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PubMed2001

Color stability of provisional restorative materials after accelerated aging.

PURPOSE: Color of 11 provisional restorative materials (4 acrylic resins and 7 resin composites) was evaluated by reflection spectrophotometry immediately after fabrication, after aging for 15 kJ/m(2), and after aging for 60 kJ/m(2) to determine relative color stability under experimental aging conditions. MATERIALS AND METHODS: Specimens of provisional restorative materials were polymerized according to manufacturers' instructions and aged in an artificial aging chamber with exposure to a total ultraviolet irradiation of 60 kJ/m(2) in increments of 15 kJ/m(2). Color was measured by CIE L*a*b* on a reflection spectrophotometer before and after aging. Color change (Delta E*) was calculated and analyzed statistically by analysis of variance with repeated measures after 15 and 60 kJ/m(2) intervals of aging. RESULTS: Statistically significant changes in color were observed after accelerated aging at both the initial and final aging intervals. Five of the 11 provisional materials tested showed perceptible color change (Delta E* from 3.6 to 9.3) after accelerated aging of 15 kJ/m(2). Seven of the 11 provisional materials tested showed perceptible color change (Delta E* from 3.4 to 9.4) after accelerated aging of 60 kJ/m(2). CONCLUSIONS: Clinically perceptible color changes (Delta E* Delta 3.3) can be expected in some acrylic resin and composite resin provisional materials after accelerated aging.

Acrylic Resins↗

PubMed2006

Comparison of a standard versus accelerated dosing regimen for D,L-sotalol for the treatment of atrial and ventricular dysrhythmias.

BACKGROUND: The current recommended starting dose of sotalol is 80 mg orally twice per day, followed by a judicious increase in dosage every 3 days under continuous telemetry monitoring. We hypothesized that sotalol administered at a higher starting dose (120 or 160 mg twice daily) would allow a more rapid attainment of therapeutic response with an acceptable safety and comparable efficacy profile. METHODS: Two hundred nine inpatients with various atrial and ventricular dysrhythmias were begun on either a standard starting dose (80 mg b.i.d.) or an accelerated dose (120 or 160 mg b.i.d.) of sotalol. In-hospital occurrences of drug-related adverse effects (proarrhythmic and others), drug efficacy, and length of hospitalization were retrospectively compared between the two groups. RESULTS: Ten patients (9.3%) in the 80 mg b.i.d. starting dose group experienced a cardiac adverse effect of sotalol as compared to 15 patients (14.9%) in the accelerated dose group (P = 0.286). The mean amount of corrected QT (QTc) prolongation over baseline was not significantly different between the two groups at hospital discharge (22.5 ms vs 21.6 ms, P = 0.898). There was a trend toward more noncardiac side effects of sotalol in the accelerated dose group: 2 (1.9%) versus 7(6.9%), P = 0.092. The average length of hospital stay was similar in the two groups (6.8 days vs 7.4 days, P = 0.558). CONCLUSION: Initiating sotalol at 120-160 mg orally twice per day marginally increases the risk of cardiac and non-cardiac side effects compared to the standard starting regimen of 80 mg b.i.d. Such an accelerated dosing regimen neither shortened hospitalization nor had any effect on treatment efficacy in this retrospective analysis.

Administration, Oral↗

PubMed2005

Rat cytomegalovirus-accelerated transplant vascular sclerosis is reduced with mutation of the chemokine-receptor R33.

Cytomegalovirus (CMV) infection accelerates transplant vascular sclerosis (TVS) and chronic rejection (CR) in both human and animal solid organ transplantation models. The host/viral mechanisms involved in this process are unclear. We examine the role of the rat CMV (RCMV)-encoded chemokine-receptor R33 in the development of TVS using a rat heart transplantation/CR model. F344 heart grafts were transplanted heterotopically into Lewis recipients. The ability of RCMV lacking the R33 gene (RCMV-Deltar33) to accelerate CR/TVS (neointimal index, NI) was compared to wild-type (WT) RCMV. Allograft recipients were infected with 1 x 10(5) pfu RCMV or RCMV-Deltar33 on postoperative day (POD) 1. Grafts from RCMV-Deltar33-infected recipients demonstrated an accelerated time to allograft CR compared to grafts from uninfected recipients (POD = 56 vs. 90), this was slower than that seen in grafts from WT-RCMV-infected recipients (POD = 45). Similarly, the degree of graft TVS formation at terminal rejection in RMCV-Deltar33 infected recipients was more severe than uninfected recipients (NI = 63 vs. 45), yet not as severe as in WT-RCMV infected recipients (NI = 83). In parallel, RCMV-Deltar33 failed to induce vascular smooth muscle cell (SMC) migration in vitro, whereas WT-RCMV induced substantial migration. The RCMV-encoded chemokine-receptor r33 is critical for RCMV-accelerated TVS/CR and vascular SMC migration.

Animals↗

PubMed1987

Acceleration of desensitization by agonist pre-treatment in the snake.

1. The kinetics of carbachol-induced desensitization have been studied in snake twitch-muscle fibres maintained in an isotonic potassium propionate solution and voltage clamped to +50 mV. 2. Microperfusion of carbachol (162-756 microM) induces a transient outward current which peaks within a few seconds and then slowly decays towards the base line. The time course of current decay estimates the time course of desensitization onset. 3. Brief exposure (30 s) to a 'conditioning' concentration of agonist (10.8 microM) accelerates the desensitization onset produced by exposure to higher 'test' concentrations of agonist (162-756 microM). 4. The acceleration of desensitization by pre-treatment with 10.8 microM-carbachol was independent of the duration of exposure between 15 and 60 s. This observation indicated that the mechanism responsible for the alteration in desensitization kinetics by treatment with 10.8 microM-carbachol differed from that responsible for the time-dependent development of desensitization produced in the presence of higher carbachol concentrations. 5. Pre-treatment with the muscarinic agonists, methylcholine and bethanechol, did not accelerate 216 microM-carbachol-induced desensitization, suggesting that the alteration of desensitization kinetics by pre-treatment was specific for nicotinic agonists. 6. The conditioning concentrations of carbachol (5.4-10.8 microM) produced no measurable outward current in muscle fibres voltage clamped to +50 mV. Further, in patch-clamp recordings it was observed that, with these concentrations of carbachol, there was no channel activity in many successful patches voltage clamped to +50 mV and, when present, the frequency of channel activity was very low. These results demonstrated that the alteration in desensitization was not the consequence of significant amounts of either receptor activation or desensitization produced by the conditioning concentration. 7. Exposure to 10.8 microM-carbachol for periods of up to 150 s did not change the amplitude of miniature end-plate currents recorded at end-plates voltage clamped to +50 mV. These results also demonstrated that the acceleration of desensitization by pre-treatment with conditioning concentrations of agonist was not due to partial desensitization occurring during the pre-treatment period. 8. Our results are consistent with the view that there are distinct populations of agonist binding sites on the acetylcholine receptor which separately regulate desensitization and channel opening.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1995

Acceleration of puberty onset in female mice by male urinary proteins.

1. Puberty onset in female mice is accelerated by exposure to conspecific adult male urine, which acts through the vomeronasal organ and the accessory olfactory system. A distinctive component of adult male mouse urine is the major urinary protein complex (MUP), which is a lipocalin; it has a hydrophobic pocket that binds small endogenous volatile molecules. The MUP gene family also codes for a hexapeptide, which has four residues in common with the N-terminal region of MUP. 2. MUP, the volatiles bound to MUP and the MUP-related hexapeptide have been tested for the induction of puberty acceleration by measuring the increase in uterus weight related to the first pro-oestrus phase. MUP, together with its bound volatiles, induces puberty acceleration. Its activity is retained even when the volatiles have been removed either by organic extraction or competition displacement with a high-affinity ligand. 3. MUP-related hexapeptide also induces puberty acceleration in female mice. In contrast, the odorants bound to MUP do not exert this effect. 4. It is proposed that the vomeronasal organ contains receptors that recognize the short N-terminal consensus sequence, N-Glu-Glu-Ala-X-Ser (where X is a polar residue), common to both MUP and the hexapeptide.

Animals↗

PubMed2006

Acceleration of AMPA receptor kinetics underlies temperature-dependent changes in synaptic strength at the rat calyx of Held.

It is well established that synaptic transmission declines at temperatures below physiological, but many in vitro studies are conducted at lower temperatures. Recent evidence suggests that temperature-dependent changes in presynaptic mechanisms remain in overall equilibrium and have little effect on transmitter release at low transmission frequencies. Our objective was to examine the postsynaptic effects of temperature. Whole-cell patch-clamp recordings from principal neurons in the medial nucleus of the trapezoid body showed that a rise from 25 degrees C to 35 degrees C increased miniature EPSC (mEPSC) amplitude from -33 +/- 2.3 to -46 +/- 5.7 pA (n=6) and accelerated mEPSC kinetics. Evoked EPSC amplitude increased from -3.14 +/- 0.59 to -4.15 +/- 0.73 nA with the fast decay time constant accelerating from 0.75 +/- 0.09 ms at 25 degrees C to 0.56 +/- 0.08 ms at 35 degrees C. Direct application of glutamate produced currents which similarly increased in amplitude from -0.76 +/- 0.10 nA at 25 degrees C to -1.11 +/- 0.19 nA 35 degrees C. Kinetic modelling of fast AMPA receptors showed that a temperature-dependent scaling of all reaction rate constants by a single multiplicative factor (Q10=2.4) drives AMPA channels with multiple subconductances into the higher-conducting states at higher temperature. Furthermore, Monte Carlo simulation and deconvolution analysis of transmission at the calyx of Held showed that this acceleration of the receptor kinetics explained the temperature dependence of both the mEPSC and evoked EPSC. We propose that acceleration in postsynaptic AMPA receptor kinetics, rather than altered presynaptic release, is the primary mechanism by which temperature changes alter synaptic responses at low frequencies.

Animals↗

PubMed2000

A Monte Carlo dosimetry-based evaluation of the 7Li(p,n)7Be reaction near threshold for accelerator boron neutron capture therapy.

Advanced methods of boron neutron capture therapy (BNCT) use an epithermal neutron beam in conjunction with tumor-targeting boron compounds for irradiation of glioblastomas and metastatic melanomas. A common neutron-producing reaction considered for accelerator-based BNCT is 7Li(p,n)7Be, whose cross section increases very rapidly within several tens of keV of the reaction threshold at 1.88 MeV. Operation in the proton energy region near threshold will have an appreciable thick target neutron yield, but the neutrons produced will have relatively low energies that require little moderation to reach the epithermal range desirable for BNCT. Because of its relatively low projected accelerator cost and the portability of the neutron source/target assembly, BNCT based on the near-threshold technique is considered an attractive candidate for widespread hospital use. A systematic Monte Carlo N-Particle (MCNP) investigation of the dosimetric properties of near-threshold neutron beams has been performed. Results of these studies indicate that accelerator proton energies between 1.93 and 1.99 MeV, using 5 cm of H2O moderator followed by thin 6Li and Pb shields, can provide therapeutically useful beams with treatment times less than one hour and accelerator currents less than 5 mA.

Beryllium↗

PubMed2000

Development and construction of a neutron beam line for accelerator-based boron neutron capture synovectomy.

A potential application of the 10B(n, alpha)7Li nuclear reaction for the treatment of rheumatoid arthritis, termed Boron Neutron Capture Synovectomy (BNCS), is under investigation. In an arthritic joint, the synovial lining becomes inflamed and is a source of great pain and discomfort for the afflicted patient. The goal of BNCS is to ablate the synovium, thereby eliminating the symptoms of the arthritis. A BNCS treatment would consist of an intra-articular injection of boron followed by neutron irradiation of the joint. Monte Carlo radiation transport calculations have been used to develop an accelerator-based epithermal neutron beam line for BNCS treatments. The model includes a moderator/reflector assembly, neutron producing target, target cooling system, and arthritic joint phantom. Single and parallel opposed beam irradiations have been modeled for the human knee, human finger, and rabbit knee joints. Additional reflectors, placed to the side and back of the joint, have been added to the model and have been shown to improve treatment times and skin doses by about a factor of 2. Several neutron-producing charged particle reactions have been examined for BNCS, including the 9Be(p,n) reaction at proton energies of 4 and 3.7 MeV, the 9Be(d,n) reaction at deuteron energies of 1.5 and 2.6 MeV, and the 7Li(p,n) reaction at a proton energy of 2.5 MeV. For an accelerator beam current of 1 mA and synovial boron uptake of 1000 ppm, the time to deliver a therapy dose of 10,000 RBEcGy ranges from 3 to 48 min, depending on the treated joint and the neutron producing charged particle reaction. The whole-body effective dose that a human would incur during a knee treatment has been estimated to be 3.6 rem or 0.75 rem, for 1000 ppm or 19,000 ppm synovial boron uptake, respectively, although the shielding configuration has not yet been optimized. The Monte Carlo design process culminated in the construction, installation, and testing of a dedicated BNCS beam line on the high-current tandem electrostatic accelerator at the Laboratory for Accelerator Beam Applications at the Massachusetts Institute of Technology.

Animals↗

PubMed2006

Accelerated evolution of conserved noncoding sequences in humans.

Changes in gene regulation likely influenced the profound phenotypic divergence of humans from other mammals, but the extent of adaptive substitution in human regulatory sequences remains unknown. We identified 992 conserved noncoding sequences (CNSs) with a significant excess of human-specific substitutions. These accelerated elements were disproportionately found near genes involved in neuronal cell adhesion. To assess the uniqueness of human noncoding evolution, we examined CNSs accelerated in chimpanzee and mouse. Although we observed a similar enrichment near neuronal adhesion genes in chimpanzee, the accelerated CNSs themselves exhibited almost no overlap with those in human, suggesting independent evolution toward different neuronal phenotypes in each species. CNSs accelerated in mouse showed no bias toward neuronal cell adhesion. Our results indicate that widespread cis-regulatory changes in human evolution may have contributed to uniquely human features of brain development and function.

Animals↗

PubMed1995

Natural assemblages of marine bacteria exhibiting high-speed motility and large accelerations.

Natural communities of marine bacteria, an isolate (FMB-Bf3) from one marine community, and Escherichia coli were examined by video microscopy for the magnitude and uniformity of their speed. Natural communities formed tight microswarms that showed higher speeds (mean = 230 microns s-1) than did E. coli (15 microns s-1) or FMB-Bf3 (mean = 62 microns s-1). Outside the microswarms, the marine bacteria slowed to 45 microns s-1. Between turns, in mid run, and while travelling in straight lines, the natural-community bacteria accelerated up to 1,450 microns s-2 while the cultured bacteria showed maximum accelerations of 70 and 166 microns s-2. The frequency distribution of speed change for the marine bacteria was skewed towards a few large negative accelerations and a range of positive accelerations. The general pattern was one of relatively slow increases in speed followed by abrupt declines. The results indicate that the mechanical generation and energetic maintenance, as well as the environmental function, of bacterial motility need reappraisal. We conclude that the standard bacterial motility parameters of low and uniform speed, derived from culture-based studies, are not necessarily applicable to marine bacterial communities.

Escherichia coli↗

PubMed2003

Cytomegalovirus-mediated upregulation of chemokine expression correlates with the acceleration of chronic rejection in rat heart transplants.

Cytomegalovirus (CMV) infections have been shown to dramatically affect solid organ transplant graft survival in both human and animal models. Recently, it was demonstrated that rat CMV (RCMV) infection accelerates the development of transplant vascular sclerosis (TVS) in both rat heart and small bowel graft transplants. However, the mechanisms involved in this process are still unclear. In the present study, we determined the kinetics of RCMV-accelerated TVS in a rat heart transplant model. Acute RCMV infection enhances the development of TVS in rat heart allografts, and this process is initiated between 21 and 24 days posttransplantation. The virus is consistently detected in the heart grafts from day 7 until day 35 posttransplantation but is rarely found at the time of graft rejection (day 45 posttransplantation). Grafts from RCMV-infected recipients had upregulation of chemokine expression compared to uninfected controls, and the timing of this increased expression paralleled that of RCMV-accelerated neointimal formation. In addition, graft vessels from RCMV-infected grafts demonstrate the increased infiltration of T cells and macrophages during periods of highest chemokine expression. These results suggest that CMV-induced acceleration of TVS involves the increased graft vascular infiltration of inflammatory cells through enhanced chemokine expression.

Animals↗

PubMed2005

Expression of interleukin-4 by recombinant respiratory syncytial virus is associated with accelerated inflammation and a nonfunctional cytotoxic T-lymphocyte response following primary infection but not following challenge with wild-type virus.

The outcome of a viral infection or of immunization with a vaccine can be influenced by the local cytokine environment. In studies of experimental vaccines against respiratory syncytial virus (RSV), an increased stimulation of Th2 (T helper 2) lymphocytes was associated with increased immunopathology upon subsequent RSV infection. For this study, we investigated the effect of increased local expression of the Th2 cytokine interleukin-4 (IL-4) from the genome of a recombinant RSV following primary infection and after a challenge with wild-type (wt) RSV. Mice infected with RSV/IL-4 exhibited an accelerated pulmonary inflammatory response compared to those infected with wt RSV, although the wt RSV group caught up by day 8. In the first few days postinfection, RSV/IL-4 was associated with a small but significant acceleration in the expansion of pulmonary T lymphocytes specific for an RSV CD8(+) cytotoxic T-lymphocyte (CTL) epitope presented as a major histocompatibility complex class I tetramer. However, by day 7 the response of tetramer-positive T lymphocytes in the wt RSV group caught up and exceeded that of the RSV/IL-4 group. At all times, the CTL response of the RSV/IL-4 group was deficient in the production of gamma interferon and was nonfunctional for in vitro cell killing. The accelerated inflammatory response coincided with an accelerated accumulation and activation of pulmonary dendritic cells early in infection, but thereafter the dendritic cells were deficient in the expression of B7-1, which governs the acquisition of cytolytic activity by CTL. Following a challenge with wt RSV, there was an increase in Th2 cytokines in the animals that had previously been infected with RSV/IL-4 compared to those previously infected with wt RSV, but the CD8(+) CTL response and the amount of pulmonary inflammation were not significantly different. Thus, a strong Th2 environment during primary pulmonary immunization with live RSV resulted in early inflammation and a largely nonfunctional primary CTL response but had a minimal effect on the secondary response.

Animals↗

PubMed1992

Symptoms after accelerated immunisation.

OBJECTIVE: To document the incidence of symptoms after accelerated immunisation with diphtheria-tetanus-pertussis vaccine. DESIGN: Controlled study of children immunised with adsorbed diphtheria-tetanus-pertussis vaccine at accelerated and standard schedules. SETTING: Colchester and north Hertfordshire. SUBJECTS: 107 children scheduled to receive immunisation at 2, 3, and 4 months of age and 115 children scheduled to receive immunisation at 3, 4 1/2 to 5, and 8 1/2 to 11 months of age. MAIN OUTCOME MEASURES: Parentally recorded symptoms, axillary temperatures, and size of local redness and swelling at the injection site during the seven days after immunisation. RESULTS: In general symptoms occurred less frequently with the accelerated schedule. Proportions of parents reporting axillary temperatures greater than 37.2 degrees C or local redness or swelling greater than 2.5 cm after the third dose of vaccine were significantly reduced in the accelerated schedule group. CONCLUSION: Immunisation at 2, 3, and 4 months of age is likely to cause fewer reactions than immunisation at 3, 4 1/2 to 5, and 8 1/2 to 11 months of age.

Diphtheria-Tetanus-Pertussis Vaccine↗

PubMed1975

Structure--activity relations for the acceleration of efflux of noradrenaline from adrenergic nerves in rabbit atria by sympathomimetic amines.

Atria from reserpine-pretreated rabbits were exposed to pargyline to inhibit monoamine oxidase (amine oxidase (flavin-containing) EC 1.4.3.4) and subsequently incubated in (-)-[3H]noradrenaline to allow the cytoplasmic accumulation of amine in adrenergic nerves. The structure-activity relations for acceleration of efflux of cytoplasmic amine were examined. The most potent agents studied were (+)- and (-)-amphetamine, beta-phenethylamine, phentermine, and mephentermine. Ability to accelerate efflux was reduced by addition of phenolic hydroxyl groups, by phenolic methylation, by beta-hydroxylation, and by N-substitution. The structure-activity relations for acceleration of efflux differ notably from those for uptake, inhibition of uptake, or release of noradrenaline from adrenergic nerves, reported in previous studies. The ability and potency of a given phenethylamine derivative to accelerate the efflux of cytoplasmic noradrenaline is probably determined by such factors as the lipid solubility of the amine, the affinity of the amine for the uptake and efflux site(s) for noradrenaline, and competition for any reserpine-resistant intraneuronal binding sites.

Animals↗

PubMed1996

Hepatic artery: variability in measurement of resistive index and systolic acceleration time in healthy volunteers.

PURPOSE: To determine the intrinsic sampling variability of measurements of hepatic artery resistive index and systolic acceleration time in healthy subjects and to estimate the components of variability attributable to the sonographer, individual measurement, and subject. MATERIALS AND METHODS: In a randomized, controlled (blinded) fashion, nine sonographers measured hepatic artery resistive index and systolic acceleration time in five healthy subjects by using Doppler ultrasound (US). Analysis of variance was used to estimate the contribution of several factors to the observed variability in measurements. RESULTS: The standard deviation for a single measurement was 0.08 for resistive index and 39 msec for systolic acceleration time. For resistive index, the estimated variance components were 0.0012 (18%), 0.0004 (6%), and 0.0050 (76%) for the subject, sonographer, and intrinsic variability, respectively. For systolic acceleration time, the estimated variance components were 59 msec (4%), 264 msec (17%), and 1,250 msec (79%) for the subject, sonographer, and intrinsic variability, respectively. CONCLUSION: Because of substantial variability in hepatic arterial measures, caution is indicated when interpreting small changes in the measurement of these Doppler US indexes.

Adult↗

PubMed2007

Frequency-dependent acceleration of relaxation involves decreased myofilament calcium sensitivity.

The force-frequency relationship is an intrinsic modulator of cardiac contractility and relaxation. Force of contraction increases with frequency, while simultaneously a frequency-dependent acceleration of relaxation occurs. While frequency dependency of calcium handling and sarcoplasmic reticulum calcium load have been well described, it remains unknown whether frequency-dependent changes in myofilament calcium sensitivity occur. We hypothesized that an increase in heart rate that results in acceleration of relaxation is accompanied by a proportional decrease in myofilament calcium sensitivity. To test our hypothesis, ultrathin right ventricular trabeculae were isolated from New Zealand White rabbit hearts and iontophorically loaded with the calcium indicator bis-fura 2. Twitch and intracellular calcium handling parameters were measured and showed a robust increase in twitch force, acceleration of relaxation, and rise in both diastolic and systolic intracellular calcium concentration with increased frequency. Steady-state force-intracellular calcium concentration relationships were measured at frequencies 1, 2, 3, and 4 Hz at 37 degrees C using potassium-induced contractures. EC(50) significantly and gradually increased with frequency, from 475 +/- 64 nM at 1 Hz to 1,004 +/- 142 nM at 4 Hz (P < 0.05) and correlated with the corresponding changes in half relaxation time. No significant changes in maximal active force development or in the myofilament cooperativity coefficient were found. Myofilament protein phosphorylation was assessed using Pro-Q Diamond staining on protein gels of trabeculae frozen at either 1 or 4 Hz, revealing troponin I and myosin light chain-2 phosphorylation associated with the myofilament desensitization. We conclude that myofilament calcium sensitivity is substantially and significantly decreased at higher frequencies, playing a prominent role in frequency-dependent acceleration of relaxation.

Actin Cytoskeleton↗

PubMed1976

Gas exchange in man during combined +Gz acceleration and exercise.

Gravity and acceleration from head to foot (+Gz) handicap gas exchange by shifting blood from thorax to dependent veins and creating a ventilation/perfusion (V/Q) mismatch in the lung. At 1 G leg exercise improves V/Q matching. Gas exchange was measured in six subjects +1, +2, and +3 Gz during rest and two levels of exercise, either unloaded pedaling or 600 kpm/min. The VO2 for pedaling was clearly related to G level, but work efficiency was unaffected. Acceleration lowered resting Pao2 while raising VE/VO2, HR, AaDo2, VD, and VD/VT. Unloaded pedaling returned VE/VO2 and HR toward their 1-G values. In contrast, at 3 G each increase in VO2 caused a fall in Pao2 and a rise in AaDo2. The VD showed no further change with exercise, while VD/VT decreased at all G levels. It thus appears that only some of the effects of acceleration are counteracted by exercise, probably by the peripheral muscle pump. Any accompanying rise in VO2 adds to the stress of acceleration, due to limitations on gas transport.

Adult↗

PubMed1980

Coronary blood flow in conscious miniature swine during +GZ acceleration stress.

One of the factors determining tolerance to +GZ acceleration may be the ability to maintain adequate coronary blood flow. Consequently, the purpose of these studies was to determine the effect of acute exposure (60 s) to several levels of positive acceleration (+GZ) on total and regional coronary blood flow in conscious adult miniature swine. Blood flow was measured with the radiolabeled microsphere technique in chronically instrumented miniature swine during 60-s exposures to accelerations of +3 GZ, +5 GZ, or +7 GZ with anti-G suit support. All levels of acceleration stress caused two- to threefold increases in coronary blood flow. The regional distribution of coronary blood flow during +GZ was similar to that under resting control conditions as long as aortic diastolic pressure was maintained. All left ventricular endocardial/epicardial flow ratios were significantly greater than one, except in two animals, during exposure to +7 GZ. These were the only animals to have aortic diastolic pressures less than 100 Torr during +GZ stress. These studies indicate that, if an animal is able to compensate and maintain a cardiovascular steady State, coronary blood flow will remain adequate for myocardial needs. However, if decompensation occurs and aortic diastolic pressure falls below a critical value, subendocardial blood flow may become inadequate.

Animals↗