New digital thermometer with fast time constant

Systemic vascular effects of hydralazine, prazosin, captopril, and nifedipine were studied in 115 anesthetized dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. At three dose levels producing comparable reductions in systemic arterial pressure (30–40% at the highest dose), these drugs had different effects on flow distribution and venous return. Hydralazine and prazosin had parallel and balanced effects on arterial resistance of the two vascular compartments, and flow distribution was unaltered. Captopril preferentially reduced arterial resistance of the compartment with a slow time constant for venous return (−26 ± 6%, −30 ± 6%, −50 ± 5% at 0.02, 0.10, and 0.50 mg∙kg−1∙h−1, respectively; [Formula: see text]) without altering arterial resistance of the fast time-constant compartment. Blood flow to the slow time-constant compartment was increased 43 ± 14% at the highest dose, and central blood volume was reduced 108 ± 15 mL. In contrast, nifedipine had a balanced effect on arterial resistance with the lowest dose (0.025 mg/kg) but caused a preferential reduction in arterial resistance of the fast time-constant compartment at higher doses (−38 ± 4% and −55 ± 2% at 0.05 and 0.10 mg/kg, respectively). Blood flow to the slow time-constant compartment was reduced 36 ± 5% at the highest dose of nifedipine, and central blood volume was increased 66 ± 12 mL. Total systemic venous compliance was unaltered or slightly reduced by each of the four drugs. These results add further evidence to the hypothesis that peripheral blood flow distribution is a major determinant of venous return to the heart.

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Analysis of venous flow transients for estimation of vascular resistance, compliance, and blood flow distribution

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-292 ◽

1987 ◽

Vol 65 (9) ◽

pp. 1884-1890 ◽

Cited By ~ 2

Author(s):

Richard I. Ogilvie ◽

Danuta Zborowska-Sluis

Keyword(s):

Time Constant ◽

Venous Return ◽

Fast Time ◽

Slow Time ◽

Venous Outflow ◽

Venous Flow ◽

Time Constants ◽

Slow Time Constant ◽

Over Time ◽

Flow Transients

We analysed venous flow transients using a long venous circuit and right heart bypass in 17 dogs after a rapid decrease in atrial pressure. A biphase curve was obtained which we decomposed into a two-compartmental model, one with a fast time constant for venous return (0.069 min) and 52% of total circulating flow [Formula: see text], and one with a slower time constant (0.456 min) and 48% of [Formula: see text]. Subsequently, separate drainage from splanchnic and peripheral beds (with the renal venous return in the peripheral bed drainage) allowed comparison of time constants and venous outflow in these beds. The sum of the venous outflow volumes over time during separate drainage was indistinguishable from the single biphasic venous outflow volume curve over time observed with a long circuit and single reservoir. The fast time constant of the biphasic curve was not different from that determined by separate drainage from the peripheral circulation. The slow time constant of the single biphasic curve of 0.456 min was hybrid of two time constants, 0.216 min in the splanchnic bed and 0.862 min in the peripheral bed. Separate drainage from peripheral and splanchnic vascular beds demonstrated that the peripheral bed constituted 70% of venous outflow in the fast time constant compartment using Caldini's technique, whereas the splanchnic bed constituted 63% of venous outflow in the slow time constant compartment. It is concluded that, although Caldini's technique demonstrates biphasic venous flow transients, neither the fast nor the slow time constant compartments resolved from this analysis represent a particular anatomical region or vascular bed.

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Effects of inotropic agents on arterial resistance and venous compliance in anesthetized dogs

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y82-136 ◽

1982 ◽

Vol 60 (7) ◽

pp. 968-976 ◽

Cited By ~ 3

Author(s):

R. I. Ogilvie

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Time Constant ◽

Right Atrial ◽

Fast Time ◽

Vascular Effects ◽

Venous Compliance ◽

Peripheral Vasculature ◽

Arterial Resistance ◽

Flat Dose

Systemic vascular effects of dopamine, dobutamine, and prenalterol were studied in 45 anesthetized open-chest dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. Dopamine (2.5–10 μg∙kg−1∙min−1) was the most active drug with dose-related increases in heart rate 6–19%, arterial pressure (Pa) 3–36%, and venous compliance 2–25%. Small doses of dopamine (2.5 and 5 μg∙kg−1∙min−1) reduced arterial resistance of the slow time-constant compartment increasing [Formula: see text] distribution to that compartment 21–42%, whereas larger doses increased both arterial resistance and venous compliance in that compartment. Arterial resistance in the fast time-constant compartment increased with all doses of dopamine. Dobutamine (2.5–10 μg∙kg−1∙min−1) modestly increased heart rate 2–11% and Pa 9–12%) without altering [Formula: see text] distribution demonstrating a relatively flat dose response. Dobutamine 2.5–5 μg∙kg−1∙min−1 increased venous compliance 5–10% while 10 μg∙kg−1∙min−1 had no effect or decreased compliance of both compartments. Prenalterol 3 μg∙kg−1∙min−1 increased Pa 9% primarily by increasing arterial resistance in the fast time-constant compartment without altering heart rate or blood flow distribution. Doses of prenalterol 10–100 times greater caused dose-dependent reductions in Pa and vascular compliance. In this animal model of the circulation with a fixed cardiac output, dopamine had the greatest effect on the peripheral vasculature and chronotropy.

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Periodicity, time constants of drainage, and the mechanical determinants of peak cardiac output during exercise

Journal of Applied Physiology ◽

10.1152/japplphysiol.00688.2018 ◽

2019 ◽

Vol 127 (6) ◽

pp. 1611-1619

Author(s):

Sheldon Magder ◽

Gabriel Famulari ◽

Brian Gariepy

Keyword(s):

Cardiac Output ◽

Computational Model ◽

Time Constant ◽

Muscle Contractions ◽

Fast Time ◽

Fractional Flow ◽

Time Constants ◽

Peripheral Muscle ◽

Muscle Region ◽

Muscle Compartment

To analyze mechanical adaptations that must occur in the cardiovascular system to reach the high cardiac outputs known to occur at peak aerobic performance, we adapted a computational model of the circulation by adding a second parallel venous compartment as proposed by August Krogh in 1912. One venous compartment has a large compliance and slow time constant of emptying; it is representative of the splanchnic circulation. The other has a low compliance and fast time constant of emptying and is representative of muscle beds. Fractional distribution between the two compartments is an important determinant of cardiac output. Parameters in the model were based on values from animal and human studies normalized to a 70 kg male. The baseline cardiac output was set at 5 L/min, and we aimed for 25 L/min at peak exercise with a fractional flow to the peripheral-muscle region of 90%. Finally, we added the equivalent of a muscle pump. Adjustments in circuit and cardiac parameters alone increased cardiac output to only 15.6 L/min because volume accumulated in the muscle compartment and limited a higher cardiac output. Addition of muscle contractions decompressed the muscle region and allowed cardiac output to increase to 23.4 L/min. The pulsatility of blood flow imposes important constraints on the adaptations of cardiac and circulatory functions because it fixes the times for filling and emptying. Flow is further limited by the limits of cardiac filling on each beat. Muscle contractions play a key role by decompressing volume that would otherwise accumulate in the muscle vasculature and by decreasing the time for stroke return to the right ventricle. NEW & NOTEWORTHY We used a computational model of the circulation and previous human and animal data to model mechanical changes in the heart and circulation that are needed to reach the known high cardiac output at peak aerobic exercise. Key points are that time constants of drainage of circulatory compartments put limits on peak flow in a pulsatile system. Muscle contractions increase the rate of return to the heart and by doing so prevent accumulation of volume in the muscle compartment and greatly increase circulatory capacity.

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A Role for Short-Term Synaptic Facilitation and Depression in the Processing of Intensity Information in the Auditory Brain Stem

Journal of Neurophysiology ◽

10.1152/jn.01030.2006 ◽

2007 ◽

Vol 97 (4) ◽

pp. 2863-2874 ◽

Cited By ~ 37

Author(s):

K. M. MacLeod ◽

T. K. Horiuchi ◽

C. E. Carr

Keyword(s):

Synaptic Plasticity ◽

Brain Stem ◽

Time Constant ◽

Cochlear Nucleus ◽

Auditory Nerve ◽

Brain Slices ◽

Fast Time ◽

Short Term ◽

Intensity Information

The nature of the synaptic connection from the auditory nerve onto the cochlear nucleus neurons has a profound impact on how sound information is transmitted. Short-term synaptic plasticity, by dynamically modulating synaptic strength, filters information contained in the firing patterns. In the sound-localization circuits of the brain stem, the synapses of the timing pathway are characterized by strong short-term depression. We investigated the short-term synaptic plasticity of the inputs to the bird's cochlear nucleus angularis (NA), which encodes intensity information, by using chick embryonic brain slices and trains of electrical stimulation. These excitatory inputs expressed a mixture of short-term facilitation and depression, unlike those in the timing nuclei that only depressed. Facilitation and depression at NA synapses were balanced such that postsynaptic response amplitude was often maintained throughout the train at high firing rates (>100 Hz). The steady-state input rate relationship of the balanced synapses linearly conveyed rate information and therefore transmits intensity information encoded as a rate code in the nerve. A quantitative model of synaptic transmission could account for the plasticity by including facilitation of release (with a time constant of ∼40 ms), and a two-step recovery from depression (with one slow time constant of ∼8 s, and one fast time constant of ∼20 ms). A simulation using the model fit to NA synapses and auditory nerve spike trains from recordings in vivo confirmed that these synapses can convey intensity information contained in natural train inputs.

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Design of a State Space Controller for an Intercooled, Regenerated (ICR) Gas Turbine Engine

Volume 2: Aircraft Engine; Marine; Microturbines and Small Turbomachinery ◽

10.1115/94-gt-374 ◽

1994 ◽

Author(s):

Karl F. Prigge ◽

Jerry W. Watts ◽

Terrence E. Dwan

Keyword(s):

Gas Turbine ◽

Time Constant ◽

Gas Turbine Engine ◽

The Other ◽

Pole Placement ◽

Inlet Temperature ◽

Fast Time ◽

Turbine Engine ◽

Power Turbine ◽

Input Control

A multi-input, multi-output (MIMO) controller for an advanced gas turbine has been developed and tested using a computer simulation. The engine modeled is a two-and-one half spool gas turbine with both an intercooler and a regenerator. In addition, variable stator vanes are present in the free-power turbine. This advanced engine is proposed for future naval propulsion for both mechanical drive ships and electrical drive ships. The designed controller controls free-power turbine speed and turbine inlet temperature using fuel flow and angle of the stator vanes. The controller will also have four modes of operation to deal with over temperature and over speed conditions. An eight state reduced order controller was used with pole placement and LQR to arrive at control gains. Both these methods required considerable insight into the problem. This insight was provided by previous experience with controller design for a less complicated engine, and also by use of a polyhedral search model of the gas turbine engine. The difficulty with a MIMO controller was that both inputs affect both of the control variables. The classical resolution of this problem is to have one input control one variable at a fast time constant and the other input control the other variable at a slow time constant. The “optimal” resolution of this problem is analyzed using the transient curves and basic control theory.

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Properties of a Calcium-Activated K+ Current on Interneurons in the Developing Rat Hippocampus

Journal of Neurophysiology ◽

10.1152/jn.2000.83.6.3453 ◽

2000 ◽

Vol 83 (6) ◽

pp. 3453-3461 ◽

Cited By ~ 21

Author(s):

Takuya Aoki ◽

Scott C. Baraban

Keyword(s):

Time Constant ◽

Pyramidal Neurons ◽

Pyramidal Cells ◽

Cell Types ◽

Current Amplitude ◽

Kinetic Properties ◽

Fast Time ◽

Peak Current ◽

Time To Peak ◽

Ca1 Pyramidal Neurons

Calcium-activated potassium currents have an essential role in regulating excitability in a variety of neurons. Although it is well established that mature CA1 pyramidal neurons possess a Ca2+-activated K+ conductance ( I K(Ca)) with early and late components, modulation by various endogenous neurotransmitters, and sensitivity to K+ channel toxins, the properties of I K(Ca) on hippocampal interneurons (or immature CA1 pyramidal neurons) are relatively unknown. To address this problem, whole-cell voltage-clamp recordings were made from visually identified interneurons in stratum lacunosum-moleculare (L-M) and CA1 pyramidal cells in hippocampal slices from immature rats (P3–P25). A biphasic calcium-activated K+ tail current was elicited following a brief depolarization from the holding potential (−50 mV). Analysis of the kinetic properties of I K(Ca)suggests that an early current component differs between these two cell types. An early I K(Ca) with a large peak current amplitude (200.8 ± 13.2 pA, mean ± SE), slow time constant of decay (70.9 ± 3.3 ms), and relatively rapid time to peak (within 15 ms) was observed on L-M interneurons ( n = 88), whereas an early I K(Ca) with a small peak current amplitude (112.5 ± 7.3 pA), a fast time constant of decay (39.4 ± 1.6 ms), and a slower time-to-peak (within 26 ms) was observed on CA1 pyramidal neurons ( n = 85). Removal of extracellular calcium or addition of inorganic Ca2+ channel blockers (cadmium, nickel, or cobalt) was used to demonstrate the calcium dependence of these currents. Addition of norepinephrine, carbachol, and a variety of channel toxins (apamin, iberiotoxin, verruculogen, paxilline, penitrem A, and charybdotoxin) were used to further distinguish between I K(Ca) on these two hippocampal cell types. Verruculogen (100 nM), carbachol (100 μM), apamin (100 nM), TEA (1 mM), and iberiotoxin (50 nM) significantly reduced early I K(Ca) on CA1 pyramidal neurons; early I K(Ca) on L-M interneurons was inhibited by apamin and TEA. Combined with previous work showing that the firing properties of hippocampal interneurons and pyramidal cells differ, our kinetic and pharmacological data provide strong support for the hypothesis that different types of Ca2+-activated K+ current are present on these two cell types.

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