Minimal effects of nitric oxide on spatial blood flow heterogeneity of the dog heart

 Eleven Beagle dogs were studied to elucidate the possible role of L-arginine-derived nitric oxide on local blood flow distribution in left and right ventricular myocardium. Local blood flow was determined in 256 samples from the left and 64 samples from the right ventricle per heart using the tracer microsphere technique (mean sample mass 319 ± 131 mg). Nitric oxide production was effectively inhibited by intravenous infusion of 20 mg/kg nitro-L-arginine methylester (L-NAME) as evidenced by a shift of the dose/response curve for the effect of intracoronary administration of bradykinin (0.004–4.0 nmol/min) on coronary blood flow. L-NAME enhanced left and right ventricular systolic pressures from 132 ± 18 to 155 ± 15 mm Hg and from 26 ± 3 to 29 ± 3 mm Hg respectively (both P = 0.043). Mean left ventricular blood flow was 1.14 ± 0.38 before and 0.99 ± 0.28 ml min^–1 g^–1 after L-NAME (P = 0.068), while right ventricular blood flow fell from 0.72 ± 0.28 to 0.53 ± 0.20 ml min^–1 g^–1 (P = 0.043). Coronary conductance of left and right ventricular myocardium fell by 31 and 43% respectively (both P = 0.043). The coefficient of variation of left ventricular blood flow was 0.26 ± 0.07 before and 0.29 ± 0.07 after L-NAME (P = 0.068), that of right ventricular blood flow was 0.27 before and after L-NAME. Skewness (0.51) and kurtosis (4.23) of left ventricular blood flow distribution were unchanged after L-NAME, while in the right ventricle skewness decreased from 0.54 to 0.09 (P = 0.043) and kurtosis (3.68) tended to decrease after L-NAME (P = 0.080). The fractal dimension (D = 1.20–1.27) and the corresponding nearest-neighbor correlation coefficient (r _n = 0.37–0.53) of left and right ventricular myocardium remained unchanged after infusion of L-NAME. From these results it is concluded that firstly, local nitric oxide release does not explain the higher perfusion of physiological high flow samples and secondly, that spatial myocardial blood flow coordination is not dependent on nitric oxide. Received: 11 July 1996 / Received after revision: 29 October 1996 / Accepted: 17 December 1996     

Crista Supraventricularis Purkinje Network and Its Relation to Intraseptal Purkinje Network

Using transparent specimens with a dual color injection, microscopy, and computer tomography, this report shows that the right and left ventricular subendocardial Purkinje networks are connected by an extensive septal network in the bovine heart. The septal network is present along the entire septum except at a free zone below ventricular valves. Being the only communication of the basal right septum with the right free wall, the supraventricular crest is an enigmatic but not, by any means, hidden muscular structure. It is one of the last structures to be activated in human heart. It is shown here that the supraventricular crest Purkinje network connects the anterosuperior right ventricular basal free wall Purkinje network to anterior right ventricular basal septal Purkinje network. It is suggested that the stimulus initiated at middle left ventricular endocardium will activate the supraventricular crest. The intraseptal connection found between the basal left ventricular subendocardial septal Purkinje network and the right ventricular basal septal Purkinje network is, probably, the pathway for the stimulus. An anatomic basis is provided to explain why the inflow tract contracts earlier than the outflow tract in the right ventricle systole. Anat Rec, 2017. © 2017 Wiley Periodicals, Inc. Anat Rec, 300:1793–1801, 2017. © 2017 Wiley Periodicals, Inc.     

Electrical analogy of diastolic pressure difference between left atrium and ventricle

We proposed a mathematical model to describe the early filling process of the left ventricle and applied the model toin vivo experiments. The solution of a second-order differential equation indicated that the pressure difference between the left atrium and ventricle during ventricular filling (PD) could be explained by a transient response, i.e. decremental oscillation, in an LCR circuit. Thereafter, we analysed the sequence of PD during vagal stimulation with two catheter-tip manometers in 12 anaesthetised dogs and evaluated changes in the parameters of the system under various haemodynamic conditions. The values of ω_n and ξ were quite stable among beats within an episode of vagal stimulation, between episodes and even among dogs, despite the changes in haemodynamic variables. Pericardiotomy and partial discommunication of the mitral valve with the left ventricular free wall by cutting the mitral chordal tendons decreased ω_n and increased ζ, mainly because of the increase in C_LV. Occlusion of the coronary vascular beds with large numbers of microspheres increased ω_n and decreased ζ, mainly because of the decrease in C_LV. Mitral obstruction with an inflated balloon (increase in R) abolished the oscillatory changes and produced and exponential decay sequence of PD. In conclusion, both the logical and experimental approaches indicated that the sequence of PD could be considered as decremental oscillation in the LCR circuit and the parameters ω_n and ξ could be good indices of the diastolic property of the left ventricle     

The effect of physical activity and physical fitness on plasma adiponectin in adults with predisposition to metabolic syndrome

The purpose of this study was to measure changes in plasma adiponectin (ApN) over 24 months of exercise intervention in middle age adults with a predisposition to metabolic syndrome and to determine if changes in ApN were more affected by physical activity or physical fitness. Thirty-six subjects completed a 24 months home-based exercise program (cycling ≥ three times per week, ≥ 45 min/session at 50–65% of VO_2peak). Body composition, blood samples, and physical fitness were studied at baseline and after 12 and 24 months of participation in the study. The prescribed physical activity was monitored via self-reported exercise diary to determine MET levels, hours, and exercise compliance. Two-tailed repeated measures ANOVA and Spearman Rank Correlation Coefficients were used to detect significant differences and associations between the variables. ApN increased significantly (P < 0.05) after 12 months in males (n = 17; 5.3 ± 1.9–7.0 ± 3.0 μg ml⁻¹) but not in females (n = 9; 8.6 ± 3.8–11.5 ± 4.0 μg ml⁻¹). The net change in ApN over 24 months was significantly correlated to the net change in VO_2peak (physical fitness) (r = 0.66; P < 0.001), whereas exercise intensity was negatively correlated to ΔApN over 12 months (r = −0.4; P ≤ 0.04) and 24 months (r = −0.45; P ≤ 0.02). Based on our results, an improvement in cardiorespiratory fitness of 15% increased plasma ApN concentration. Our findings suggest that moderate physical activity performed over many months induces positive changes in the plasma ApN concentration in adults with a predisposition to metabolic syndrome.     

Individual differences in the responses to endurance and resistance training

Large individual differences in the responsiveness of cardiorespiratory fitness (VO_2peak) to endurance training have been observed in healthy subjects. We tested the hypothesis that subjects with a poor responsiveness to endurance training might benefit from resistance training in terms of aerobic fitness. The study population consisted of sedentary healthy male and female subjects (n=91, 42±5 year) assigned to either a training (n=73) or a control group (n=18). The randomized cross-over study design included a 2-week laboratory-controlled endurance or resistance training period with a 2-month detraining period between the interventions. Large individual differences were observed in the changes of VO_2peak (ΔVO_2peak) after both the endurance (average 8±6 %, P<0.001, range −5 to +22%) and resistance training (average 4±5%, P<0.001, range −8 to +16%). The average increase in ΔVO_2peak between genders was similar after both the endurance (8±6% for both genders, P=ns) and resistance training (3±5% for males and 5±6% for females, P=ns). There was no linear relationship between the changes in VO_2peak after each training intervention (r=−.09, P=ns). On the contrary, when the study group was divided into quartiles according to the endurance training response (1±3, 6±1, 9±1, and 16±3% increase in VO_2peak), the group with the lowest response to endurance training increased VO_2peak after the resistance training intervention (ΔVO_2peak 7±5%, P<0.001). The individual responsiveness of VO_2peak to exercise training is related to the mode of training. The healthy males and females whose training response is low after endurance training seem to result in a marked improvement in their cardiorespiratory fitness by resistance training.     

Association between serum cortisol and progesterone concentrations and the infiltration of immune cells in the endometrium of gilts with vaginal discharge

The objective of the study was to investigate an association between serum cortisol and progesterone (P₄) concentrations and the distribution of immune cells in the endometrium of the gilts with vaginal discharge. Genital organs from 39 Landrace×Yorkshire crossbred gilts culled owing to vaginal discharge problem were collected from two commercial swine herds in Thailand. The estrous stage and gross pathology were examined. Blood samples were collected from the jugular vein prior to being slaughtered. Serum P₄ and cortisol were analyzed by means of enzyme immunoassay. The samples observed were in inactive (n = 4), follicular (n = 10), and luteal (n = 25) phases. They, afterwards, were processed in hematoxylin and eosin sections. The endometrium of the gilts was histologically divided into three layers, i.e., epithelial, subepithelial connective tissue, and glandular connective tissue layers. Immune cells, i.e., lymphocytes, neutrophils, eosinophils, macrophages, and plasma cells, in each layer were quantified under a light microscope (×400). The results revealed that mean serum cortisol was 430.6 ± 68.3 nmol/l. Serum P₄ varied by ovarian status. Serum P₄ of the gilts in the luteal phase was higher than those in the follicular phase (88.3 ± 7.7 versus 20.6 ± 6.2 nmol/l, P < 0.05). As for the endometrium condition, the gilts were classified into acute/subacute endometritis (n = 13), chronic endometritis (n = 9), and normal endometrium (n = 17). Neutrophils were the main local immune cells in the epithelial layer. Lymphocytes were the dominant population in the subepithelial and glandular connective tissue layers. Generally, the serum cortisol tended to negatively correlate with lymphocytes in the subepithelial connective tissue layer (r = −0.28, P = 0.081). In the gilts with acute/subacute endometritis, no correlation among serum cortisol, P₄, and immune cells was observed. In chronic endometritis gilts, only a negative correlation was remarked between P₄ and epithelial lymphocytes (r = −0.83, P = 0.010), epithelial neutrophils (r = −0.79, P = 0.019), and subepithelial neutrophils (r = −0.73, P = 0.025). In the gilts with normal endometrium, P₄ negatively correlated with subepithelial neutrophils (r = −0.55, P = 0.022) while positively correlated with subepithelial macrophages (r = 0.54, P = 0.024) and subepithelial eosinophils (r = 0.60, P = 0.011).     

Actions of myristyl-FRCRCFa, a cell-permeant blocker of the cardiac sarcolemmal Na-Ca exchanger, tested in rabbit ventricular myocytes

 In cardiac muscle, the electrogenic Na-Ca exchanger plays important roles in determining action potential shape and in the beat-to-beat homeostasis of intracellular calcium. In this study we tested the actions of a putative cell-permeant blocker of the cardiac sarcolemmal Na-Ca exchange, ”Myristyl- (Myr-) FRCRCFa”. Experiments were performed using isolated rabbit right ventricular myocytes and whole-cell patch-clamp at 35–37°C. The Na-Ca exchange current (I _Na-Ca), L-type calcium current (I _Ca,L), inward rectifier potassium current (I _K1) and delayed rectifier potassium current (I _K) were compared in untreated cells and cells incubated in a solution containing N-myristylated FRCRCFa. With other major currents blocked, I _Na-Ca was measured as the Ni-sensitive component of current during a voltage ramp applied from the holding potential of –40 mV, between +80 and –120 mV (ramp velocity 0.1 V s^–1). In untreated cells, I _Na-Ca at +60 mV was 7.1±0.6 pA/pF and at –100 mV was –2.7±0.3 pA/pF (n=9). After a 15-min pre-incubation with 20 μM Myr-FRCRCFa, I _Na-Ca was reduced to 4.2±0.3 pA/pF at +60 mV and –1.5±0.2 pA/pF at –100 mV (P<0.02; n=7). After incubation with 20 μM Myr-FRCRCFa for 1 h, I _Na-Ca at both potentials was further reduced (2.3±0.8 pA/pF at +60 mV; –0.9±0.3 pA/pF at –100 mV; P<0.008 compared with control; n=4). Under selective recording conditions for I _Ca,L, there was little difference in I _Ca,L density between untreated and cells incubated with Myr-FRCRCFa. A Boltzmann fit to the I _Ca,L/V relation showed no significant alteration of half-maximal activation potential or slope factor of activation. I _K1 was also largely unaffected by pre-incubation of cells with Myr-FRCRCFa. I _K, measured as deactivating tail current following 1-s test depolarisations to a range of test potentials, was also not significantly altered by Myr-FRCRCFa. The suppression of I _Na-Ca in cells incubated in Myr-FRCRCFa suggests that addition of the myristyl group to FRCRCFa peptide conveys cell permeancy to the peptide and that Myr-FRCRCFa applied externally to rabbit ventricular myocytes is moderately effective as an I _Na-Ca blocker. I _Ca,L, I _K1 and I _K were largely unaffected by Myr-FRCRCFa. N-Myristylation of such conformationally constrained hexapeptides may, therefore, provide a means of producing cell-permeant inhibitors of the cardiac Na-Ca exchanger. Received: 6 February 1997 / Received after revision: 8 April 1998 / Accepted: 9 April 1998     

Double outlet right ventricle in a calf

Double outlet right ventricle is a conotruncal malformation where both great arteries (aorta and pulmonary trunk) arise from the right ventricle. A 2-month-old Holstein calf was slaughtered due to severe respiratory distress. At necropsy, the heart was enlarged, globose, and had ventricular and atrial septal defects. The only outlet for the left ventricle was a large ventricular septal defect located at 6 cm distance from the heart apex and involved atrial septum too. The right ventricle was enlarged and markedly thickened with a left to right free wall ratio of 2.5:2 and prominent papillary muscles. The aorta arose from the right ventricular infundibulum adjacent to pulmonary trunk. Two valvular hematomas were observed on the edge of the right atrioventricular valve. The lungs were rubbery with ecchymotic and petechial hemorrhages and did not collapse after removing from thoracic cavity. Enhanced lobular pattern was evident on both the capsular and cut surfaces of the liver. Histopathological examination of the lungs revealed thickening of alveolar septa, hemorrhages, and infiltration of hemosiderophages within alveoli. Periportal hepatocellular fatty changes, substitution of centrilobular and midzonal hepatocytes by red blood cells, and dilation of midzonal and periportal sinusoids were seen in the liver. To our knowledge, this particular combination of cardiac defects has not been previously described in domestic animals and the pathological lesions observed in the calf may be resulted as a sequel to left–right blood shunting and heart failure.     

Transmural distribution of biochemical markers of total protein and collagen synthesis,myocardial contraction speed and capillary density in the rat left ventricle in angiotensin ll-induced hypertension

The effect of angiotensin II-induced hypertension on selected biochemical parameters was studied in Sprague-Dawley rats. Angiotensin II infusion at rates of 41.7 μg h^-1 kg^-1 and 12.5 μg h^-1 kg^-1 for 2, 5, 10 and 15 days elevated the systolic blood pressure from 143 ± 7 mmHg to 215–230 mmHg (P < 0.001) and 185–195 mmHg (P < 0.001), respectively. The left ventricular weight/body weight ratio increased 10–14% (P < 0.05) and 23–32% (P < 0.001) after 2–15 days in rats treated at the lower and higher infusion rates, respectively. Prolyl 4-hydroxylase (PH) activity, a marker of collagen synthesis, was evenly distributed in the left ventricle. PH activity increased by about 100% in both subendocardial and subepicardial layers of the left ventricular wall after angiotensin II infusion for 10 days at 41.7 γ h^-1 kg^-1, but remained unaltered at 12.5 μg h^-1 kg^-1. No change was observed in hydroxyproline concentration. Myosin isoenzymes (V₁-V₃), which reflect myocardial contractility, were unevenly distributed in the left ventricular wall: the proportion of the fast-turnover isoenzyme (V₁) was smaller in the subendocardial layer than in the subepicardial layer. The proportion of V_l decreased after treatment in both layers. Alkaline phosphatase activity, a marker of capillary density, was evenly distributed transmurally in the left ventricular wall. Angiotensin II caused a slight decrease in this activity in both myocardial layers. The results suggest that the elevation of blood pressure leads to transmurally evenly distributed changes in biochemical parameters reflecting collagen synthesis, capillary density and contractile properties of the myocardium.     

Stroke volume equation for impedance cardiography

The study's goal was to determine if cardiac output (CO), obtained by impedance cardiography (ICG), would be improved by a new equation N, implementing a square root transformation for dZ/dt_max/Z₀, and a variable magnitude, mass-based volume conductor V_c. Pulmonary artery catheterisation was performed on 106 cardiac surgery patients pre-operatively. Post-operatively, thermodilution cardiac output (TDCO) was simultaneously compared with ICG CO. dZ/dt_max/Z₀ and Z₀ were obtained from a proprietary bioimpedance device. The impedance variables, in addition to left ventricular ejection time T_LVE and patient height and weight, were input using four stroke volume (SV) equations: Kubicek (K), Sramek (S), Sramek-Bernstein (SB), and a new equation N. CO was calculated as SV × heart rate. Data are presented as mean ± SD. One way repeated measures of ANOVA followed by the Tukey test were used for inter-group comparisons. Bland-Altman methods were used to assess bias, precision and limits of agreement. P<0.05 was considered statistically significant. CO implementing N (6.06±1.48 l min⁻¹) was not different from TDCO (5.97±1.41 l min⁻¹). By contrast, CO calculated using K (3.70±1.53 l min⁻¹), S (4.16±1.83 l min⁻¹) and SB (4.37±1.82 l min⁻¹) was significantly less than TDCO. Bland-Altman analysis showed poor agreement between TDCO and K, S and SB, but not between TDCO and N. Compared with TDCO, equation N, using a square-root transformation for dZ/dt_max/Z₀, and a mass-based V_C was superior to existing transthoracic impedance techniques for SV and CO determination.     

Specific function and morphology of the right ventricle of the heart during ischemic injury of the left ventricle

Focal ischemia of the left ventricular myocardium was modeled by surgical ligation of the descending branch of the left coronary artery at the junction of the lower and middle thirds of this artery in anesthetized rabbits. Contractility and morphological characteristics of the right ventricular myocardium were evaluated 24, 72, and 120 h after treatment. Significant morphofunctional changes in the right ventricle manifested in the development of severe extracellular edema and increase in the area of damaged and destroyed myofibrils. However, the actual and maximum intraventricular pressure remained unchanged under these conditions. The degree of cardiomyocyte apoptosis increased on day 1, but returned to normal in the follow-up period. Our study demonstrated high sensitivity of the right ventricle to left ventricular dysfunction and early activation of compensatory mechanisms. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 145, No. 4, pp. 392–394, April, 2008     

Left ventricular flow propagation velocity measurement: Is it cast in stone?

This study aims to investigate the measurement of left ventricular flow propagation velocity, V _p, using phase contrast magnetic resonance imaging and to assess the discrepancies resulting from inflow jet direction and individual left ventricular size. Three V _p measuring techniques, namely non-adaptive (NA), adaptive positions (AP) and adaptive vectors (AV) method, were suggested and compared. We performed the comparison on nine healthy volunteers and nine post-infarct patients at four measurement positions, respectively, at one-third, one-half, two-thirds and the conventional 4 cm distances from the mitral valve leaflet into the left ventricle. We found that the V _p measurement was affected by both the inflow jet direction and measurement positions. Both NA and AP methods overestimated V _p, especially in dilated left ventricles, while the AV method showed the strongest correlation with the isovolumic relaxation myocardial strain rate (r = 0.53, p < 0.05). Using the AV method, notable difference in mean V _p was also observed between healthy volunteers and post-infarct patients at positions of: one-half (81 ± 31 vs. 58 ± 25 cm/s), two-thirds (89 ± 32 vs. 45 ± 15 cm/s) and 4 cm (98 ± 23 vs. 47 ± 13 cm/s) distances. The use of AV method and measurement position at one-half distance was found to be the most suitable method for assessing diastolic dysfunction given varying left ventricular sizes and inflow jet directions.     

Low total haemoglobin mass, blood volume and aerobic capacity in men with type 1 diabetes

Blood O₂ carrying capacity affects aerobic capacity (VO_2max). Patients with type 1 diabetes have a risk for anaemia along with renal impairment, and they often have low VO_2max. We investigated whether total haemoglobin mass (tHb-mass) and blood volume (BV) differ in men with type 1 diabetes (T1D, n = 12) presently without complications and in healthy men (CON, n = 23) (age-, anthropometry-, physical activity-matched), to seek an explanation for low VO_2max. We determined tHb-mass, BV, haemoglobin concentration ([Hb]), and VO_2max in T1D and CON. With similar (mean ± SD) [Hb] (144 vs. 145 g l^?1), T1D had lower tHb-mass (10.1 ± 1.4 vs. 11.0 ± 1.1 g kg^?1, P < 0.05), BV (76.8 ± 9.5 vs. 83.5 ± 8.3 ml kg^?1, P < 0.05) and VO_2max (35.4 ± 4.8 vs. 44.9 ± 7.5 ml kg^?1 min^?1, P < 0.001) than CON. VO_2max correlated with tHb-mass and BV both in T1D (r = 0.71, P < 0.01 and 0.67, P < 0.05, respectively) and CON (r = 0.54, P < 0.01 and 0.66, P < 0.001, respectively), but not with [Hb]. Linear regression slopes were shallower in T1D than CON both between VO_2max and tHb-mass (2.4 and 3.6 ml kg^?1 min^?1 vs. g kg^?1, respectively) and VO_2max and BV (0.3 and 0.6 ml kg^?1 min^?1 vs. g kg^?1, respectively), indicating that T1D were unable to reach similar VO_2max than CON at a given tHb-mass and BV. In conclusion, low tHb-mass and BV partly explained low VO_2max in T1D and may provide early and more sensitive markers of blood O₂ carrying capacity than [Hb] alone.     

The relationship between monocarboxylate transporters 1 and 4 expression in skeletal muscle and endurance performance in athletes

The purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and endurance performance in trained cyclists. Ten well-trained cyclists (mean ± SD; age 24.4 ± 2.8 years, body mass 73.2 ± 8.3 kg, VO_2max 58 ± 7 ml kg⁻¹ min⁻¹) completed three endurance performance tasks [incremental exercise test to exhaustion, 2 and 10 min time trial (TT)]. In addition, a muscle biopsy sample from the vastus lateralis muscle was analysed for MCT1 and MCT4 expression levels together with the activity of citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD). There was a tendency for VO_2max and peak power output obtained in the incremental exercise test to be correlated with MCT1 (r = −0.71 to −0.74; P < 0.06), but not MCT4. The average power output (P _average) in the 2 min TT was significantly correlated with MCT4 (r = −0.74; P < 0.05) and HAD (r = −0.92; P < 0.01). The P _average in the 10 min TT was only correlated with CS activity (r = 0.68; P < 0.05). These results indicate the relationship between MCT1 and MCT4 as well as cycle TT performance may be influenced by the length and intensity of the task.     

Validity of the two-parameter model in estimating the anaerobic work capacity

The curvature of the power–time (P–t) relationship (W′) has been suggested to be constant when exercising above critical power (CP) and to represent the anaerobic work capacity (AWC). The aim of this study was to compare W′ to (1) the total amount of work performed above CP (W _90s′) and (2) the AWC, both determined from a 90s all-out fixed cadence test. Fourteen participants (age 30.5±6.5 years; body mass 67.8±10.3 kg), following an incremental VO_2max ramp protocol, performed three constant load exhaustion tests set at 103±3, 97±3 and 90±2% P-VO_2max to calculate W′ from the P–t relationship. Two 90s all-out efforts were also undertaken to determine W _90s′ (power output—time integral above CP) and AWC (power output—time integral above the power output expected from the measured VO₂). W′ (13.6±1.3 kJ) and W _90s′ (13.9±1.1 kJ; P=0.96) were not significantly different but were lower than AWC (15.9±1.2 kJ) by 24% (P=0.03) and 17%, respectively (P=0.04). All these variables were correlated (P<0.001) but great extents of disagreement were reported (0.2±6.4 kJ between W′ and W _90s′, 2.3±7.2 kJ between W′ and AWC, and 2.1±4.3 kJ between W _90s′ and AWC). The underestimation of AWC from both W′ and W _90s′ can be explained by the aerobic inertia not taking into consideration when determining the two latter variables. The low extents of agreement between W′, W _90s′ and AWC mean the terms should not be used interchangeably.     

Sigma-optokinetic nystagmus in squirrel monkeys elicited by stationary stripe patterns illuminated by regular and random-interval flash sequences

 Eye position and angular velocity were measured in squirrel monkeys (Saimiri sciureus) by means of the electromagnetic scleral search-coil technique. Horizontal sigma-optokinetic nystagmus (sigma-OKN) was elicited by a stationary, stroboscopically illuminated, periodic, vertical-stripe pattern lining a vertical cylinder. The relationship between the mean slow-phase eye angular velocity, V_e, of sigma-OKN and the product of pattern period, P_s, and flash frequency, f_s, was determined. When V_e approximated k·P_s·f_s (deg·s^–1) and k was an integer ≥l, the sigma-paradigm was fulfilled. Sigma-OKN could be evoked in different ”modes”, whereby k approximated 1, 2,…n. The sigma-OKN properties of squirrel monkeys were similar to those measured for sigma-OKN in the ”stare” mode in man, with the exception of a long-lasting optokinetic afternystagmus (sigma-OKAN) appearing in the monkey. A considerable amount of temporal variability in flash sequence intervals (”temporal noise”), causing retinal error signals that interfered with the sigma-paradigm, was accepted by the visuo-motor system without interruption of sigma-OKN. This observation was explained by the operation of a short memory device for perception of visual motion. The internal gain, g_i, which relates the retinal ”error” displacement velocity, V_r, and V_e depended, in turn, on V_r according to a function resembling the known relationship between neuronal activity of NOT (nucleus of the optic tract) nerve cells and V_r. This observation may be taken as direct proof that sigma-OKN can be explained by a centrally preprogrammed relationship between the retinal velocity, V_r, and the OKN slow-phase eye velocity, V_e. It is stipulated that the sum of V_r and efference copy signals generated in cortical or subcortical gaze centers is the essential component controlling the perceived velocity of the sigma-movement, whereby a short-term integrator plays a role for squirrel monkey sigma-OKN. When the flash frequency, f_s, was modulated periodically according to a sinewave or ”triangular” function at a rate below 0.5 cycles·s^–1, V_e was found to respond with a corresponding modulation, provided the modulation amplitude did not exceed 50% of the mean flash rate. When the latter occurred, nonlinear responses could be observed. A similar response was found when the speed of ”real” optokinetic stimuli was varied sinusoidally. Under these experimental conditions, however, the amplitude of the V_e variation yielded up to 1.0 approximately linear responses. Received: 4 May 1998 / Accepted: 3 September 1998     

Evidence of increased electro-mechanical delay in the left and right ventricle after prolonged exercise

We assessed the time delay from the onset of QRS (Q) to peak systolic (S′) and diastolic (E′) tissue velocities in the left (LV) and right ventricle (RV) before and after prolonged exercise. Nineteen well-trained runners (mean ± SD age, 41 ± 9 years) had tissue-Doppler echocardiography performed before and after an 89 km ultra-marathon race. Longitudinal tissue motion was analysed in LV basal and mid-wall segments and RV free wall. Electromechanical coupling was assessed by the delay between Q and S′ as well as E′ tissue velocities. Average data for all segments were adjusted for the R–R interval. Comparisons were made by paired t-tests. An increase in electro-mechanical delay (EMD) was reported post-exercise in systole (Q–S′ LV: 131 ± 20 vs. 175 ± 27 ms; RV: 171 ± 34 vs. 258 ± 35 ms; P < 0.05) and diastole (Q–E′ LV: 486 ± 51 vs. 647 ± 44 ms; RV: 500 ± 80 vs. 690 ± 75 ms; P < 0.05). Further, post-race peak tissue velocities in basal LV and RV wall segments were reduced (P < 0.05). Recovery from prolonged running was associated with an increased “EMD”, and reduced peak tissue velocities, in both ventricles.     

Changes in heart rate recovery after high-intensity training in well-trained cyclists

Heart rate recovery (HRR) after submaximal exercise improves after training. However, it is unknown if this also occurs in already well-trained cyclists. Therefore, 14 well-trained cyclists (VO_2max 60.3 ± 7.2 ml kg⁻¹ min⁻¹; relative peak power output 5.2 ± 0.6 W kg⁻¹) participated in a high-intensity training programme (eight sessions in 4 weeks). Before and after high-intensity training, performance was assessed with a peak power output test including respiratory gas analysis (VO_2max) and a 40-km time trial. HRR was measured after every high-intensity training session and 40-km time trial. After the training period peak power output, expressed as W kg⁻¹, improved by 4.7% (P = 0.000010) and 40-km time trial improved by 2.2% (P = 0.000007), whereas there was no change in VO_2max (P = 0.066571). Both HRR after the high intensity training sessions (7 ± 6 beats; P = 0.001302) and HRR after the 40-km time trials (6 ± 3 beats; P = 0.023101) improved significantly after the training period. Good relationships were found between improvements in HRR_40-km and improvements in peak power output (r = 0.73; P < 0.0001) and 40-km time trial time (r = 0.96; P < 0.0001). In conclusion, HRR is a sensitive marker which tracks changes in training status in already well-trained cyclists and has the potential to have an important role in monitoring and prescribing training.     

Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

The first stage of the two‐stage arterial switch operation (ASO) for transposition of the great arteries (TGA) is associated with depressed ventricular function and an unstable immediate post‐operative course. It is unclear if this is because of the acute increase in afterload of the thin‐walled, low‐pressure ventricle by pulmonary artery banding (PAB). To determine the acute effects of afterload increase on the contractile function of thin‐walled ventricles, we studied the right ventricular pressure–volume relations of seven sheep before and 30 min after PAB using combined pressure–conductance catheters during inflow reduction. Load independent indices of systolic and diastolic performance were derived from these relations. Pulmonary artery banding increased the mean ratio between right and left ventricular systolic pressure from 0.34 ± 0.05 to 0.64 ± 0.10, P < 0.05 (mean ± SD). There were no significant changes in heart rate and end‐systolic volume after banding although there was an incremental trend in the end‐diastolic volume and stroke volume. Right ventricular output (530 ± 163–713 ± 295 mL min^–1, P < 0.05), slope of the end‐systolic pressure–volume relation (ESPVR) (3.7 ± 2.8–10.0 ± 4.8 mmHg mL^–1, P < 0.05) and slope of the pre‐load recruitable stroke work (PRSW) relation (9.6 ± 1.8–15.0 ± 3.1 mmHg, P < 0.05) were significantly increased indicating improved contractile state after banding. The diastolic function curve was unchanged after banding although the right ventricle (RV) was operating at a larger end‐diastolic volume. Hence, the RV of sheep responded to acute pressure overload by demonstrating enhanced contractility and evidence of the Frank–Starling mechanism without associated change in right ventricular diastolic performance.