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At least 1,099 records · Page 61Linked to original sources
PubMed2007

Specific beta1-adrenergic receptor silencing with small interfering RNA lowers high blood pressure and improves cardiac function in myocardial ischemia.

OBJECTIVES: Beta-blockers are widely used and effective for treating hypertension, acute myocardial infarction (MI) and heart failure, but they present side-effects mainly due to antagonism of beta2-adrenergic receptor (AR). Currently available beta-blockers are at best selective but not specific for beta1 or beta2-AR. METHODS: To specifically inhibit the expression of the beta1-AR, we developed a small interfering RNA (siRNA) targeted to beta1-AR. Three different sequences of beta1 siRNA were delivered into C6-2B cells with 90% efficiency. RESULTS: One of the three sequences reduced the level of beta1-AR mRNA by 70%. The siRNA was highly specific for beta1-AR inhibition with no overlap with beta2-AR. To test this in vivo, systemic injection of beta1 siRNA complexed with liposomes resulted in efficient delivery into the heart, lung, kidney and liver, and effectively reduced beta1-AR expression in the heart without altering beta2-AR. beta1 siRNA significantly lowered blood pressure of spontaneously hypertensive rats (SHR) for at least 12 days and reduced cardiac hypertrophy following a single injection. Pretreatment with beta1 siRNA 3 days before induction of MI in Wistar rats significantly improved cardiac function, as demonstrated by dP/dt and electrocardiogram following the MI. The protective mechanism involved reduction of cardiomyocyte apoptosis in the beta1 siRNA-treated hearts. CONCLUSIONS: The present study demonstrates the possibility of using siRNA for treating cardiovascular diseases and may represent a novel beta-blocker specific for beta1-AR.

Animals↗
PubMed1999

IL-1ra administration does not improve cardiac function in patients with severe sepsis.

PURPOSE: The purpose of this study was to investigate the effects of interleukin-1 receptor antagonist (IL-1ra) on myocardial function in septic patients. MATERIALS AND METHODS: A subgroup of patients from a prospective, randomized, double-blind, placebo-controlled, multicenter trial was studied from 63 academic medical centers in the United States, Canada, and Europe. A subgroup of 71 patients with severe sepsis in whom vasoactive support was little altered during the study was included. The patients were randomized to receive either placebo (n = 29) or IL-1ra at a dose of 1 mg/kg/h (n = 20) or 2 mg/kg/h (n = 22). RESULTS: Hemodynamic measurements were taken at baseline, and 1, 2, 3, 4, 8, and 12 hours after placebo or IL-1ra administration. No significant differences in hemodynamic parameters were observed between the groups or over time during the study period. CONCLUSIONS: IL-1ra administration has no effect on cardiac function in septic patients.

Blood Gas Analysis↗
PubMed2006

Long-term assessment of cardiac function after dose-dense and -intense sequential doxorubicin (A), paclitaxel (T), and cyclophosphamide (C) as adjuvant therapy for high risk breast cancer.

OBJECTIVES: This study evaluated the incidence of late cardiotoxicity after dose-dense and -intense adjuvant sequential doxorubicin (A), paclitaxel (T), and cyclophosphamide (C) for breast cancer (BC) with > or = 4 involved ipsilateral axillary lymph nodes. METHODS: Patients were enrolled from 1994 to 2001 after definitive BC surgery if > or =4 axillary nodes were involved. Planned treatment was A 90 mg/m(2) q 14 days x 3, T 250 mg/m(2) q 14 days x 3, C 3 g/m(2 )q 14 days x 3 with filgrastim (G) support. Left ventricular ejection fraction (LVEF) was monitored using equilibrium radionuclide angiography (ERNA) before the initiation of chemotherapy, and after three cycles of each chemotherapeutic agent. At a median follow-up of 7 years, we obtained ERNA scans on 32 patients to evaluate the long-term cardiotoxicity of this regimen. RESULTS: Eighty-five eligible patients enrolled on the treatment protocol. Clinical heart failure developed in one patient. Seven (8%) patients had LVEF < 50% at the end of therapy. No cardiac-related deaths occurred. Thirty-two (46%) of 69 surviving patients have consented to late cardiac imaging. At a median follow-up of 7 years, the median absolute change in LVEF from baseline was -5.5%; [range (-8%) to (+36%)], and from the end of chemotherapy was -2.0%; [range (-25%) to (+16%)]. Four patients (12%) had a LVEF < 50%; two of these four patients had an LVEF of < 50% at the end of chemotherapy. CONCLUSIONS: Late development of asymptomatic decline in cardiac function may occur after dose-dense and -intense adjuvant therapy, but is uncommon.

Aged↗
PubMed1977

Cardiac function under myocardial ischemia.

The hemodynamic and metabolic changes, during coronary occlusion and during coronary perfusion with non-oxygenated solution, were studied in anesthetized dogs. Coronary perfusion with non-oxygenated Tyrode's solution was performed through a cannula inserted into the left circumflex coronary artery. Left ventricular peak systolic and end-diastolic pressure (LVSP and LVEDP) were measured, and peak LV-dp/dt/IIP calculated. Stroke volume was measured, and the changed of the local myocardial segment length were recorded by a strain gauge arch sutured on that portion of the myocardium perfused through the left circumflex coronary artery. The efflux of lactic acid into the venous blood from the myocardium perfused through the left circumflex coronary artery was calculated. After 10 sec of coronary occlusion, LVSP, SV, and peak LV-dp/dt/IIP declined; LVEDP elevated and a systolic bulge appeared on the local myocardial segment length curve. There was almost no change in these parameters during 3 min of perfusion with non-oxygenated solution. The efflux of lactic acid was more marked during the perfusion with non-oxygenated solution than during coronary occlusion. The delay of the depression of cardiac function during perfusion with the non-oxygenated solution could be related partly to the "wash-out" of metabolites, such as lactic acid, accumulated in the anoxic myocardium.

Animals↗
PubMed1999

Effects of L-arginine on endothelial and cardiac function in rats with heart failure.

We examined the effects of chronic oral L-arginine treatment on endothelial and cardiovascular function in rats with heart failure induced by coronary artery ligation. Both heart failure and sham-operated rats were treated with either L-arginine in drinking water (12.5 or 50 g/l) or water placebo for 8 weeks following surgery. Plasma L-arginine levels in heart failure rats (153 +/- 11 microM) were lower than sham rats (201 +/- 13 microM, P < 0.05). The lower dose L-arginine treatment improved endothelium-dependent relaxation of isolated aortic rings of heart failure rats, while the higher dose of L-arginine treatment did not. Neither low nor high dose of L-arginine treatment improved hemodynamic parameters in heart failure rats. Thus, chronic oral L-arginine treatment at a dose of 12.5 g/l in drinking water improves endothelium-dependent relaxation, but fails to improve in vivo cardiac function in rats with heart failure.

Animals↗
PubMed2004

Differences in the effects of Na+-H+ exchange inhibitors on cardiac function and apoptosis in guinea-pig ischemia-reperfused hearts.

The protective effects of the Na+-H+ exchange (NHE) inhibitors SM-198110 (2-[[(aminoiminomethyl) amino] carbonyl]-4-chloro-1H-indole-1-propanesulfonic acid monohydrate) and SM-197378 (N-(aminoiminomethyl)-1-methyl-7-(sulfooxy)-4-(trifluoromethyl)-1H-indole-2-carboxamide monohydrate) were investigated in perfused Langendorff guinea-pig hearts subjected to ischemia (40 min) and reperfusion (40 min). The recovery of left ventricular developed pressure (LVDP) from ischemia by reperfusion was 39.0% in the control, while in the hearts pretreated with SM-198110 or SM-197378 (10(-7) M), it was about 100%. The ATP level, monitored simultaneously by (31)P-nuclear magnetic resonance spectrometry, was already higher than the control value at the end of the ischemic period, and the elevation in Na+ or Ca2+ fluorometric signals induced during ischemia was suppressed. In post-treated hearts, the LVDP recovery rate was significantly higher with SM-198110 than with SM-197378. By in vitro electron paramagnetic resonance spectrometry, SM-197378 was found to directly quench the active oxygen radical, whereas SM-198110 had no effect. Numbers of apoptotic cardiomyocytes after ischemia (1 h) followed by reperfusion (5 h) were significantly lower in SM-197378-treated than in SM-198110-treated hearts, consistent with the level of activity of caspase-3. These results suggest that the antioxidant effects of NHE inhibitors have an important role in apoptosis during ischemia-reperfusion, but apoptosis is not a major manifestation of cardiac function during postischemic recovery, and that NHE-sensitive mechanisms of reperfusion injury promote both necrotic and apoptotic processes death.

Animals↗
PubMed2004

Pyrroloquinoline quinone (PQQ) decreases myocardial infarct size and improves cardiac function in rat models of ischemia and ischemia/reperfusion.

As pyrroloquinoline quinone (PQQ) is a redox cofactor in mammals, we asked if it is cardioprotective. Rats were subjected to 2 h of left anterior descending (LAD) coronary artery ligation without reperfusion (model 1, ischemia). In model 2 (ischemia/reperfusion), rats were subjected to 17 or 30 min of LAD occlusion and 2 h of reperfusion. PQQ (15-20 mg/kg) was given i.p., either 30 min before LAD occlusion (Pretreatment) or i.v. at the onset of reperfusion (Treatment). In model 1, PQQ reduced infarct size (10.0 +/- 1.5 vs 19.1 +/- 2.1%, P < 0.01). In model 2, either PQQ Pretreatment or Treatment also reduced infarct size (18.4 +/- 2.3 and 25.6 +/- 3.5% vs 38.1 +/- 2.6%, P < 0.01). PQQ resulted in higher LV developed pressure and LV (+)dP/dt after 1-2 h of reperfusion (P < 0.05), and fewer ventricular fibrillation episodes. PQQ dose (5-20 mg/kg) was inversely related to infarct size. PQQ reduced myocardial tissue levels of malondialdehyde (MDA), an indicator of lipid peroxidation (316 +/- 88 vs 99 +/- 14 nmol/g, P < 0.01). PQQ given either as Pretreatment or as Treatment at the onset of reperfusion is highly effective in reducing infarct size and improving cardiac function in a dose-related manner in rat models of ischemia and ischemia/reperfusion. The optimal dose in this study, which exhibited neither renal nor hepatic toxicity, was 15 mg/kg, but lower doses may also be efficacious. We conclude that PQQ, which appears to act as a free radical scavenger in ischemic myocardium, is a highly effective cardioprotective agent.

Animals↗
PubMed1984

Vasodilatory action of HA1004 [N-(2-guanidinoethyl)-5-isoquinolinesulfonamide], a novel calcium antagonist with no effect on cardiac function.

A novel compound, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA1004) was found to be a potent relaxant of blood vessels. Rabbit aortic strips contracted by 18 mM KCl relaxed in the presence of HA1004, with an ED50 value of 2.2 X 10(-6) M. The isolated guinea-pig atria on right ventricular papillary muscles did not respond to HA1004, even at a concentration of 3 X 10(-4) M. HA1004, like verapamil, produced a competitive inhibition of the Ca++-induced contraction of the depolarized rabbit aorta. The pA2 value of HA1004 for the Ca++-induced contraction was 6.60. Atropine, propranolol, theophylline or indomethacin had no effect on the HA1004-induced relaxation. HA1004 (3 X 10(-6) M) inhibited the contraction produced by Ca++ ionophore, A23187, whereas verapamil or diltiazem had no effect on this contraction, even at a concentration of 3 X 10(-5) M. Moreover, HA1004 produced a competitive inhibition of Ca++-induced contraction of the A23187-treated aorta and inhibited the phenylephrine-induced contraction elicited in ca++-free solution, thereby suggesting that this drug affects intracellular rather than extracellular Ca++. The present findings indicate that HA1004 is a novel calcium antagonistic vasodilator with no effect on cardiac function and is apparently of a different class of calcium antagonist from verapamil.

Animals↗
PubMed2001

Effects of left ventricular assist device on cardiac function: experimental study of relationship between pump flow and left ventricular diastolic function.

The left ventricular assist device (LVAD) with centrifugal pump has two characteristics. One is a pump flow wave of the centrifugal pump, consisting of the pulsatile flow of the native heart and the nonpulsatile flow of the centrifugal pump. The other is that the centrifugal pump fills from the native heart not only in the systolic phase, but also in the diastolic phase. In the case of the apex outlet LVAD with centrifugal pump, blood flows from the left atrium through the left ventricle to the pump. Pump flow is regulated by preload, and preload is regulated by diastolic hemodynamics. The aim of this study is to analyze the relationship between pump flow and the diastolic hemodynamics of the native heart. Ten anesthetized intact pigs were studied after placement of an LVAD. Data were recorded with the LVAD off (control) and the LVAD on. The assist rate was changed to 25%, 50%, and 75%. The indexes of left ventricular (LV) diastolic function included LV myocardial relaxation (time constant of isovolumic pressure decay [Tau] and maximum negative dP/dt [LV dP/dt min]) and LV filling (peak filling rate [PFR], time to peak filling rate [tPFR], and diastolic filling time [DFT]). Stroke volume decreased significantly in 75% assist. LV end-systolic pressure decreased significantly in 50% and 75% assist. LV end-diastolic volume decreased as assist rate increased, but there were no significant changes. Stroke work decreased significantly in 50% and 75% assist. LV dP/dt min decreased significantly in 50% and 75% assist. Tau prolonged as assist rate increased, but there were no significant changes. DFT shortened significantly in 75% assist. PFR increased significantly in 75% assist. tPFR shortened significantly in 50% and 75% assist. In this study, LV relaxation delayed as an increasing of pump assist rate, but it suggested a result of reduction of cardiac work. Also, it was suggested that LVAD increases the pressure difference between the left atrium and the left ventricle in the diastolic phase. This phenomenon is due to the filling of the left ventricle. In this study it was suggested that as pump assist rate increases, it is more effective to keep cardiac function in the diastolic phase.

Animals↗
PubMed2001

Transoesophageal acoustic quantification for evaluation of cardiac function during laparoscopic surgery.

Pneumoperitoneum may be poorly tolerated in patients with marginal cardiopulmonary function. Transoesophageal echocardiography is a relatively non-invasive technique that can track changes in left ventricular cavity area using acoustic quantification and has been found to provide a reliable, real-time estimation of left ventricular function. We evaluated mid-papillary fractional area change during pneumoperitoneum in 17 healthy adult patients (group 1) and 17 with hypertension and/or ischaemic heart disease (group 2) undergoing laparoscopic cholecystectomy. Peritoneal insufflation led to significant (p < 0.01) decreases in fractional area change and an increase in mean blood pressure. There was no significant change in heart rate. Patients with cardiovascular disease who had a > 30% decrease in fractional area change following carbon dioxide insufflation (group 2B) were given an intravenous infusion of glyceryl trinitrate. In groups 1 and 2A, fractional area change improved slightly with head-up tilt and continued to improve over the course of surgery. Glyceryl trinitrate led to a significant increase in fractional area change and a decrease in mean blood pressure back to baseline values. We conclude that peritoneal insufflation of carbon dioxide results in a significant increase in cardiac workload that is well tolerated in patients with no cardiovascular disease. Coexisting cardiovascular disease can result in even more pronounced impairment of cardiac function, which may not be predictable by clinical assessment or adequately determined by routine monitoring. We recommend the use of transoesophageal acoustic quantification as a monitor in these patients and the administration of glyceryl trinitrate to ameliorate myocardial stress.

Adult↗
PubMed2006

Apelin and cardiac function in hemodialyzed patients: possible relations?

BACKGROUND: Apelin, a newly discovered adipocytokine, is produced by white adipose tissue and is also expressed in the kidney and heart. Increasing evidence suggests a role for apelin in the pathology of the cardiovascular system. Cardiovascular disease is a major contributor to the mortality and morbidity in patients with chronic renal failure. The aim of this study was to assess associations between apelin, coronary artery disease (CAD) and echocardiographic parameters in hemodialyzed patients. PATIENTS AND METHODS: We investigated plasma apelin levels (using commercially available kits) in 81 nondiabetic, clinically stable hemodialyzed patients (38 females, 43 males) with and without CAD. RESULTS: Patients with CAD were significantly older, with significantly increased left ventricular internal end-diastolic dimension (LVIDd), left ventricular internal end-systolic dimension (LVISd), right ventricle (RV), left atrium (LA), interventricular septum in diastole, left ventricle posterior wall in diastole (LVPW), aorta, pulmonary artery, significantly lower ejection fraction and apelin than patients without CAD. We observed statistically significant correlations between apelin and echocardiographic parameters: LVIDd, LVISd, RV, LA, right atrium, LVPW, aorta, and serum lipids: cholesterol, LDL, triglycerides. In multiple logistic regression analysis, the only associate of apelin was LVIDd. CONCLUSIONS: Apelin level was significantly lower in dialyzed patients with CAD and it was associated with cardiac function. Apelin might be involved in the pathophysiology of cardiovascular disease in chronic renal failure. Since apelin is an inotrope in normal and failing hearts, this finding may have clinical implications for future use of apelin as a novel inotropic agent also for patients with uremic cardiomyopathy.

Aged↗
PubMedDate not supplied

Improvement of cardiac function by dry weight optimization based on interdialysis inferior vena caval diameter.

In hemodialysis (HD) patients, the diameter of the inferior vena cava (IVC) serves for evaluation of the amount of body fluid. IVC measurement is usually performed immediately before and/or after an HD session. In the present study, we examined the validity of IVC diameter in the interdialysis period (interdialytic IVC) for dry weight (DW) optimization. In 100 HD patients, interdialytic IVC was measured ultrasonographically. The average maximum IVC diameter during quiet expiration (IVCe) was 14.2+/-3.8 mm. In 32 patients with volume dependent hypertension, the interdialytic IVCe was > 16 mm in 29 of 32. Thus, we defined an interdialytic IVCe > 16 mm as a hypervolemic state. Next, by screening 306 HD patients ultrasonographically, 31 patients with left ventricular volume overload were chosen based on criteria of an interdialytic IVCe > 16 mm, together with a left ventricular ejection fraction (EF) < 55%. After the DW was lowered to obtain an interdialytic IVCe < 16 mm, 25 of the 31 patients had a significant increase in EF, decrease in diastolic left ventricular dimension, and amelioration of hypertension. In conclusion, interdialytic IVCe is considered to be a useful parameter for DW optimization. In hypervolemic patients with IVCe > 16 mm, reduction in DW is expected to improve volume overload and cardiac function.

Adult↗
PubMed1996

Diltiazem improves cardiac function and exercise capacity in patients with idiopathic dilated cardiomyopathy. Results of the Diltiazem in Dilated Cardiomyopathy Trial.

BACKGROUND: Evidence is arising that calcium antagonists in idiopathic dilated cardiomyopathy (IDC) may have beneficial effects on virus-induced cardiopathology, alcohol toxicity, micro-circulatory disorders, and impaired calcium cycling, all possibly involved in the pathogenesis of the disease. Thus, the effect of adjunct diltiazem (60 to 90 mg TID) on standard treatment was investigated. METHODS AND RESULTS: The Diltiazem in Dilated Cardiomyopathy (DiDi) trial was a randomized, double-blind, placebo-controlled, multicenter trial of 186 patients (92 receiving diltiazem, 94 receiving placebo) with IDC diagnosed by coronary angiography, catheterization of the left side of the heart, and a left ventricular ejection fraction of < 0.50 (mean, 0.34 +/- 0.11). The effect of adjunct diltiazem treatment on transplant listing-free survival, hemodynamics, exercise capacity, and subjective status was investigated. During the 24-month study period, 33 patients dropped out of the study; 153 patients finished the study protocol. Twenty-seven patients died or had a listing for heart transplantation: 16 in the placebo group and 11 in the diltiazem group. The transplant listing-free survival rate was 85% for diltiazem and 80% for placebo recipients (P = .444). After 24 months, only diltiazem significantly increased cardiac index at rest (P = .01) and under a workload (P = .02), systolic and diastolic pressures (P = .003 and P = .004), stroke volume index (P = .003), and stroke work index (P = .000) and decreased both pulmonary artery pressure under workload (P = .007) and heart rate (P = .001). Diltiazem also increased exercise capacity (P = .002) and subjective well-being (P = .01). Adverse reactions were minor and evenly distributed in both groups, except for an increase in the PQ interval in the diltiazem group. CONCLUSIONS: In patients with IDC, the adjunct therapy of diltiazem improves cardiac function, exercise capacity, and subjective status without deleterious effects on transplant listing-free survival.

Calcium Channel Blockers↗
PubMed2001

Long-term treatment with neutral endopeptidase inhibitor improves cardiac function and reduces natriuretic peptides in rats with chronic heart failure.

OBJECTIVE: Increased secretion of atrial and brain natriuretic peptide (ANP and BNP) from hearts is known to exhibit favorable effects in patients and animals with heart failure, and inhibition of neutral endopeptidase (NEP), an enzyme that degrades ANP and BNP, may further increase these peptide levels. However, it is still unknown whether such elevation of the ANP and BNP may offer a therapeutic benefit to the progression of chronic heart failure (CHF). We examined the effects of ONO-9902, a novel NEP inhibitor, on changes in hemodynamic parameters, NEP activity and neurohumoral factors in rats with CHF induced by left coronary artery ligation (CAL). METHODS: Male Wistar rats (220-240 g) were subjected to induction of acute myocardial infarction by CAL. Rats were orally treated with ONO-9902 (300 mg/kg/day) from the 1st to 6th week after the operation. Hemodynamic and/or biochemical assessments were performed at the 1st and 6th weeks after the operation. RESULTS: A single administration of ONO-9902 inhibited the plasma and kidney NEP activities and thereby further augmented the elevation of plasma ANP concentration in rats with CAL at the 1st week after the operation. In rats with CAL at the 6th week after the operation, the left ventricular end-diastolic pressure (LVEDP) increased and cardiac output index (COI) decreased as compared with those of sham-operated rats. These changes were accompanied by marked increases in the plasma ANP, BNP and endothelin-1 (ET-1). Chronic treatment with ONO-9902 attenuated the increase in LVEDP and the decrease in COI. These changes were associated with a decrease in plasma ANP, BNP and ET-1 concentrations. CONCLUSIONS: The results suggest that chronic treatment with NEP inhibitor improves depressed cardiac function in rats with CHF. ONO-9902 may offer a new and possible therapeutic approach in patients with CHF.

Analgesics, Non-Narcotic↗
PubMed2005

Progressive attenuation of myocardial vascular endothelial growth factor expression is a seminal event in diabetic cardiomyopathy: restoration of microvascular homeostasis and recovery of cardiac function in diabetic cardiomyopathy after replenishment of local vascular endothelial growth factor.

BACKGROUND: Diabetic cardiomyopathy (DCM) is characterized by microvascular pathology and interstitial fibrosis, which leads to progressive heart failure; however, the pathogenesis of DCM remains uncertain. METHODS AND RESULTS: Using the streptozotocin-induced diabetic rat model, we evaluated the natural course of DCM over a period of 1 year by serial echocardiography, Western blot analysis for vascular endothelial growth factor (VEGF), endothelial progenitor cell assays, myocardial blood flow measurements, and histopathologic analysis that included terminal dUTP nick end-labeling (TUNEL), capillary and cardiomyocyte density, and fibrosis area. Downregulation of myocardial VEGF expression preceded all other features of DCM and was followed by increased apoptosis of endothelial cells, decreased numbers of circulating endothelial progenitor cells, decreased capillary density, and impaired myocardial perfusion. Apoptosis and necrosis of cardiomyocytes ensued, along with fibrosis and progressive diastolic and then systolic dysfunction. To provide further evidence of the central role of VEGF in the pathophysiology of DCM, we replenished myocardial VEGF expression using naked DNA gene therapy via direct intramyocardial injection of plasmid DNA encoding VEGF (phVEGF165). VEGF-replenished rats showed increased capillary density, decreased endothelial cell and cardiomyocyte apoptosis, and in situ differentiation of bone marrow-derived endothelial progenitor cells into endothelial cells. These anatomic findings were accompanied by significant improvements in cardiac function. CONCLUSIONS: These findings suggest that downregulation of VEGF may compromise microvascular homeostasis in the myocardium and thereby play a central role in the pathogenesis of DCM.

Animals↗
PubMed1996

Anti-CD18 antibodies improve cardiac function following cardiopulmonary bypass in dogs.

PURPOSE: Cardiopulmonary bypass is associated with activation of neutrophils, which may adhere to vascular endothelium causing lung, heart, and brain injury. We tested whether blocking neutrophil adherence would improve organ function following cardiopulmonary bypass in dogs. MATERIALS AND METHODS: All dogs received a standard anesthetic, and then one group (n = 6) received 2 hours of cardiopulmonary bypass followed by 4 hours of observation. A second group (n = 6) received a monoclonal antibody (6 mg/kg) to CD18, a neutrophil adherence factor, immediately before cardiopulmonary bypass. A third group (n = 6) did not receive cardiopulmonary bypass or antibody. RESULTS: Using flow cytometry we found that the antibody bound essentially all neutrophil CD18 sites. All three groups had similar gas exchange and hemodynamics. Lung and heart histology results were similar between groups. By echocardiography, five animals receiving cardiopulmonary bypass alone showed regional wall abnormalities, whereas only one receiving antibody showed wall motion abnormality (P < .05). Following cardiopulmonary bypass, intracellular myocardial pH was higher (P < .05) in the antibody-treated group compared with the group that had cardiopulmonary bypass alone (7.23 +/- 0.05 v 7.07 +/- 0.07 respectively). CONCLUSION: Monoclonal antibodies to CD18 can prevent the deterioration in cardiac function routinely observed following cardiopulmonary bypass.

Analysis of Variance↗
PubMed1998

The effects of desflurane on cardiac function as measured by conductance volumetry in swine.

UNLABELLED: The purpose of the investigation was to assess the effects of desflurane (DES) on left ventricular heart function during basal barbiturate anesthesia in a closed-pericardium, closed-chest acute swine model. The study was performed in 11 normoventilated adult pigs. Hemodynamic measurements were obtained using arterial, central venous, and pulmonary artery catheters, as well as a conductance volumetry and tip manometry catheter placed in the left ventricle. Hemodynamic measurements were recorded during basal pentobarbital anesthesia and with the addition of 1%, 2%, 4%, and 6% DES. DES dose-dependently decreased mean arterial pressure, systemic vascular resistance, left ventricular end-systolic pressure, dP/dtMAX and dP/dtMIN. At doses >1%, decreases in CO, stroke volume, ejection fraction, end-systolic elastance, preload recruitable stroke work, preload adjusted maximal power, and peak filling rate were observed. Heart rate decreased at 4% and 6% DES. Isovolumetric relaxation time increased only at 6% DES. We conclude that smaller doses of DES have a significant cardiodepressive effect in the setting of barbiturate infusion, as measured by conductance volumetry. IMPLICATIONS: Desflurane, in very small doses, depressed cardiac function during pentobarbital anesthesia with ketamine and benzodiazepine premedication in swine, as assessed by conductance volumetry and left ventricular pressure and volume relationship analysis. These results suggest that desflurane, in combination with certain anesthetics, can be cardiodepressive even in very small doses.

Anesthetics, Inhalation↗
PubMed1997

Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and reperfusion.

BACKGROUND: Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing reperfusion damage by the application of C1 esterase inhibitor (C1-INH). METHODS AND RESULTS: Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. C1-INH was administered during the first 5 minutes of coronary reperfusion Compared with the NaCl controls, C1-INH reduced myocardial injury (48.8 +/- 7.8% versus 73.4 +/- 4.0% necrosis of area at risk, P < or = .018). C1-INH treatment significantly reduced circulating C3a and slightly attenuated C5a plasma concentrations. Myocardial protection was accompanied by reduced plasma concentration of creatine kinase and troponin-T. C1-INH had no effect on global hemodynamic parameters, but local myocardial contractility was markedly improved in the ischemic zone. In the short-axis view, 137 degrees of the anteroseptal region showed significantly improved wall motion at early and 29 degrees at late reperfusion with C1-INH treatment. CONCLUSIONS: C1-INH significantly protects ischemic tissue from reperfusion damage, reduces myocardial necrosis, and improves local cardiac function.

Anaphylatoxins↗