamma aminobutyric acid A receptor (GABA_AR) in nucleus tractus solitarius were increased in chronic stress rats, which were counteracted by NPY pretreatment. We conclude that chronic stress-induced baroreflex hypersensitivity could be blocked by NPY pretreatment. Furthermore, the altered expressions of neurotransmitters and receptors in the brainstem might contribute to this process.

Moderate cardiac‐selective overexpression of angiotensin II type 2 receptor protects cardiac functions from ischaemic injury

We hypothesized that moderate cardiac-selective overexpression of the angiotensin II type 2 receptor (AT2R) would protect the myocardium from ischaemic injury after a myocardial infarction (MI) induced by coronary artery ligation. For in vitro studies, adenoviral vector expressing genomic DNA of AT2R and enhanced green fluorescence protein (EGFP) was used to overexpress AT2R in rat neonatal cardiac myocytes. Expression of AT2R, measured by real-time PCR and immunostaining, demonstrated efficient transduction of AT2R in a dose-dependent pattern. The AT2R constitutively induced apoptosis in rat neonatal cardiac myocytes in dose-dependent patterns. For in vivo studies, 4 × 10(10) vector genomes (vg) of recombinant adeno-associated virus serotype 9 (rAAV9)-chicken β actin promoter-AT2R was injected into the left ventricle of 5-day-old Sprague-Dawley rats. At 6 weeks of age, hearts were harvested and expression of AT2R determined by real-time PCR and Western blotting. Expression was increased onefold over control hearts, and no apoptosis was detected. Two subsequent in vivo studies were performed. In a prevention study, 4 × 10(10) vg of rAAV9-CBA-AT2R was injected into the left ventricle of 5-day-old Sprague-Dawley rats and MI was induced at 6 weeks of age. For a post-treatment study, 4 × 10(10) vg of rAAV9-CBA-AT2R was administrated to the peri-infarcted myocardium area immediately after MI in 6-week-old animals. For both in vivo studies, cardiac functions were assessed using echocardiography and haemodynamic measurements 4 weeks after coronary artery ligation. In the in vivo studies, the rats subjected to MI showed significant decreases in fractional shortening and rate of change of left ventricular pressure, with increased left ventricular end-diastolic pressure and ventricular hypertrophy. For the prevention study, the moderate cardiac-selective overexpression of AT2R attenuated these MI-induced impairments and also caused a decrease in ventricular wall thinning. In the post-treatment study, the overexpression of AT2R partly reversed the MI-induced cardiac dysfunction. Myocardial infarction also induced the upregulation of angiotensin II type 1 receptor, angiotensin-converting enzyme and collagen I mRNA expression, all of which were attenuated by the overexpression of AT2R. It is concluded that moderate cardiac-selective overexpression of AT2R protects heart function from ischaemic injury, which may be mediated, at least in part, through modulation of components of the cardiac renin-angiotensin system and collagen levels in the myocardium.

The role of RhoA/Rho kinase signalling pathway in myocardial fibrosis in rats with type 2 diabetes

The role of RhoA/Rho kinase signalling pathway in myocardial fibrosis in rats with type 2 diabetes

Left atrial dilatation and ST-T changes predict cardiovascular outcome in chronic hemodialysis patients

The left atrium (LA) is afterload-sensitive, meaning that it responds to changes in left ventricular diastolic pressure, and left atrial volumetric remodeling has been reported. We prospectively examined the effects of LA enlargement and ST-T changes on cardiovascular outcome of chronic hemodialysis (HD) patients. Echocardiography was performed twice, a mean interval of 2.1 ± 0.4 years apart, and LA size, left ventricular mass index (LVMI), and other indices were evaluated. The prognostic value of ST-T changes and LA dilatation for cardiovascular events was investigated in a cohort of 112 HD patients. The LVDd, interventricular septum thickness, fractional shortening, and LVMI values were higher in the HD patients with ST-T changes and LA dilatation at the second echocardiography. Moreover, LV hypertrophy (LVH) and new cardiovascular events were more common in HD patients with both ST-T changes and LA dilatation (p = 0.0127). Interdialysis weight gain, presence of ST-T changes and LA dilatation, and use of calcium channel blockers were significantly associated with LVH, and the odds ratios were 1.740, 2.870, and 0.304, respectively. Over a mean follow-up period of 2.1 ± 0.4 years, 27 patients experienced new cardiovascular event. A Cox proportional hazard analysis revealed that complication of coronary artery diseases, the presence of ST-T changes and LA dilatation, and serum albumin levels were significantly associated with incident cardiovascular events, and the hazard ratios were 3.898, 5.182, and 0.185 (1 g/dl per year increase), respectively. In a Kaplan-Meier analysis, incident cardiovascular events were significantly less common in HD patients without ST-T changes and LA dilatation than those with (p < 0.0001), 50% event-free period was about 2 years in HD patients with ST-T changes and LA dilatation. In conclusion, ST-T changes and LA dilatation predict the cardiovascular outcome of chronic HD patients. Detecting ST-T changes on ECG and LA dilatation is useful for monitoring cardiovascular risk in chronic HD patients.

Hemodynamic Changes during Hepatic Vascular Exclusion: Use of Intraoperative Transesophageal Echocardiography a Case Series

The aim of this clinical observation was to compare intraoperative transesophageal echocardiography (TEE) and pulmonary artery catheterization (PAC) during hepatic vascular exclusion (HEV). Five non-cirrhotic patients to undergo HVE for major liver resection have been observed. Hemodynamic parameters: pulmonary arterial wedge pressure (PCWP), cardiac index (CI), cardiac output (CO), and systemic vascular resistance (SVR) have been monitored by PAC. Left ventricular end-diastolic area (LVEDA), left ventricular end-systolic area (LVESA), left ventricular end-diastolic pressure (LVEDP), cardiac index (CI), cardiac output (CO), and fractional area changes (FAC) have been monitored by TEE. Hemodynamic variables were assessed before clamping (), at 5 and 30 minutes after clamping (, ) and 15 minutes after unclamping (). No significant difference between PCWP and LVEDP was found. LVEDP significantly decreased at and compared to (); PCWP showed the same trend. A correlation was found between SV and LVEDP (, ) as well as CI (, ). Data confirm that intraoperative TEE may be a reliable method for hemodynamic monitoring during major liver resections.

Effects of Polysaccharides Extracted from Zhu Zi Shen (Rhizoma Panacis Majoris) on Oxidative Stress and Hemodynamics in Rats with Adriamycin-induced Chronic Heart Failure

To probe into the intervening action of polysaccharides of Zhu Zi Shen (Rhizoma Panacis Majoris) (PZZS) on oxidative stress and hemodynamics in rats with adriamycin-induced chronic congestive heart failure (CHF). After SD rats were successfully modeled with adriamycin, they were randomly divided into a normal control group, a model group, a PZZS group, and a captopril group, and were administrated respectively. At the end of experiment, the hemodynamic function, whole heart weight index, and the blood CK, SOD, MDA, NO, NOS were detected; and the myocardial morphological examinations were carried out. Compared with the normal control group, the arterial systolic pressure (SBP), diastolic pressure (DBP), mean arterial pressure (MAP), heart rate (HR), left ventricular systolic peak (LVSP), and left ventricular pressure change rate (dp/dt(max)) significantly decreased, and left ventricular end diastolic pressure (LVEDP), whole heart weight index, the blood CK, MDA, NO, NOS significantly increased in the model group. PZZS significantly improved the hemodynamic function, lowered the MDA and NO levels, and decreased the CK and NOS activities in the CHF rats. PZZS can improve the hemodynamic function, and alleviate the oxidative stress reaction in the CHF rat.

Non-Geometric Echocardiographic Indices of Ventricular Function in Patients with a Fontan Circulation

Complex anatomy and limited windows complicate echocardiographic assessments of ventricular function in Fontan patients. For the Pediatric Heart Network Fontan Cross-Sectional Study, data were acquired from which mean ventricular pressure change during isovolumetric contraction (dP/dt(ic)), Tei index, and maximal systolic annular velocity (S') could be measured. The purpose of this study was to compare these nongeometric indices of ventricular function to cardiac magnetic resonance (CMR) measurements of ventricular ejection fraction (EF). Echocardiographic and CMR studies were performed prospectively using standardized protocols; measurements were completed by core laboratories. Data from both modalities were available from 137 patients. A weak but statistically significant correlation was observed between mean dP/dt(ic) and CMR-derived EF (r= 0.20, P= .022). This correlation was strengthened when preload was taken into account (r= 0.30, P=.001). Statistically significant correlations did not exist between CMR-derived EF and the Tei index or S'. Among Fontan patients, the correlation between CMR-derived EF and nongeometric echocardiographic indices of ventricular function is not strong. Of the indices evaluated, however, mean dP/dt(ic) appears to be the best.

Reflexes from pulmonary arterial baroreceptors in dogs: interaction with carotid sinus baroreceptors

In contrast to the reflex vasodilatation occurring in response to stimulation of baroreceptors in the aortic arch, carotid sinuses and coronary arteries, stimulation of receptors in the wall of pulmonary arteries results in reflex systemic vasoconstriction. It is rare for interventions to activate only one reflexogenic region, therefore we investigated how these two types of reflexes interact. In anaesthetized dogs connected to cardiopulmonary bypass, reflexogenic areas of the carotid sinuses, aortic arch and coronary arteries and the pulmonary artery were subjected to independently controlled pressures. Systemic perfusion pressure (SPP) measured in the descending aorta (constant flow) provided an index of systemic vascular resistance. In other experiments, sympathetic efferent neural activity was recorded in fibres dissected from the renal nerve (RSNA). Physiological increases in pulmonary arterial pressure (PAP) induced significant increases in SPP (+39.1 ± 10.4 mmHg) and RSNA (+17.6 ± 2.2 impulses s(−1)) whereas increases in carotid sinus pressure (CSP) induced significant decreases in SPP (−42.6 ± 10.8 mmHg) and RSNA (−42.8 ± 18.2 impulses s(−1)) (P < 0.05 for each comparison; paired t test). To examine possible interactions, PAP was changed at different levels of CSP in both studies. With CSP controlled at 124 ± 2 mmHg, the threshold, 'set point' and saturation pressures of the PAP–SPP relationship were higher than those with CSP at 60 ± 1 mmHg; this rightward shift was associated with a significant decrease in the reflex gain. Similarly, increasing CSP produced a rightward shift of the PAP–RSNA relationship, although the effect on reflex gain was inconsistent. Furthermore, the responses to changes in CSP were influenced by setting PAP at different levels; increasing the level of PAP from 5 ± 1 to 33 ± 3 mmHg significantly increased the set point and threshold pressures of the CSP–SPP relationship; the reflex gain was not affected. These results indicate the existence of interaction between pulmonary arterial and carotid sinus baroreceptor reflexes; physiological and pathological states that alter the stimulus to one may alter the reflex responses from the other.

Beneficial effects of angiotensin (1–7) in diabetic rats with cardiomyopathy

This study was designed to investigate the effect of angiotensin (1-7), a Mas receptor agonist, and A-779, a Mas receptor antagonist, in rats with diabetic cardiomyopathy (DC). Rats treated with a single injection of streptozotocin (50 mg/kg, intraperitoneal), developed DC after 8 weeks. The extent of DC was assessed by measuring the left ventricular weight/body weight (LVW/BW) ratio, absolute LVW, left ventricular developed pressure (LVDP), maximum change in left ventricular pressure over time (dp/dtmax), minimum change in left ventricular pressure over time (dp/dtmin), left ventricular (LV) protein content, LV collagen content, lipid profile, and serum nitrite/nitrate concentration. Test drug treatment was given from week 4 to week 8. Angiotensin (1-7) treatment attenuated DC by significantly increasing LVDP, dp/dtmax, dp/dtmin, serum nitrite/nitrate concentration and significantly decreasing the LVW/BW ratio and LV collagen content. For the first time, this study has documented that endogenous angiotensin (1-7) regulates lipid profile in rats, and that treatment with angiotensin (1-7) significantly attenuates diabetes-induced changes in lipid profile. However, LV protein content and absolute LVW remain unaffected after treatment. Angiotensin (1-7) significantly attenuates DC in rats because of vasodilatory, antiproliferative and anifibrotic properties but also because of a significant decrease in dyslipidemia, the major culprit for cardiac dysfunctions in diabetes.

Respiratory systolic variation test in acutely impaired cardiac function for predicting volume responsiveness in pigs

Predicting the response of cardiac output (CO) to volume administration remains difficult, in particular in patients with acutely compromised cardiac function, where, even small amounts of i.v. fluids can lead to volume overload. We compared the ability to predict volume responsiveness of different functional haemodynamic parameters, such as pulse pressure variation (PPV), stroke volume variation (SVV), the static preload parameter right atrial pressure (RAP), and global end-diastolic volume (GEDV) with the recently proposed respiratory systolic variation test (RSVT) in acutely impaired cardiac function. In 13 mechanically ventilated pigs, cardiac function was acutely reduced by continuous application of verapamil to reach a decrease in peak change of left ventricular pressure over time (dP/dt) of 50%. After withdrawal of 20 ml kg(-1) BW blood to establish hypovolaemia, four volume loading steps of 7 ml kg(-1) BW using the shed blood and 6% hydroxyethylstarch 130/0.4 were performed. Volume responsiveness was considered as positive, if CO increased more than 10%. Receiver operating characteristic curve analysis revealed an area under the curve (AUC) of 0.88 for the RSVT, 0.84 for PPV, 0.82 for SVV, 0.78 for RAP, and 0.77 for GEDV. Functional parameters of cardiac preload, including the RSVT, allow prediction of fluid responsiveness in an experimental model of acutely impaired cardiac function.

Influence of fluvastatin on cardiac function and baroreflex sensitivity in diabetic rats

To investigate whether fluvastatin is able to ameliorate the impaired cardiac function or baroreflex sensitivity (BRS) in rats with type 1 diabetes. Type 1 diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ) and then administered fluvastatin (1.5, 3.0, and 6.0 mg·kg(-1)·d(-1)) for 30 d. Food and drink intake was recorded every day. Fasting blood glucose (FBG) level, blood lipid level, cardiac function and BRS were measured in diabetic rats after fluvastatin treatment for 30 d. The polydipsia, polyphagia and abnormal biochemical indexes of blood were significantly ameliorated by the the 3.0- and 6.0-mg doses of fluvastatin in STZ-induced diabetic rats. FBG was decreased in diabetic rats after fluvastatin treatment for 30 d. The left ventricular systolic pressure (LVSP) and the maximum rate of change of left ventricular pressure in the isovolumic contraction and relaxation period (±dp/dt(max)) were elevated, and left ventricular diastolic pressure (LVEDP) was decreased by fluvastatin. The attenuated heart rate responses to arterial blood pressure (ABP) increase induced by phenylephrine (PE) and ABP decrease induced by sodium nitroprusside (SNP) were reversed by the 3.0-mg dose of fluvastatin. Fluvastatin regulates blood lipid levels and decreases the FBG level in diabetic rats. These responses can protect the diabetic heart from complications by improving cardiac function and BRS.

Interaction between hydrogen sulfide and nitric oxide on cardiac protection in rats with metabolic syndrome.

To investigate the interaction between hydrogen sulfide (H2S)/cystathionine gamma-lyase (CSE) system and nitric oxide (NO)/nitric oxide synthase (NOS) system on cardiac protection in metabolic syndrome (MS) rats. Forty one male Sprague-Dawley rats were randomly divided into 6 groups: control group, MS group, H2S donor group, CSE inhibitor group, NOS inhibitor group, and NO donor group. The MS rat model was established by a high-fat diet of 16 weeks. Rats in control and MS groups were subjected to normal saline and the other four groups were respectively subjected to sodium hydrosulfide (NaHS, 56 μmol/kg), D,L-propargylglycine (PPG, 37.5 mg/kg), Nψ-nitro-L-arginine methyl ester (L-NAME, 18 mg/kg), L-Arginine (500 mg/kg) every day. Four weeks later, the obesity indices, blood sugar of oral glucose tolerance test in each time point (0,30,60, and 120 minutes) and blood lipids (cholesterol, triglyceride, high density lipoprotein, low density lipoprotein) were measured. The computer-based electrophysiological recorder system was used to measure the changes of the left ventricular systolic pressure (LVSP), the left ventricular end diastolic pressure (LVEDP), the maximal rate of pressure increase in the contraction phase (+dP/dtmax), and the maximal rate of pressure decrease in the diastole phase (-dP/dtmax). H2S and NO concentration in plasma and myocardium, as well as CSE, constitutive NOS (cNOS), and inducible NOS (iNOS) activities in myocardium were measured with colorimetric method. Reverse transcription-polymerase chain reaction was used to assess the gene expression of CSE and endothelial NOS (eNOS) mRNAs. Compared with control group, the obesity indices, blood sugar at each time point, and blood lipids significantly increased in MS group (P<0.05). H2S and NO concentration in plasma and myocardium, CSE and cNOS activities in myocardium, the expressions of CSE mRNA and eNOS mRNA, and the myocardial function significantly decreased in MS group (P<0.05). Compared with MS group, NO concentration in plasma and myocardium, cNOS and iNOS activities in myocardium, and the expression of eNOS mRNA significantly increased in CSE inhibitor group (P<0.05). However, activities of cNOS and iNOS in myocardium and the expression of eNOS mRNA were significantly decreased in H2S donor group (P<0.01), while the myocardial function significantly increased (P<0.05). H2S concentration in plasma and myocardium, and the expression of CSE mRNA significantly increased in NOS inhibitor group (P<0.05). However, in NO donor group, the CSE activity in myocardium and the expression of CSE mRNA significantly decreased (P<0.05). And the myocardial function was improved significantly (P<0.05). Both the H2S/CSE and NO/NOS systems appear to have a mutual down-regulation effect on myocardium in MS rats. Meanwhile, exogenous H2S and NO supplement is cardioprotective in rat model of MS.

Protective effect of carnosine on adriamycin-induced oxidative heart damage in rats

Oxidative stress is one of the major factors involved in the pathogenesis of adriamycin (ADR)-induced cardiac dysfunction. The present study examined the antioxidant protective effects of carnosine (CAR) on adriamycin-induced cardiac damage in rats. Female Sprague Dawley rats were divided into four groups. Control (CONT, n=8, saline only i.v.); carnosine (CAR, n=8.10 mg/kg/day, i.v.); adriamycin (ADR, n=10.4 mg/kg four times every 2 days for 8 days, i.v.) alone and carnosine with adriamycin (CAR+ADR, n=10). Carnosine was given one week before adriamycin treatment and following one week with adriamycin treatment. After measurement of physiological functions, blood samples were collected for biochemical assays. The hearts were excised for hemodynamic study. Comparisons between different groups were made using ANOVA and posthoc Tukey test. Adriamycin produced evident cardiac damage revealed by; hemodynamic changes - decreased left ventricular developed pressure (p=0.01), the maximum-minimum rates of change in left ventricular pressure (± dP/dt, p=0.01), electrocardiogram (ECG) changes (elevated ST, decreased R-wave, p=0.001), cardiac injury marker changes (increased creatine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase), plasma antioxidant enzymes activity changes (decreased superoxide dismutase, glutathione peroxidase, catalase activities, p=0.03) and lipid peroxidation (elevated malondialdehyde, p=0.05) to the control and carnosine groups. Carnosine treatment caused significant attenuation (p=0.05) of cardiac dysfunction induced by adriamycin (CAR+ADR), revealed by normalization of the ventricular function, ECG and biochemical variables. An increase in oxidative stress, superoxide dismutase, glutathione peroxidase levels, catalase inactivation and cardiac dysfunction induced by adriamycin were prevented by carnosine.

The use of sildenafil to treat pulmonary hypertension associated with interstitial lung disease

Limited data suggest a benefit following sildenafil treatment in patients with pulmonary hypertension (PH) and interstitial lung disease (ILD). The role of sildenafil in the management of PH in ILD is not clear. We report our experience of ILD patients with PH after 6-month sildenafil therapy. We reviewed 15 patients (mean age 55 ± 15 years; 8 men) with ILD (mean FVC 52.6 ± 15.4%) and PH (mean right ventricular systolic pressure 73.8 ± 17.8 mm Hg). Median brain natriuretic peptide: 37 (5-452) pmol/L; mean 6MWD: 156 ± 101 m. Following 6-month treatment with sildenafil, brain natriuretic peptide levels were lower (n = 12, P = 0.03), 6MWD was higher (n = 6, P < 0.05), but no change in right ventricular systolic pressure (n = 11) was demonstrated. Our observations suggest that sildenafil may be useful in the management of PH in ILD. Controlled trials are warranted before therapeutic recommendations can be made.

Effects of a novel ultrasound contrast agent with long persistence on right ventricular pressure: Comparison with SonoVue

This work investigated the effect of infusion of a self-made ultrasound contrast agent with long persistence (named ZHIFUXIAN) on rat right ventricular pressure and made a preliminary evaluation on the relative safety of the novel microbubbles. Normal saline, SonoVue and ZHIFUXIAN were injected through caudal vein at the total volume of 0.5 ml for each injection. The right ventricular systolic pressure (RVSP) and end-diastolic pressure (RVEDP) were monitored and the changes of the pressure were compared with baseline readings. RVSP increased when saline, SonoVue or ZHIFUXIAN were injected, the greatest change being after SonoVue (about 2 mm Hg), but there was no statistical significance compared with baseline ( P > 0.05). There was no significant difference in RVSP between saline, SonoVue and ZHIFUXIAN at any time point. Also, there was no significant difference in RVEDP between groups at each time point and between different time points in each group. The results indicate that the self-made microbubbles effect on right ventricular hemodynamics is equivalent to that of normal saline at the same volume needed for effective enhanced imaging, demonstrating that it does not produce changes in right ventricular blood pressure under the study conditions. Pathological examination also showed it had no obvious influence on lung, liver and kidney.

Left-to-right systolic ventricular interaction in patients undergoing biventricular stimulation for dilated cardiomyopathy

Left-to-right systolic ventricular interaction (i.e., the phenomenon by which the left ventricle contributes to most of the flow and to two-thirds of the pressure generated by the right ventricle) originates from transmission of systolic forces between the ventricles through the interventricular septum and from the mechanical effect of the common muscle fibers encircling their free walls. As a consequence, any reduction of left ventricular free wall function translates in lower right ventricular pressure or function. We investigated whether systolic ventricular interaction could be evidenced in nine patients with dilated cardiomyopathy in whom a biventricular pacemaker was implanted. Changes in right and left ventricular pressures were measured with high-fidelity catheters, before and after periods of biventricular pacing from the right atrium with different stimulation intervals to the right and left ventricles, respectively. The steady-state changes of left and right ventricular systolic pressure obtained from any single pacing interval combination were considered. We then calculated, with a two-level mixed regression analysis of the entire data set, the relation between changes in left and right systolic pressures: the presence of a statistically significant slope was assumed as evidence of ventricular interaction. The slope of the regression replaced the crude pressure ratio as an estimate of the gain of the interaction; its value compared with values observed in experimental studies. Moreover, its dependence on septal elastance and on right ventricular volume was similar to that already demonstrated for ventricular interaction gain. In conclusion, the linear relationship we found between systolic pressure changes in the two ventricles of patients with dilated cardiomyopathy during biventricular pacing could be explained in terms of ventricular interaction.

Feasibility of In Vivo Pressure Measurement Using a Pressure-Tip Catheter via Transventricular Puncture

Pressure-tip catheters (PTCs) are used to evaluate ventricular mechanics during surgical repair of congenital heart disease in children. Studies in infants require miniaturized sensors. We compared the safety and accuracy of a 2-Fr ultraminiature PTC with a 5-Fr PTC. In 10 piglets (weight 19-22 kg), a 5-Fr PTC was inserted through a 3-mm apical puncture with a #11 blade. A 20-gauge angiocatheter was inserted using a separate site. A 2-Fr PTC was threaded through the angiocatheter lumen. The angiocatheter was withdrawn, leaving the 2-Fr PTC within the left ventricle (LV). Left ventricular pressure (LVP) changes were measured during three inferior vena caval occlusions. Reliability coefficients demonstrated correlation between the 2-Fr PTC and 5-Fr PTC for LV end-diastolic pressure (0.90-0.95), peak LVP (0.92-0.99), and the maximal (0.87-0.93) and minimal (0.89-0.94) first derivatives of LVP. Bland-Altman analysis demonstrated agreement for all variables. Blood loss was trivial with pressure manipulation and catheter placement and removal. Pressure measurements using the 2-Fr PTC were accurate and comparable with those from the 5-Fr PTC. Transventricular placement of a 2-Fr PTC is feasible and should allow evaluation of ventricular mechanics during surgical repair of congenital heart disease.