Angular momentum transport in turbulent flow between independently rotating cylinders.

We present measurements of the angular momentum flux (torque) in Taylor-Couette flow of water between independently rotating cylinders for all regions of the (Ω1, Ω2) parameter space at high Reynolds numbers, where Ω1 (Ω2) is the inner (outer) cylinder angular velocity. We find that the Rossby number Ro = (Ω1 - Ω2)/Ω2 fully determines the state and torque G as compared to G(Ro = ∞) ≡ G∞. The ratio G/G∞ is a linear function of Ro(-1) in four sections of the parameter space. For flows with radially increasing angular momentum, our measured torques greatly exceed those of previous experiments [Ji et al., Nature (London), 444, 343 (2006)], but agree with the analysis of Richard and Zahn [Astron. Astrophys. 347, 734 (1999)].

Velocity statistics distinguish quantum turbulence from classical turbulence.

By analyzing trajectories of solid hydrogen tracers, we find that the distributions of velocity in decaying quantum turbulence in superfluid 4He are strongly non-Gaussian with 1/v(3) power-law tails. These features differ from the near-Gaussian statistics of homogenous and isotropic turbulence of classical fluids. We examine the dynamics of many events of reconnection between quantized vortices and show by simple scaling arguments that they produce the observed power-law tails.

On the neural connection.

Discoveries concerning cardiac neural-electrical modulation and local neural remodeling provide powerful new approaches for the development of novel antiarrhythmic strategies. This "view" of developments in this emerging field highlights recent advances and suggests that additional neurally targeted investigations have considerable potential for prevention of arrhythmic diseases.

Blowout bifurcations and the onset of magnetic activity in turbulent dynamos.

The transition to magnetic-field self-generation in a turbulent, electrically conducting fluid is shown to exhibit intermittent bursting characterized by distinct scaling laws. This behavior is predicted on the basis of prior analysis of a type of bifurcation (called a blowout bifurcation) occurring in chaotic systems with an invariant phase space submanifold. The predicted scalings are shown to be consistent with numerical solutions of the governing magnetohydrodynamic equations, and implications for recently implemented experimental programs are discussed.

Intraventricular pressure dynamics in ventriculocholecystic shunting: a telemetric study.

Extracranial cerebrospinal fluid shunting is the current mainstay of therapy for hydrocephalus. The generally preferred extracranial site for cerebrospinal fluid absorption is the peritoneal space; however, the cardiac atrium and the pleura are also commonly used. On occasion other CSF recipient sites, such as the gallbladder, are used secondarily when the more common absorptive spaces are unavailable or unsuitable. The gallbladder, though, exhibits its own pressure dynamics in response to physiological stimuli. The effects of gallbladder contraction on intraventricular pressure (IVP) in the presence of a ventriculocholecystic (VGB) shunt are unknown. We had the opportunity to place a VGB shunt in a 4-year-old child who was coupled to a noninvasive telemonitor. After a period of acclimation, we examined the IVP dynamics of that shunting system both pre- and postprandially. We found that before ingestion of food, the gallbladder provides a CSF recipient site similar to that of the peritoneal space. However, after ingestion of a meal containing fat, we found that IVP rose more than 10 cm water in a stereotypic fashion consistent with postprandial gallbladder contraction. The increase in IVP lasted for several hours reaching a peak at approximately 75 min postprandially. We conclude that the VGB shunt is a viable alternative for extracranial cerebrospinal fluid shunting; however, one must be aware of the peculiar dynamics of this shunt in relation to food ingestion and the potential for unusually high IVPs.

Circular polarization excitation and detection in (14)N NQR.

Circular polarization excitation and detection of (14)N NQR signal are reported. A theoretical model is presented in terms of fictitious spin-1/2 operators and is compared to experiments performed on a powder crystalline sample of RDX. It is shown that in spin-1 systems with finite asymmetry--unlike previously reported NMR and symmetric spin-3/2 NQR systems (Chen et al., J. Magn. Reson. 54, 324--327, 1983; Weber and Hahn, Phys. Rev. 120, 365--375, 1960)-the circular polarization nature of the signal is due to powder orientation effects in polycrystalline samples. Sensitivity improvements up to a factor of the square root of 2 are reported using the same hardware and switching modes from linear polarization to circular polarization; this also is shown to result from the polycrystalline nature of the samples.

Pharmacological block of the slow component of the outward delayed rectifier current (I(Ks)) fails to lengthen rabbit ventricular muscle QT(c) and action potential duration.

1. The effects of I(Ks) block by chromanol 293B and L-735,821 on rabbit QT-interval, action potential duration (APD), and membrane current were compared to those of E-4031, a recognized I(Kr) blocker. Measurements were made in rabbit Langendorff-perfused whole hearts, isolated papillary muscle, and single isolated ventricular myocytes. 2. Neither chromanol 293B (10 microM) nor L-735,821 (100 nM) had a significant effect on QTc interval in Langendorff-perfused hearts. E-4031 (100 nM), on the other hand, significantly increased QTc interval (35.6+/-3.9%, n=8, P<0.05). 3. Similarly both chromanol 293B (10 microM) and L-735,821 (100 nM) produced little increase in papillary muscle APD (less than 7%) while pacing at cycle lengths between 300 and 5000 ms. In contrast, E-4031 (100 nM) markedly increased (30 - 60%) APD in a reverse frequency-dependent manner. 4. In ventricular myocytes, the same concentrations of chromanol 293B (10 microM), L-735,821 (100 nM) and E-4031 (1 microM) markedly or totally blocked I(Ks) and I(Kr), respectively. 5. I(Ks) tail currents activated slowly (at +30 mV, tau=888.1+/-48.2 ms, n=21) and deactivated rapidly (at -40 mV, tau=157.1+/-4.7 ms, n=22), while I(Kr) tail currents activated rapidly (at +30 mV, tau=35.5+/-3.1 ms, n=26) and deactivated slowly (at -40 mV, tau(1)=641.5+/-29.0 ms, tau(2)=6531+/-343, n=35). I(Kr) was estimated to contribute substantially more to total current density during normal ventricular muscle action potentials (i.e., after a 150 ms square pulse to +30 mV) than does I(Ks). 6. These findings indicate that block of I(Ks) is not likely to provide antiarrhythmic benefit by lengthening normal ventricular muscle QTc, APD, and refractoriness over a wide range of frequencies.

Multiple agents potentiate alpha1-adrenoceptor-induced conduction depression in canine cardiac purkinje fibers.

BACKGROUND: Halothane more so than isoflurane potentiates an alpha1-adrenoceptor (alpha1-AR)-mediated action of epinephrine that abnormally slows conduction in Purkinje fibers and may facilitate reentrant arrhythmias. This adverse drug interaction was further evaluated by examining conduction responses to epinephrine in combination with thiopental and propofol, which "sensitize" or reduce the dose of epinephrine required to induce arrhythmias in the heart, and with etomidate, which does not, and responses to epinephrine with verapamil, lidocaine, and l-palmitoyl carnitine, a potential ischemic metabolite. METHODS: Action potentials and conduction times were measured in vitro using two microelectrodes in groups of canine Purkinje fibers stimulated at 150 pulses/min. Conduction was evaluated each minute after exposure to 5 microm epinephrine (or phenylephrine) alone or with the test drugs. Changes in the rate of phase 0 depolarization (Vmax) and the electrotonic spread of intracellular current were measured during exposure to epinephrine with octanol to evaluate the role of inhibition of active and passive (intercellular coupling) membrane properties in the transient depression of conduction velocity. RESULTS: Lidocaine (20 microm) and octanol (0.2 mm) potentiated alpha1-AR-induced conduction depression like halothane (0.4 mm), with maximum depression at 3-5 min of agonist exposure, no decrease of Vmax, and little accentuation at a rapid (250 vs. 150 pulses/min) stimulation rate. Thiopental (95 microm), propofol (50 microm), and verapamil (2 microm) similarly potentiated epinephrine responses, whereas etomidate (10 microm) did not. Between groups, the decrease of velocity induced by epinephrine in the presence of (10 microm) l-palmitoyl carnitine (-18%) was significantly greater than that resulting from epinephrine alone (-6%; 0.05

The role of the delayed rectifier component IKs in dog ventricular muscle and Purkinje fibre repolarization.

1. The relative contributions of the rapid and slow components of the delayed rectifier potassium current (IKr and IKs, respectively) to dog cardiac action potential configuration were compared in ventricular myocytes and in multicellular right ventricular papillary muscle and Purkinje fibre preparations. Whole-cell patch-clamp techniques, conventional microelectrode and in vivo ECG measurements were made at 37C. 2. Action potential duration (APD) was minimally increased (less than 7%) by chromanol 293B (10 microM) and L-735,821 (100 nM), selective blockers of IKs, over a range of pacing cycle lengths (300-5000 ms) in both dog right ventricular papillary muscles and Purkinje fibre strands. D-Sotalol (30 microM) and E-4031 (1 microM), selective blockers of IKr, in the same preparations markedly (20-80%) lengthened APD in a reverse frequency-dependent manner. 3. In vivo ECG recordings in intact anaesthetized dogs indicated no significant chromanol 293B (1 mg kg-1 i.v.) effect on the QTc interval (332.9 +/- 16.1 ms before versus 330.5 +/- 11.2 ms, n = 6, after chromanol 293B), while D-sotalol (1 mg kg-1 i.v.) significantly increased the QTc interval (323.9 +/- 7.3 ms before versus 346.5 +/- 6.4 ms, n = 5, after D-sotalol, P < 0.05). 4. The current density estimated during the normal ventricular muscle action potential (i.e. after a 200 ms square pulse to +30 mV or during a 250 ms long 'action potential-like' test pulse) indicates that substantially more current is conducted through IKr channels than through IKs channels. However, if the duration of the square test pulse or the 'action potential-like' test pulse was lengthened to 500 ms the relative contribution of IKs significantly increased. 5. When APD was pharmacologically prolonged in papillary muscle (1 microM E-4031 and 1 microg ml-1 veratrine), 100 nM L-735,821 and 10 microM chromanol 293B lengthened repolarization substantially by 14.4 +/- 3.4 and 18. 0 +/- 3.4% (n = 8), respectively. 6. We conclude that in this study IKs plays little role in normal dog ventricular muscle and Purkinje fibre action potential repolarization and that IKr is the major source of outward current responsible for initiation of final action potential repolarization. Thus, when APD is abnormally increased, the role of IKs in final repolarization increases to provide an important safety mechanism that reduces arrhythmia risk.

Telemetric assessment of intracranial pressure changes consequent to manipulations of the Codman-Medos programmable shunt valve.

INTRODUCTION: Noninvasive manipulation of programmable shunt valves may allow customization of intracranial pressure (ICP) dynamics in individual shunted patients. Manipulations of the recently FDA-approved Codman-Medos variable pressure valve (VPV) are monitored by radiographic changes in the valve mechanism, necessitating a skull radiograph with each pressure change. We wished to assess the in vivo impact of VPV manipulations on ICP changes using a noninvasive telemonitor as an alternative to radiographic confirmation and as a method for validating the ICP changes. METHODS: TeleSensor devices (Radionics) were implanted in-line with 12 VPV shunt systems. ICP was assessed telemetrically in the supine position whenever the valve pressure was adjusted (both before and 2-5 min after the manipulation). RESULTS: Valve manipulation was confirmed by radiograph for the initial manipulations only and matched the telemetric pressure changes observed in all cases. Confirmed manipulations of the valve were generally followed by a near equivalent relative change in ICP (

Cardiac effects of non-depolarizing neuromuscular blocking agents pancuronium,vecuronium, and rocuronium in isolated rat atria.

Pancuronium, vecuronium, and rocuronium produce different cardiac effects. Using spontaneously beating right and electrically stimulated left rat atria, while measuring developed force, effective refractory period, and heart rate, we determined and compared the concentration-dependent cardiac effects of the compounds. The preparations were exposed to five progressively increasing concentrations of these compounds (10(-9), 10(-8), 10(-7), 10(-6), and 10(-5) mol/L). Pancuronium increased heart rate; vecuronium and rocuronium produced positive inotropic effects; and vecuronium shortened refractoriness. These effects may be the result of a blockade of the M2 muscarinic receptors. However, the concentrations required to produce changes were higher than those observed in patients under neuromuscular blockade.

Effects of the optical isomers of verapamil on electrophysiological properties of the heart in conscious dogs.

We compared the cumulative dose-response relations of verapamil (0.1, 0.2 and 0.4 mg kg(-1)) in different R/S enantiomer ratios (100/0, 90/10, 80/20, 50/50 and 20/80) on the electrophysiological and hemodynamic characteristics of the heart using the conscious dogs. A reduction of mean arterial pressure occurred with 20R/80S producing a 3-times greater decrease than 100R/0S, but an increase in heart rate occurred with 20R/80S producing a 9-times greater increase than 100R/0S. Increased heart rate was concurrent with decreased mean arterial pressure most prevalent with a higher ratio of S-isomer that produced a greater reduction in mean arterial pressure and increase in heart rate at lower overall verapamil doses. Atrio-ventricular conduction time increased 3-5 min after each infusion, with 20R/80S producing a 4-times greater effect than 100R/0S. These results indicate that the peripheral and cardiac electrophysiologic properties of various nonracemic verapamil mixtures are mainly attributable to the concentration of S-isomer.

The role of glycolysis in myocardial calcium control.

Because glycolysis is thought to be important for maintenance of cellular ion homeostasis, the aim of the present study was to examine the role of glycolysis in the control of cytosolic calcium ([Ca2+]i) and cell shortening during conditions of increased calcium influx. Thus, [Ca2+]i and unloaded cell shortening were measured in fura-2/AM loaded rat ventricular myocytes. All cells were superfused with Tyrode's solution containing glucose and pyruvate (to preserve oxidative metabolism), and glycolysis was inhibited by iodoacetate (IAA, 100 microM). Calcium influx was increased, secondary to an increase in intracellular sodium, by addition of veratrine (1 microgram/ml), or directly by either elevating [Ca2+]o from 2 to 5 mM or by exposing the cells to isoproterenol (1 to 100 nm). Veratrine exposure caused a time-dependent increase in both diastolic and systolic [Ca2+]i that resulted in cellular calcium overload and hypercontraction. The rate of increase in [Ca2+]i was more rapid in IAA-treated than in untreated myocytes, leading to a 13+/-3 v 5+/-2% increase (P<0.05) in diastolic [Ca2+]i after 5 min of exposure. The corresponding increases in systolic [Ca2+]i were 43+/-6 and 24+/-5% (P<0.05). Elevated [Ca2+]o resulted in increased [Ca2+]i transient amplitudes and cell shortening. These responses were each attenuated by inhibiting glycolysis, so that the increase was 38+/-5 v 68+/-9% ([Ca2+]i transient amplitude, P<0.05) and 41+/-11 v 91+/-18% (cell shortening, P<0.05). Inhibition of glycolysis did not, however, affect the increase in calcium transient or cell shortening during addition of isoproterenol. We conclude that glycolysis plays an essential role in the maintenance of intracellular calcium homeostasis during severe calcium overload. Glycolysis was also essential for signalling the inotropic effect that accompanied elevation in extracellular calcium, while the changes in intracellular calcium following administration of isoproterenol were not influenced by glycolysis in the present model.

Action-potential duration and contractility in canine cardiac tissues: action of inotropic drugs.

1. Inotropic and electrophysiologic effects of veratrine, vesnarinone, d-sotalol and tetraethylammonium (TEA) were compared. Action-potential duration (APD) and contractility were measured in isolated canine Purkinje fiber and ventricular trabecular muscle preparations by using standard microelectrode techniques. Each drug significantly increased APD and force development in either tissue. 2. Drug-induced increases in force development were normalized to increases in APD. The order of efficacy was found to be vesnarinone>veratrine>TEA in ventricular myocardium, whereas it was veratrine>>vesnarinone=d-sotalol=TEA in Purkinje fibers. 3. The force-APD relation was linear for all drugs in the concentrations used. 4. Simultaneous measurements of APD, force development and intracellular sodium ion activity (a(i)Na) in the presence of either veratrine or lidocaine indicated a linear relation between force development and changes in a(i)Na. 5. The relation between APD and force development was different in ventricular and Purkinje fiber preparations. Differences in the veratrine sensitivity of the force-APD relation observed between Purkinje and ventricular preparations suggest that a(i)Na-dependent changes in Na+/Ca2+ exchange may play a more important role in regulation of force generation in Purkinje fibers than in ventricular myocardium.

Intraventricular pressure dynamics in patients with ventriculopleural shunts: a telemetric study.

Extracranial CSF shunting to the pleural absorptive surface is sometimes used as an alternative to ventriculoperitoneal shunting. The pressure dynamics of this type of shunt would be expected to differ from peritoneal shunting due to active changes in pleural pressures caused by the ventilatory cycle. We have had opportunity to examine the in vivo intraventricular pressure (IVP) dynamics of ventriculopleural shunts utilizing a commercially available implantable telemonitor (Telesensor; Radionics, Burlington, Mass.). Four patients with ventriculopleural shunts were monitored telemetrically while supine and at increments of head elevation to 90 degrees. Two patients with 'medium' grade differential pressure valves exhibited IVPs which were never greater than zero. One patient with an in-line antisiphoning device in the shunt system appeared to have IVPs closely resembling those seen in shunting to the peritoneal space. Another patient with valve opening pressure set at 19 cm of water consistently had supine intraventricular pressures less than 10 cm of water that readily fell to zero with minimal head elevation. We conclude that the negative intrapleural pressures generated by the ventilatory cycle tend to cause IVPs in ventriculopleural shunts to be lower than those expected in peritoneal shunting. This observation suggests that ventriculopleural shunts may be appropriate for patients requiring very low intraventricular pressures in order to resolve their hydrocephalic symptoms.

Reversal of hypothermia-induced action potential lengthening by the KATP channel agonist bimakalim in isolated guinea pig ventricular muscle.

1. ATP-sensitive potassium (KATP) channel openers shorten cardiac ventricular muscle action potential duration (APD), reduce resting and developed contractile force, and have been shown to provide cardioprotection when given before, during, and after either short-term ischemia or long-term hypothermia. The authors' aim was to determine the concentration-dependent effect of the potent KATP channel opener bimakalim on transmembrane action potential changes induced by mild (27 degrees C) and moderate (20 degrees C) hypothermia in isolated guinea pig ventricular muscle. 2. Conventional microelectrode techniques were used to record action potentials (APs) in single myocytes during normothermia (37 degrees C) and hypothermia in the presence and absence of 0.1 to 30 mumol.l-1 bimakalim. 3. Hypothermia alone increased APD and depolarized the diastolic membrane potential (DMP): APD90 = 141.7 +/- 7.0 msec and DMP -86.2 +/- 1.4 mV (n = 6) at 37 degrees C versus 235.7 +/- 7.8 msec and -75.6 +/- 1.0 mV at 20 degrees C (n = 7). At 37 degrees C, bimakalim (0.1-10 mumol.l-1) shortened APD in a concentration-dependent fashion. 4. APD90 was markedly reduced from 141.7 +/- 7.0 msec without bimakalim to 9.5 +/- 2.6 msec with 10 mumol.l-1 bimakalim (n = 6); this effect was blocked by glibenclamide. DMP was hyperpolarized by bimakalim. More bimakalim was required to shorten APs during mild and moderate hypothermia. The 50% effective concentration (EC50) of bimakalim required to maximally shorten APD90 was 0.96 +/- 0.10 mumol.l-1 at 37 degrees C; this increased to 3.96 +/- 0.24 mumol.l-1 at 27 degrees C, and to 12.34 +/- 0.72 mumol.l-1 at 20 degrees C. Relative to hypothermia-induced depolarization, bimakalim hyperpolarized DMP toward drug-free values obtained at 37 degrees C. 5. These results indicate that hypothermia shifts the bimakalim concentration APD90 response curve to the right such that 13 times more bimakalim is required at 20 degrees C shorten APD by the same amount as at 37 degrees C. Bimakalim also reverses hypothermia-induced AP lengthening and tends to reverse the hypothermia-induced decrease in DMP. 6. These findings aid in our understanding of the cardioprotective effects of KATP channel openers during hypothermia.

Diazepam-induced Ca(2+)-channel blockade reduces hypothermia-induced electromechanical changes in isolated guinea pig ventricular muscle.

Calcium-channel blockers reduce the in vitro effects of hypothermia and benzodiazepines have been reported to reduce inward calcium flow through L-type cardiac-calcium channels. Thus, this study was designed to determine if diazepam could reduce hypothermia-induced changes in ventricular papillary muscle electromechanical activity. Conventional microelectrode techniques were used while force was recorded using a miniature force transducer. Six experimental groups of electrically paced papillary muscles were formed (n = 6 per group). One was exposed to one microM nisoldipine and four were exposed to one of four diazepam concentrations (0.1, 1.0, 10 or 100 microM). A final group had no drug and provided a time-matched control. The effects were determined at 37 degrees C and then at 27 degrees C. At 37 degrees C, diazepam initially increased and then reduced inotropy and APD90. Nisoldipine reduced both APD90 and inotropy. At 27 degrees C, 100 microM diazepam and nisoldipine (1.0 microM) reduced the hypothermia-induced lengthening of APD and the increase in force. Although diazepam reduced the hypothermia-induced alterations, the concentration required to do so (100 microM) suggests that this effect has little role in clinical use.

Influence of hypothermia on the cardiac effects of propranolol observed in isolated rat atria.

UNLABELLED: 1. The purpose was to determine if hypothermia influences cardiac responses to propranolol. 2. Rat atria were used and 11 test groups were created; 3 control groups were maintained at 35, 28 or 20 degrees C. Two additional groups, at each temperature, were exposed to 1.2 or 40 mumol/l propranolol. Developed force and effective refractory period (ERP) were measured. 3. At 35 degrees C, propranolol decreased developed force and lengthened ERP. At 28 degrees C, propranolol did not affect developed force, but ERP was lengthened. At 20 degrees C, 1.2 microM propranolol neither affected developed force or ERP, but 40 microM reduced developed force and lengthened ERP. CONCLUSION: hypothermia reduced propranolol's usual negative inotropic effect.

Electrical restitution in diseased human ventricular myocardium.

Action potential configuration and electrical restitution were studied in diseased human ventricular muscle by comparing the characteristics of hypertrophic (HYP) and dilated (DIL) human ventricular preparations. Conventional microelectrode techniques were used to evaluate action potentials evoked at increasingly longer diastolic intervals. The steady-state action potential duration (APD90) was significantly longer in DIL than in HYP preparations (393 +/- 5 ms, n = 4 and 296 +/- 11 ms, n = 4, respectively; P < 0.001, mean +/- SEM). In the dilated preparations studied at long diastolic intervals, the initial period of rapid repolarization (phase 1) was absent, and the rate of final repolarization (phase 3) was reduced. Electrical restitution relations in these preparations were fitted as the sum of two exponentials. The time constant of the fast component was significantly longer in DIL than in HYP preparations (242 +/- 9 ms and 121 +/- 4 ms, respectively; P < 0.001). No difference was observed in the time constants for the slow component of restitution in the two groups. Electrical restitution was also studied in single human ventricular myocytes by using patch clamp techniques. The initial 600 ms period of restitution was fitted in these cells to a monoexponential function. The time constant for this period of the restitution relation was significantly longer, while the estimated amplitude of this early rising phase was significantly lower in human cells obtained from DIL hearts than the respective parameters obtained in the healthy canine and guinea pig cells also examined. The observed changes in the restitution kinetics of the dilated human heart are, likely, the consequence of alterations in the ionic currents that underlie the cardiac action potential.