Significant Reduction In Stroke Volume Research Articles

Perinatal nicotine exposure alters development of cardiac performance

Perinatal nicotine exposure alters development of brainstem neurons, including those involved in the control of breathing and cardiovascular function. Whether or not perinatal nicotine exposure alters development of cardiac performance is unknown. Pregnant rats were exposed to nicotine plus saccharin in drinking water beginning on the 4thday of gestation. Developing fetuses were exposed via the placental circulation, and exposure continued via breast milk after birth, up until the day of study. Plasma cotinine levels in the nicotine‐exposed pups ranged from 50‐100 ng/ml. Control neonates drank water with saccharin, but no nicotine. Animals aged postnatal day 10‐12 (P10‐P12) were lightly anesthetized with isoflurane, and cardiac function was assessed non‐invasively with echocardiography. Compared to controls (N=13), nicotine‐exposed pups (N=13) had reduced body weight (28.4 ± 1 vs. 21 ± 1 g, P=0.00032), significant reductions in stroke volume (39.1 ± 1 vs. 33.7 ± 1.7 μL/beat, P=0.027) and cardiac output (14.0 ± 0.8 vs. 12.4 ± 1 ml/min, P=0.011), and had significantly slower isovolumetric contraction (15 ± 1 vs. 22 ± 2 ms, P=0.005) and relaxation times (21 ± 1 vs. 33 ± 3 ms, P=0.04). There were also trends toward a lower heart rate (P=0.055), ejection fraction (P=0.065) and left ventricular wall thickness (P=0.059) in the nicotine exposed animals. These are the first data showing that perinatal nicotine exposure alters development of the heart’s pumping capacity.

Carotid Reservoir Pressure Decrease After Prolonged Head Down Tilt Bed Rest in Young Healthy Subjects Is Associated With Reduction in Left Ventricular Ejection Time and Diastolic Length.

BackgroundThe arterial pressure waveform reflects the interaction between the heart and the arterial system and carries potentially relevant information about circulatory status. According to the commonly accepted ‘wave transmission model’, the net BP waveform results from the super-position of discrete forward and backward pressure waves, with the forward wave in systole determined mainly by the left ventricular (LV) ejection function and the backward by the wave reflection from the periphery, the timing and amplitude of which depend on arterial stiffness, the wave propagation speed and the extent of downstream admittance mismatching. However, this approach obscures the ‘Windkessel function’ of the elastic arteries. Recently, a ‘reservoir-excess pressure’ model has been proposed, which interprets the arterial BP waveform as a composite of a volume-related ‘reservoir’ pressure and a wave-related ‘excess’ pressure.MethodsIn this study we applied the reservoir-excess pressure approach to the analysis of carotid arterial pressure waveforms (applanation tonometry) in 10 young healthy volunteers before and after a 5-week head down tilt bed rest which induced a significant reduction in stroke volume (SV), end-diastolic LV volume and LV longitudinal function without significant changes in central blood pressure, cardiac output, total peripheral resistance and aortic stiffness. Forward and backward pressure components were also determined by wave separation analysis.ResultsCompared to the baseline state, bed rest induced a significant reduction in LV ejection time (LVET), diastolic time (DT), backward pressure amplitude (bP) and pressure reservoir integral (INTPR). INTPR correlated directly with LVET, DT, time to the peak of backward wave (bT) and stroke volume, while excess pressure integral (INTXSP) correlated directly with central pressure. Furthermore, Δ.INTPR correlated directly with Δ.LVET, and Δ.DT, and in multivariate analysis INTPR was independently related to LVET and DT and INTXSP to central systolic BP.ConclusionThis is an hypothesis generating paper which adds support to the idea that the reservoir-wave hypothesis applied to non-invasively obtained carotid pressure waveforms is of potential clinical usefulness.

Optimizing sprint interval exercise for post-exercise hypotension: A randomized crossover trial

ABSTRACT This study aimed to examine the effects of manipulating the rest intervals during sprint interval training (SIT) on post-exercise hypotension and within-session oxygen consumption. Thirty healthy, trained adults (aged 30.9 ± 8.7 years; 14 males, 16 females; BMI 22.1 ± 2.3 kg/m2; VO2max 50.7 ± 7.8 ml/kg/min) completed two different SIT protocols (4x 30-seconds all-out cycling sprints) with a one-week washout period. Sprint bouts were separated by either 1 (R1) or 3 (R3) minutes of active recovery. Both before and throughout the 45 min after the training, peripheral systolic (pSBP) and diastolic (pDBP) blood pressure, central systolic (cSBP) and diastolic (cDBP) blood pressure, aortic pulse wave velocity (aPWV), stroke volume (SV), and heart rate (HR) were assessed. Throughout the SIT protocols, oxygen consumption (VO2) was monitored. There were no significant differences in time spent at 75%, 85%, 95%, and 100% of maximal VO2 between R1 and R3. After R3, there was a significant reduction in pSBP, pDBP, cSBP, cDBP, and aPWV. After R1, there were no changes in the respective parameters. There were significant interaction effects in pSBD (p < 0.001), pDBP (p < 0.001), cSBP (p < 0.001), cDBP (p = 0.001), and aPWV (p = 0.033). HR significantly increased after both conditions. Only R1 resulted in a significant reduction in SV. Longer resting intervals during SIT bouts seem to result in more substantial post-exercise hypotension effects. Time spent at a high percentage of maximal VO2 was not affected by rest interval manipulation.

Intramuscular Ricin Poisoning of Mice Leads to Widespread Damage in the Heart, Spleen, and Bone Marrow.

Ricin, a lethal toxin derived from castor oil beans, is a potential bio-threat due to its high availability and simplicity of preparation. Ricin is prepared according to simple recipes available on the internet, and was recently considered in terrorist, suicide, or homicide attempts involving the parenteral route of exposure. In-depth study of the morbidity developing from parenteral ricin poisoning is mandatory for tailoring appropriate therapeutic measures to mitigate ricin toxicity in such instances. The present study applies various biochemical, hematological, histopathological, molecular, and functional approaches to broadly investigate the systemic effects of parenteral intoxication by a lethal dose of ricin in a murine model. Along with prompt coagulopathy, multi-organ hemorrhages, and thrombocytopenia, ricin induced profound morpho-pathological and functional damage in the spleen, bone marrow, and cardiovascular system. In the heart, diffuse hemorrhages, myocyte necrosis, collagen deposition, and induction in fibrinogen were observed. Severe functional impairment was manifested by marked thickening of the left ventricular wall, decreased ventricular volume, and a significant reduction in stroke volume and cardiac output. Unexpectedly, the differential severity of the ricin-induced damage did not correlate with the respective ricin-dependent catalytic activity measured in the various organs. These findings emphasize the complexity of ricin toxicity and stress the importance of developing novel therapeutic strategies that will combine not only anti-ricin specific therapy, but also will target ricin-induced indirect disturbances.

Clinical manifestations following intramuscular exposure of mice to a lethal dose of ricin

Abstract Ricin a plant toxin derived from seeds of Ricinus communis, irreversibly inactivates ribosomes by site-specific depurination, thereby arresting cell protein synthesis, while its clinical manifestations following intramuscular exposure have not yet been investigated in depth. Here we report an extensive pathological study of intramuscular intoxication with a lethal dose of ricin in a murine model. Ricin injection caused neutrophilia, thrombocytopenia and coagulopathy. Although histopathological alternations including hemorrhages, vessel congestion and focal necrosis were observed in various organs, major insults were limited to the spleen, bone marrow (BM) and cardiovascular system. Intensive atrophy, evident in the BM and splenic white pulps, were accompanied be severe depletion of megakaryocytes in both organs. Moreover, splenic T and B lymphocytes, NK cells, macrophages and dendritic cells decreased significantly. The most striking damage was in the heart, where we observed diffuse hemorrhages, myocyte disconnection, loss of striation, interstitial edema, collagen deposition and elevated levels of serum cardiac troponin. Finally, echocardiography revealed marked thickening of the walls, along with sequential decrease in left ventricular volume. These were accompanied by a significant reduction in stroke volume and cardiac output, while the ejection fraction remained unaltered. Measurements of the toxin direct catalytic performance in the spleen, BM and heart of the ricin-intoxicated mice revealed no substantial 28S rRNA depurination. The lack of measurable ricin catalytic activity in conjunction with the striking clinical disorders observed, suggests that ricin affects these organs in an indirect manner.

Faim2 contributes to neuroprotection by erythropoietin in transient brain ischemia.

Delayed cell death in the penumbra region of acute ischemic stroke occurs through apoptotic mechanisms, making it amenable to therapeutic interventions. Fas/CD95 mediates apoptotic cell death in response to external stimuli. In mature neurons, Fas/CD95 signaling is modulated by Fas-apoptotic inhibitory molecule 2 (Faim2), which reduces cell death in animal models of stroke, meningitis, and Parkinson disease. Erythropoietin (EPO) has been studied as a therapeutic strategy in ischemic stroke. Erythropoietin stimulates the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway, which regulates Faim2 expression. Therefore, up-regulation of Faim2 may contribute to neuroprotection by EPO. Male Faim2-deficient mice (Faim2-/- ) and wild-type littermates (WT) were subjected to 30min of middle cerebral artery occlusion (MCAo) followed by 72h of reperfusion. EPO was applied before (30min) and after (24 and 48h) MCAo. In WT mice application of EPO at a low dose (5000U/kg) significantly reduced stroke volume, whereas treatment with high dose (90000U/kg) did not. In Faim2-/- animals administration of low-dose EPO did not result in a significant reduction in stroke volume. Faim2 expression as measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) increased after low-dose EPO but not with high dose. An extensive phenotyping including analysis of cerebral vessel architecture did not reveal confounding differences between the genotypes. In human post-mortem brain Faim2 displayed a differential expression in areas of penumbral ischemia. Faim2 up-regulation may contribute to the neuroprotective effects of low-dose erythropoietin in transient brain ischemia. The dose-dependency may explain mixed effects of erythropoietin observed in clinical stroke trials.

Abstract TMP32: Intra-arterial ALD401 Cell Therapy is Associated With Reduction in Stroke Volume at 90 Days in a Subset of the RECOVER-stroke Trial

Background: Stroke is a leading cause of major long-term disability worldwide. Despite availability of IV tPA and mechanical thrombectomy, over half of treated patients have significant disability. Cell based therapy is a promising in pre-clinical studies in improving stroke recovery. Brain infarct volume is a major predictor of stroke outcome and may decrease with this treatment. We hypothesized that patients treated with intra-arterial stem cell therapy will have a significant reduction in stroke volume compared to non-treated patients. Methods: The RECOVER-Stroke trial is a randomized, sham-controlled study to determine the safety and efficacy of processed autologous bone marrow cells (ALD-401) injection via intracarotid infusion in ischemic stroke patients. Ischemic stroke patients were double-blind randomized into 2 groups, receiving ALD-401 injection or sham procedure between 9-19 days post anterior circulation ischemic stroke. All enrolled patients at 1 of 8 sites in the trial were included in this analysis. Two blinded physicians used OSIRIX software to analyze stroke volume on DWI/ 24h CT brain and MRI at 90, 180, 365 days post intervention. Volumes were compared between the 2 groups at these timepoints. Results: A total of 11 patients at our center (out of 48 multicenter patients) were included in this study, 6 patients receiving sham procedure and 5 patients receiving ALD-401. The two groups did not show any significant difference in their baseline variables including age, Mean baseline stroke volumes were not significantly different between ALD-401 (103.9±96.2ml) and sham groups (70.2±46ml), p=0.53. The stroke volume reduction in the ALD-401 was 22.9±15.5ml vs. 4.04±12.5ml in the sham group (p=0.046). On day 180 and 365, both groups did not show any further significant stroke volume reduction from day 90. Conclusion: In this exploratory analysis from one center in the multi-center RECOVER-Stroke trial, intra-arterial stem cell injection with ALD-401 was associated with significant reduction in stroke volume at 90 days post therapy compared to sham procedure in subacute ischemic stroke patients.

Abstract P114: Mas Receptor Deficiency Increases Diastolic Blood Pressure and Reduces Cardiac Function in Obese Female Mice

Objective: We recently demonstrated that protection of female mice from obesity-induced hypertension was associated with increased plasma concentrations of angiotensin-(1-7) (Ang-(1-7)). Ang-(1-7) is a ligand for Mas receptors (MasR), where the peptide has been reported to promote endothelial release of nitric oxide and reduce blood pressure. In this study, we hypothesized that MasR deficiency will abolish protection of female high fat (HF)-fed mice from the development of obesity-induced hypertension. Methods and Results: Female (8 weeks, C57BL/6) wild type (MasR+/+) and whole body MasR deficient mice (MasR-/-) were fed a HF diet (60% Kcal as fat) for 16 weeks. MasR deficiency had no effect on the development of obesity or glucose intolerance in HF-fed female mice. At week 16 of HF feeding, blood pressure was quantified by radiotelemetry. Deficiency of MasR resulted in a significant decrease in pulse pressures of HF-fed females (24hr average: MasR+/+, 37.7 ± 1.5 mmHg; MasR-/-, 33.1 ± 1.0 mmHg; P&lt;0.05). Diastolic blood pressures (DBP) of HF-fed female MasR-/- mice were modestly elevated during the night cycle compared to controls (DBP night: MasR+/+, 91.5 ± 2.0 mmHg; MasR-/-, 96.6 ± 1.3 mmHg; P=0.06). However, systolic blood pressure, mean arterial pressure and heart rate were not significantly different between genotypes. Assessment of left ventricular function by ultrasound demonstrated significant reductions in stroke volume (MasR+/+, 44.3 ± 1.6 μl; MasR-/-, 36.3 ± 2.1 μl), ejection fraction (MasR+/+, 57.1 ± 1.2; MasR-/-, 50.1 ± 2.7%) and fractional shortening (MasR+/+, 29.7 ± 0.8; MasR-/-, 25.3 ± 1.7%) in HF-fed MasR-/- females compared to controls. Conclusion: These results demonstrate that MasR deficiency promotes elevated diastolic blood pressures and reduced cardiac function in obese female mice, suggesting that the Ang-(1-7)/MasR axis protects females from obesity-hypertension. Moreover, these results suggest that MasR agonists may be effective therapies for obesity-associated cardiovascular conditions.

Catheter based selective hypothermia reduces stroke volume during focal cerebral ischemia in swine

BackgroundTotal body hypothermia is an established neuroprotectant in global cerebral ischemia. The role of hypothermia in acute ischemic stroke remains uncertain. Selective application of hypothermia to a region of focal...

PREOPERATIVE CORRECTION OF WATER-ELECTROLYTE DISTURBANCES IN PATIENTS WITH ACUTE INTESTINAL OBSTRUCTION CAUSED BY COLON CANCER

Comparative evaluation of preoperative infusion therapy in 50 patients with acute intestinal obstruction of tumour genesis has been performed and parameters of central hemodynamic and water sectors of organism were studied. The patients had a statistically significant reduction of extracellular sector, hypokalaemia, hypornatremia. Central hemodynamic parameters were characterized by a significant reduction in stroke volume and heart rate increase. Mean arterial pressure and peripheral vascular resistance, resistivity reduced in comparison with control group. The study showed that infusion therapy, which includes a balanced colloid solution (HES 130/ 04) and a balanced 700 ml and 1700 ml (average) crystalloid solution and is conducted for 3 hours reduces the severity of water-electrolyte and hemodynamic changes, reduces the need in vasopressor support, and to a certain extent improves outcomes of surgical treatment.

Group III/IV muscle afferents impair limb blood in patients with chronic heart failure

ObjectiveTo better understand the hemodynamic and autonomic reflex abnormalities in heart-failure patients (HF), we investigated the influence of group III/IV muscle afferents on their cardiovascular response to rhythmic exercise. MethodsNine HF-patients (NYHA class-II, mean left ventricular ejection-fraction: 27±3%) performed single leg knee-extensor exercise (25/50/80% peak-workload) under control conditions and with lumbar intrathecal fentanyl impairing μ-opioid receptor-sensitive muscle afferents. ResultsCardiac-output (Q) and femoral blood-flow (QL) were determined, and arterial/venous blood samples collected at each workload. Exercise-induced fatigue was estimated via pre/post-exercise changes in quadriceps strength. There were no hemodynamic differences between conditions at rest. During exercise, Q was 8–13% lower with Fentanyl-blockade, secondary to significant reductions in stroke volume and heart rate. Lower norepinephrine spillover during exercise with Fentanyl revealed an attenuated sympathetic outflow that likely contributed to the 25% increase in leg vascular conductance (p<0.05). Despite a concomitant 4% reduction in blood pressure, QL was 10–14% higher and end-exercise fatigue attenuated by 30% with Fentanyl-blockade (p<0.05). Conclusion/practice/implicationsAlthough group III/IV muscle afferents play a critical role for central hemodynamics in HF-patients, it also appears that these sensory neurons cause excessive sympatho-excitation impairing QL which likely contributes to the exercise intolerance in this population.

Acute Hypovolemia Does Not Affect Dynamic Cerebral Autoregulation in Humans

While it is well known that cerebral perfusion pressure is the primary determinant of cerebral blood flow, it has been suggested that cardiac output and stroke volume may also play an important role. To test the role of stroke volume and cardiac output on dynamic cerebral autoregulation we performed sit to stand tests on a group of volunteers prior to and following administration of furosemide to reduce blood volume. These subjects were participating in a larger artificial gravity study. As expected furosemide resulted in a significant reduction in stroke volume while seated (63±5 vs. 51±4 mL, P=0.000). In contrast cardiac output was unchanged due to increases in heart rate (72±3 vs 94±3 bpm, P=0.000). Upon standing subjects demonstrated similar drops in SV, cardiac output and increases in HR from pre to post infusion. Blood pressure was unchanged by infusion while sitting and had similar drops upon standing (−20±4 vs −21±12 mmHg). Similarly cerebral flow velocity decreases were unchanged (−15±7 vs −17±8 mmHg). Examination of the Autoregulatory Index found no change from pre to post infusion (4.7±0.6 vs 4.8±0). These data demonstrate that hypovolemia and reduced stroke volume do not affect dynamic cerebral autoregulation or the cerebrovascular response to standing. Further work is needed to determine the role of cardiac output. Supported by NASA and VA.

Heart rate variability and baroreceptor sensitivity following exercise-induced hyperthermia in endurance trained men

We evaluated the effect of exercise-induced hyperthermia (EIH) on autonomic nervous system (ANS) function in the early (<80 min) and late (24 and 48 h) stages of recovery. Eight males underwent three repeated 6 min 70° head-up tilts (HUT1, HUT2 and HUT3), each separated by 10-min supine rest in a non-exercise/non-heat stress control state (NHS). On a separate day, three 6 min 70° HUT were performed following EIH (esophageal temperature ≥ 40°C) and repeated after 24 and 48 h of recovery. Heart rate, stroke volume (SV), mean arterial pressure and cardiac output ([Formula: see text]) were evaluated during the last min prior to a change in posture. Responses to 70° HUT were compared to the same challenge performed without prior exercise and under a NHS condition. Relative to NHS, [Formula: see text] was maintained during the repeated HUT's following EIH, despite significant reductions in SV and sustained elevations in esophageal temperature (p < 0.05). The preserved [Formula: see text] appears to be due to increased HR (HUT1: NRS = 76 ± 3 beats min(-1), EIH = 126 ± 6 beats min(-1)) stemming from modulation of the ANS toward sympathetic dominance. Parasympathetic withdrawal was evidenced by a reduction in root mean squared successive difference (i.e., HUT1: NHS = 66 ± 12 ms, EIH = 9 ± 1 ms) of heart rate variability and paralleled by a reduction in baroreceptor sensitivity for all HUT's following EIH (p < 0.05). Despite significant modulation in ANS activity, Q is maintained and participants do not become orthostatic intolerant/syncopal during the short-term recovery period following EIH. Normal ANS and cardiovascular function is restored following 24 h of recovery.

Multi-site and multi-depth near-infrared spectroscopy in a model of simulated (central) hypovolemia: lower body negative pressure

PurposeTo test the hypothesis that the sensitivity of near-infrared spectroscopy (NIRS) in reflecting the degree of (compensated) hypovolemia would be affected by the application site and probing depth. We simultaneously applied multi-site (thenar and forearm) and multi-depth (15–2.5 and 25–2.5 mm probe distance) NIRS in a model of simulated hypovolemia: lower body negative pressure (LBNP).MethodsThe study group comprised 24 healthy male volunteers who were subjected to an LBNP protocol in which a baseline period of 30 min was followed by a step-wise manipulation of negative pressure in the following steps: 0, −20, −40, −60, −80 and −100 mmHg. Stroke volume and heart rate were measured using volume-clamp finger plethysmography. Two multi-depth NIRS devices were used to measure tissue oxygen saturation (StO2) and tissue hemoglobin index (THI) continuously in the thenar and the forearm. To monitor the shift of blood volume towards the lower extremities, calf THI was measured by single-depth NIRS.ResultsThe main findings were that the application of LBNP resulted in a significant reduction in stroke volume which was accompanied by a reduction in forearm StO2 and THI.ConclusionsNIRS can be used to detect changes in StO2 and THI consequent upon central hypovolemia. Forearm NIRS measurements reflect hypovolemia more sensitively than thenar NIRS measurements. The sensitivity of these NIRS measurements does not depend on NIRS probing depth. The LBNP-induced shift in blood volume is reflected by a decreased THI in the forearm and an increased THI in the calf.Electronic supplementary materialThe online version of this article (doi:10.1007/s00134-010-2128-6) contains supplementary material, which is available to authorized users.

Use of afterload hemodynamic stress as a practical method for assessing cardiac performance in rats with heart failure

After myocardial infarction, the hemodynamics under basal conditions might appear to be unaltered, which makes it difficult to identify cardiac dysfunction by the usual approaches. Thus, we tested the response to sudden afterload stress in infarcted rats with apparently normal ejection function. Control (CT) and infarcted (MI) Wistar rats with various MI sizes were submitted to echocardiography 30 days after coronary occlusion, followed by assessment of hemodynamics under basal conditions and during a pharmacologically induced sudden pressure overload (phenylephrine 15-25 microg/kg, i.v.). Coronary occlusion resulted in cardiac remodeling proportional to MI size, although several functional parameters such as systolic pressure (SP), stroke volume (SV), and stroke work (SW) of all MI rats were similar to those of CT rats. However, the afterload stress that was produced led to a relative preservation of SV and an increase of SW in CT rats; MI rats exhibited a significant reduction in SV and SW generation, although global cardiac function was normal under basal conditions, as indicated by regular echocardiography and hemodynamics assessment. Thus, we propose the use of sudden pharmacologically induced afterload stress as a practical and efficient procedure for identifying impaired performance of the heart in anesthetized rats, providing an additional physiological variable to be evaluated in experimental therapeutic studies.

Alteration in hemodynamic effects of interleukin 2 after treatment with indomethacin in anesthetized rats

The cardiovascular effects of interleukin 2 (IL2), were investigated in animals pretreated with indomethacin. Bolus intravenous administration of IL2 alone caused a significant reduction in cardiac output over time. Pretreatment with indomethacin significantly accentuated the reduction in cardiac output produced by IL2. The administration of IL2 or indomethacin alone or combined had no significant effects on dP/dt, heart rate or plasma troponin levels. As well, administration of either compound alone or combined had limited effects on mean circulatory filling pressure and arterial blood pressure. Injection of IL2 alone significantly increased resistance to venous return and arterial resistance at 3h post injections. Pretreatment with indomethacin caused IL2 to produce a significantly greater increase in arterial resistance and resistance to venous return. Administration of IL2 and indomethacin combined also produced significant reduction in stroke volume than IL2 or indomethacin alone. The injection of IL2 or indomethacin alone or combined had no significant impact on blood volume. Acute administration of IL2 appears to have no negative inotropic or chronotropic effects and its impact in reducing cardiac output is the result of an increase in vascular resistance. It seems that activation of prostanoids, possibly prostacyclin, has an acute beneficial effect in attenuating the initial negative effects of IL2 on cardiac output.

Diastolic function: the influence of pneumoperitoneum and Trendelenburg positioning during laparoscopic hysterectomy

Several reports concerning the haemodynamic changes during gynaecologic laparoscopy have been published so far, and the effects of head-down tilt and pneumoperitoneum have not been clearly separated. However, its main effect seems to be an increase in systemic vascular resistance. We investigated how the augmented afterload can affect diastolic function. : Our study involved 20 healthy women, classified as having ASA status I: 10 undergoing laparoscopic hysterectomy and 10 undergoing conventional open hysterectomy. Measurements were made in awake patients and after induction of anaesthesia and then repeated after carbon dioxide insufflation and head-down positioning and at the end of surgery. Diastolic function was primarily studied by transthoracic echocardiography. We observed that pneumoperitoneum caused a significant reduction in stroke volume, cardiac output and left ventricular end-diastolic volume; the diastolic filling times showed a progressive reduction in the E-velocity (the velocity of early mitral inflow, corresponding to the ventricular passive filling phase, measured by pulsed-wave Doppler), a prolonged deceleration time and an augmented isovolumetric relaxation time. After head-down tilting, stroke volume, cardiac output and left ventricular end-diastolic volume increased in both laparoscopic hysterectomy and conventional open hysterectomy groups. We have found that pneumoperitoneum has important effects on left ventricular volumes, causing a drop in left ventricular end-diastolic volume; it also affects diastolic function with a delay in deceleration time and isovolumetric relaxation time without any effects on intracavitary pressures.

Pulmonary Hemodynamic Responses to Intravenous Prostaglandin E2 in Broiler Chickens

Prostaglandin E(2) (PGE(2)) affects pulmonary arterial pressure (PAP), pulmonary vascular resistance (PVR), and respiratory rate (RR) in mammals, but no information previously was available regarding avian pulmonary responses to PGE(2). Two experiments were conducted in which 45- to 55-d-old male broiler chickens were infused i.v. with PGE(2) at the lowest rate (30 mug/min for 4 min) that reliably reduced PAP during pilot studies. When compared with preinfusion (control) values in experiment 1, PGE(2) reduced PAP from 19 +/- 1 to 16 +/- 1 mmHg (P < 0.001) and reduced mean systemic arterial pressure from 111 +/- 6 to 81 +/- 5 mmHg (P < 0.001) but did not significantly reduce heart rate (HR; control: 338 +/- 9 beats/min; PGE(2): 320 +/- 12 beats/min; P > 0.05). Infusing PGE(2) also reduced the RR from 57 +/- 2 to 46 +/- 4 breaths/min (P < 0.001) and reduced the percentage saturation of hemoglobin with oxygen (%HbO(2)) from 85 +/- 2 to 77 +/- 3%HbO(2) (P < 0.001). After the PGE(2) infusion ceased, the PAP, mean systemic arterial pressure, RR, and %HbO(2) recovered within 8 min to levels that did not differ from preinfusion control values. In experiment 2, an ultrasonic flow probe was surgically implanted on 1 pulmonary artery to measure cardiac output (CO). When compared with preinfusion control values, PGE(2) reduced CO from 140 +/- 6 to 111 +/- 5 mL/kg of BW x min (P < 0.001), reduced PAP from 25 +/- 2 to 21 +/- 1 mmHg (P < 0.001), and reduced RR from 49 +/- 4 to 35 +/- 4 breaths/min (P < 0.001). The reduction in CO was caused by a reduction in HR from 305 +/- 9 to 260 +/- 9 beats/min without a significant reduction in stroke volume (control: 0.46 +/- 0.02 mL/kg of BW x beat; PGE(2): 0.43 +/- 0.02 mL/kg of BW x beat; P = 0.158). After the PGE(2) infusion ceased the CO, PAP, RR, and HR recovered within 9 min to levels that did not differ from preinfusion control values. The PVR, calculated as PAP/CO, was not altered by PGE(2) (control: 0.18 +/- 0.01 relative resistance units; PGE(2): 0.20 +/- 0.02 relative resistance units; P > 0.723). These results indicate that in broilers PGE(2) reduced PAP by reducing CO rather than by acting as a pulmonary vasodilator to lower PVR. The PGE(2)-induced reductions in PAP would benefit broilers that are susceptible to pulmonary hypertension syndrome by reducing their right ventricular overload; however, the reductions in CO and RR combined with the onset of systemic arterial hypoxemia would accelerate the pathophysiological progression leading to terminal pulmonary hypertension syndrome.

Changes in Pulse Character andMental Status Are Late Responses to Central Hypovolemia

Objective. Manual assessment of radial arterial pulse character remains an important determinant of physiological status in military andcivilian casualties. This study hypothesized that changes in radial pulse character andmental status (presyncopal symptoms) in humans occur only during the later stages of progressive reductions in central blood volume in close association with systolic blood pressure (SBP). Methods. Pulse character (i.e., normal, weak, absent), estimated stroke volume (SV), SBP, anddiastolic blood pressure were measured continuously during baseline supine rest andduring progressive reductions of central blood volume to cardiovascular collapse with application of lower body negative pressure (LBNP) in 19 healthy human volunteer subjects. Results. LBNP resulted in a progressive reduction in SV. At early stages of LBNP, both radial pulse character andSBP were well-maintained. Although both radial pulse character andSBP decreased with subsequent increases in LBNP, these changes occurred only after an approximate 55% reduction in SV andwere associated with the onset of presyncopal symptoms. Changes in mental status did not occur until the point of cardiovascular collapse. Conclusions. In this model of progressive central hypovolemia secondary to application of LBNP in humans, radial pulse character score decreased in concert andwas highly correlated with decreases in SBP. In support of our hypothesis, changes in pulse character, SBP, andmental status occurred only after significant reductions in SV, suggesting that these standard vital signs may not be early indicators of central hypovolemia.

Effects of Knee Surgery on Cardiac Function in Soccer Players

To evaluate the effects of knee surgery on hematocrit and hemoglobin concentration and on resting cardiac parameters as measured by echocardiography. Ten soccer players who underwent knee surgery were evaluated before (T1) and after (T2) hospitalization within a 7-day interval. After hospitalization, end diastolic volume and stroke volume were significantly reduced (P < 0.05) by 14 and 22%, respectively. Despite a significant increase in resting heart rate (T1: 68 +/- 3.3 beats/ min, T2: 72 +/- 3.1 beats/min, P < 0.05), cardiac output was significantly decreased (T1: 4.89 +/- 0.56 liters/min; 3.95 +/- 0.62 liters/min, P < 0.05). The ejection fraction was 65% at T1 and fell to 58% at T2 (P < 0.05). After hospitalization, significant decreases in hemoglobin concentration and hematocrit were observed, suggesting a fall in blood volume. In soccer players, knee surgery leads to resting cardiac deconditioning, which is characterized by a significant reduction in stroke volume.