Changes In SV Research Articles

Silicon nitride encapsulation of sulfide passivated GaAs/AlGaAs microdisk lasers

SiNx encapsulation of sulfide passivated GaAs/AlGaAs surfaces was examined with respect to the SiNx deposition conditions and applied to GaAs/AlGaAs microdisk lasers. The SiNx encapsulation is a method for preserving the positive effects (e.g., reduced surface recombination velocity, Sv) of the sulfide passivation by inhibiting the oxidation process of the air-exposed semiconductor. GaAs-based microdisks, with diameters of 2–10 μm, provide a very sensitive probe of the surface recombination since the resonator mode is in close proximity to the edge of the disk (∼<0.5 μm) and the carrier diffusion length is typically several microns. An ammonium sulfide solution was used for the S passivation. The SiNx was deposited by plasma-enhanced chemical vapor deposition (PECVD) at 50 or 300 °C, with and without post-deposition annealing (300–400 °C), or by electron cyclotron resonance chemical vapor deposition (ECR-CVD) at 100 °C. Photoluminescent measurements of GaAs/InGaP epitaxial structures provided an indication of the relative change in Sv. The GaAs/AlGaAs microdisks do not lase without sulfide treatment when optically pumped at 77 K. With the sulfide treatment alone, cw lasing was achieved but the lifetime was only several seconds. A dramatic increase in the laser lifetime was obtained using PECVD-deposited SiNx at 300 °C. The laser output for the PECVD SiNx (300 °C) encapsulated microdisks could be increased by nearly an order of magnitude by annealing at 400 °C for 300 s or by cw operation for several hours. Initial results using the ECR-deposited SiNx films suggest improved performance (lower threshold, stability) compared to the PECVD SiNx. The laser performance is correlated with the photoluminescence results.

Respiration‐synchronous fluctuations in stroke volume, heart rate and arterial pressure in humans.

1. Simultaneous recordings of beat-to-beat left cardiac stroke volume (SV, pulsed ultrasound Doppler), mean arterial pressure (MAP) and heart rate (HR) were obtained in ten healthy young adults during spontaneous respiration at supine rest, before and after cholinergic blockade by atropine (0.035 mg kg-1). 2. Respiration-synchronous fluctuations in SV, HR, cardiac output (CO) and MAP were quantified by spectral analysis of the recordings of each of these variables. 3. Before atropine administration, respiration-synchronous fluctuations in HR and SV were prominent. The changes in HR and SV were inversely related and variation in SV was the main source of respiratory variability in CO. Respiration-synchronous fluctuations in MAP were mainly caused by variations in CO. 4. After cholinergic blockade, respiratory HR variations were eliminated, whereas the respiratory fluctuations in SV persisted. The fluctuations in CO and MAP increased. In this situation, mechanically induced variations in SV were not counteracted by inverse HR fluctuations and the influence on CO thus increased. 5. The main source of respiratory fluctuations in MAP in supine humans is thus variation in SV, while inverse, vagally mediated HR variations tend to reduce the fluctuations in CO and MAP.

Abnormal Hemodynamic Response to Valsalva Maneuver in Patients with Atrial Septal Defect Evaluated by Doppler Echocardiography

Hemodynamic responses to the Valsalva maneuver were studied in eight healthy subjects (group 1) and eight patients with ASD (group 2) using Doppler echocardiography. The acute changes of aortic blood flow profiles during the Valsalva maneuver were investigated on a basis of beat-to-beat estimation. During the active strain phase (phase 2), group 1 showed a significant decrease in systolic blood pressure, SV and CO with reflex tachycardia; in group 2, there was a significant decrease in SV and CO with reflex tachycardia, but not systolic blood pressure. The percentage decreases in SV and CO in group 2 were significantly less than those in group 1 (23 +/- 16 percent vs 48 +/- 10 percent for SV, p less than 0.01; 17 +/- 12 percent vs 40 +/- 13 percent for CO, p less than 0.05). After release of strain phase (phase 4), group 1 showed significant reversed changes in systolic blood pressure, SV and heart rate, indicating an overshoot effect which was, however, not observed in group 2. Thus, patients with ASD presented abnormal Valsalva response which was characterized by the absence of phase 4 overshoot and a less marked phase 2 change. The findings suggest that the decremental effect of impaired venous return on stroke output during active strain may be attenuated by the increased pulmonary blood volume due to left-to-right shunt. In patients with ASD, the lesser decrement of CO during phase 2 may not provoke sufficient sympathetic activity to induce overshoot response in phase 4.

Usefulness of Continuous Wave Doppler Measures as Indicators of Exercise-Induced Alterations in Myocardial Contractility

The authors examine the utility of using the CW Doppler measures of peak acceleration (PkA) and peak velocity (PkV) of blood flow in the ascending aorta as measures of alterations in myocardial contractility due to cardioselective β-blockade. Using upright cycle ergometry, 18 physically active men (mean age, years 25.2; VO2peak, 42.3 ml x kg-1 x min-1) exercised at 20, 40, and 60% VO2peak in three consecutive 6-minute stages after administration of either a placebo (P) or 100 mg of atenolol (A). CW Doppler measures were obtained, as was stroke volume (SV; CO2 rebreathing), heart rate (HR), and blood pressure. At 60% VO2peak, PkA averaged 37.0% less (P < 0.01) while PkV was 10.1% less (P < 0.05) with A than with P;SV was 22.5% higher (P < 0.01) while HR was 18.8% lower (P < 0.01) with A. Mean arterial pressure (MAP) was a significant covariate for PkA (P < 0.01) but not PkV. Absolute between-condition alterations in PkV (PkVp–a) shared a significant proportion of variance with SVp–a (R2 = 0.29, P < 0.05) while the amount of shared variance with PkAp–a was nonsignificant (R2 = 0.22). Since MAP was lower in A by 10.6% (P < 0.05), the increased SV in A was attributed to decreased afterload and not increased myocardial contractility. Approximately 68% of the variance in PkAp–a and 75% of PkVp–a cannot be explained by β1-blocker associated changes in either SV or MAP. Most likely, the majority of this unexplained variance is due to the suppression of catecholamine-induced increases in myocardial contractility seen with β1-blockade. Both PkA and PkV were significantly reduced (P < 0.01, P < 0.05, respectively) with A compared with P. These findings are consistent with the interpretation that Doppler measures of PkA and PkV are sensitive to changes in myocardial inotropic state when such measures are compared serially within the same subjects.

Cardiovascular and respiratory effects of three rapidly acting barbiturates in dogs

SUMMARY The cardiovascular and respiratory effects of 3 rapidly acting barbiturates, thiopental sodium, thiamylal sodium, and methohexital sodium, were studied in dogs from completion of injection until 12.5 minutes after injection. The doses administered were 19.4 mg of thiopental/kg of body weight, 18.4 mg of thiamylal/kg, and 9.7 mg of methohexital/kg, which were chosen as equipotent doses necessary to inhibit the laryngoscopic reflex in 50% of the population. To determine the cardiovascular and respiratory effects for each drug, the values at each measurement time following injection were compared with baseline values (T0). At the 15- and 30-second measurement times following thiopental administration, stroke volume (sv) decreased; heart rate (hr), left atrial pressure, and mean pulmonary arterial pressure increased; and cardiac index (ci), myocardial contractility, and systemic and pulmonary vascular resistances were not different from baseline values. Mean arterial pressure (map) was not different from the baseline value at 15 seconds, but was increased from 30 seconds to 2 minutes. All values except hr had returned to baseline values by 7.5 minutes. At all measurement times, arterial oxygen tension and arterial pH were decreased, and arterial carbon dioxide tension increased from baseline values. Although the cardiovascular and respiratory changes following administration of thiamylal and methohexital were similar to those described for thiopental, some differences were found. Following thiamylal administration, systemic vascular resistance increased at 1 minute, pulmonary vascular resistance increased at 1 and 2 minutes, and myocardial contractility increased at 1 and 2 minutes. Following methohexital administration, map decreased at 15 seconds, and sv decreased at all measurement times. Cardiac index increased at 30 seconds, 1 minute, and 2 minutes; myocardial contractility increased at 1, 2, and 2.5 minutes; and blood-gas and pH had returned to baseline by 12.5 minutes. To determine differences between drugs, the cardiovascular and respiratory values for each drug were compared at each measurement time. Changes in hr and sv induced by the 3 drugs were similar at all measurement times. Mean arterial pressure at 15 and 30 seconds was lower following methohexital administration than after thiopental or thiamylal administration. Cardiac index was higher at 1 minute following methohexital administration, compared with that after thiamylal administration, whereas systemic vascular resistance was higher at 1 minute following thiamylal administration, compared with that after methohexital administration. The increase in left atrial pressure was greater following thiamylal administration than after thiopental administration at 30 seconds to 5 minutes or after methohexital administration at 1 to 5 minutes. Mean pulmonary arterial pressure was significantly higher at 2 to 4 minutes following thiamylal administration than after methohexital administration. Pulmonary vascular resistance was higher at 1 minute following thiamylal administration, compared with that after thiopental and methohexital administration. At 1 and 2 minutes, myocardial contractility was significantly higher following methohexital administration, compared with that after thiobarbiturate administration. Arterial oxygen tension was lower at 12.5 minutes following administration of the thiobarbiturates, compared with that after methohexital administration. When compared with methohexital administration, arterial carbon dioxide tension was higher at 7.5 and 12.5 minutes following thiamylal administration. The decrease in pH following thiamylal administration was greater at all measurement times, compared with that after thiopental and methohexital administration.

Mathematical modelling of trabecular bone structure: The evaluation of analytical and quantified surface to volume relationships in the femoral head and iliac crest

The three-dimensional architecture of trabecular bone has structural trends related to physical function as described by Wolff's law. Mathematical modelling provides a means of analysing these structures through the use of simplified representations. A single measure of mineralized bone volume per unit volume of structure ( Vv) and the surface area of mineralized bone per unit volume of structure ( Sv) does not identify a particular architecture in any detail; the way in which Sv changes in relation to Vv does provide this information as the structure remodels. A series of structures using the elements of plates and rods were created. The rates of change of Sv with respect to Vv for trabecular structures give insight into differences in such models. Structures in the femoral head and iliac crest were analysed by power curve regression. In the principal compressive region, just above the medical cortex, advanced osteoarthritis was associated with a preferential loss of rods from the normal trabecular structure, resulting in a more plate-like architecture. The iliac crest remodelling that takes place in the osteoporotic appears to be the result of a generalised bone loss with some of the thinner elements of the structure being removed completely, resulting in an increase in unit cell dimension. The consequence of changing unit cell size has a major impact on surface availability for osteoblastic and osteoclastic activity. The simple plate model as a basis for the stereological analysis of trabecular structures is therefore limited because of the mixed plate and rod nature of trabecular architecture.

The effect of plasma volume expansion on the response to carotid occlusion in the non-human primate

The purpose of this study was to investigate the effects of plasma volume expansion on the cardiac and peripheral components of the baroreceptor reflex. Nine male Rhesus monkeys were chronically instrumented to measure arterial pressure and aortic blood flow. The aortic arch was denervated at the time of surgery. Bilateral carotid artery occlusion (BCO) was used to elicit the carotid sinus reflex both before and after 25% plasma volume expansion with an iso-osmotic dextran solution. The BCO elicited significant increases in heart rate (HR, 29.8 ± 5.3 bpm) mean arterial pressure (MAP, 55.0 ± 8.2 mm Hg) and total peripheral resistance (TPR, 0.076 ± 0.01 mm Hg/ml/min) coupled with a significant reduction in mean aortic flow (AF, −246.9 ± 55.3 ml/min) and stroke volume (SV, −2.86 ± 0.36 ml). Volume expansion significantly attenuated the HR (15.2 ± 5.8 bpm), MAP (30.4 ± 4.4 mm Hg) and TPR (0.036 ± 0.006 mm Hg/ml/min) response to carotid sinus hypotension. The changes in mean AF and SV elicited by BCO, however, were not significantly different between the control and volume expansion conditions. These data suggest that plasma volume expansion significantly attenuates the baroreceptor reflex control of circulation with a similar reduction in both the peripheral resistance and heart rate components of the response.

20℃, 30℃, および40℃における30分間運動中の心拍出量, 一回拍出量, および心拍数について

Cardiovascular responses during 30 min of exercise in 20°C, 30°C, and 40°C(R.H.50%) were measured in six male Japanese. The subjects exercised on a bicycle ergometer at the two kinds of work loads, i.e., 300 and 600kgm/min. Cardiac output(Q) was detennined with the CO2 rebreathing method at the 5th, 15th, and 30th min of exercise. Oxygen uptake(VO_2), heart rate(HR), rectal temperature(Tr), and mean skin temperature(Ts) were also measured. VO_2 and Q did not change siguificantly during exercise in all environments. Analysis of variance showed that the factor of ambient temperature had no siguificant effects on VO_2 and Q. HR increased with time and SV decreased with time during exercise. The largest change in HR and SV occured between the 5th min and the 15th min of exercise. Tr increased with time during exercise. The marked increase in Tr occured between the 15th min and 30th min of exercise. The regression equations of HR on Q and SV on Q in each time of exercise were calculated. The analysis of covariance showed that the elevation of regression line of HR on Q in the 5th min of exercise was significantly lower than those in the 15th min and the 30th min of exercise. Similarly, the elevation of regression line of SV on Q in the 5th min of exercise was significantly higher than those in the 15th min and the 30th min of exercise. From the regression equation of SV on Tr the adjusted values of SV for each time of exercise were calculated in order to exclude differences in Tr. The adjusted values of SV in the 5th min of exercise was siguificantly higher than those in the 15th min and the 30th min of exercise. So the alterations in HR and SV observed between the 5th min and the 15th min of exercise may accounted for by other than the change in internal body temperature.

The haemodynamic effects of flunitrazepam in anaesthetized patients with valvular or coronary artery lesions.

The Haemodynamic effects of flunitrazepam (FLU) 1.25 mg X m-2 administered intravenously were studied in 18 anaesthetized cardiac patients suffering from isolated mitral (MIT, n = 6), aortic (AOR, n = 6) or coronary (COR, n = 6) lesions. A placebo group of 18 clinically similar patients was used to assess the stability of the cardiovascular parameters under the conditions of the study. Heart rate, systemic arterial pressure, cardiac output and central venous pressure changes were measured 2, 5, 8 and 12 min after FLU or saline injection and compared with reference values collected before the start of the haemodynamic test. In the FLU group, the cardiovascular state of all the patients developed following the same pattern and the greatest differences were observed at 12 min post-injection. These differences, expressed as a percentage of the initial values were (* P less than 0.05; ** P less than 0.001; ns = non-significant): mean systemic arterial pressure: COR, -18% (**);MIT, -13% (*); AOR, -23% (**); heart rate: COR, 0% (ns); MIT, -10% (*); AOR, -12% (*); cardiac output: COR, -15% (**); MIT, -13% (*); AOR, -16% (**); stroke volume: COR, -12%(*);MIT, 0% (ns);AOR,-3%(ns). This shows some differences concerning the SV and heart rate changes in the valvular and COR patients. As compared to the data from the literature, most of the haemodynamic effects of FLU seem relatively independent of the initial level of consciousness.

Nitrous oxide activates the supraspinal pain inhibition system.

The effects th groups the changes in CO and SV were due mainly to a reduced demand of oxygen transport and expected changes in sympatho-adrenergic tone rather than to myocardial depression.