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T E Gayeski

Publications and source records attributed to T E Gayeski.

At least 19 recordsLinked to original sources
PubMed1998

Lack of lung hemorrhage in humans after intraoperative transesophageal echocardiography with ultrasound exposure conditions similar to those causing lung hemorrhage in laboratory animals.

This study investigated the phenomenon of ultrasonically induced lung hemorrhage in humans. Multiple experimental laboratories have shown that diagnostic ultrasound exposure can cause hemorrhage in the lungs of laboratory animals. The left lung of 50 patients (6 women, 44 men, mean age 61 years) was observed directly by the surgeon after routine intraoperative transesophageal echocardiography was performed. From manufacturer specifications the maximum derated intensity in the sound field of the system used was 186 W/cm2, the maximum derated rarefactional acoustic pressure was 2.4 MPa, and the maximum mechanical index was 1.3. The lowest frequency used was 3.5 MHz. This exposure exceeds the threshold found for surface lung hemorrhage seen on gross observation of laboratory animals. No hemorrhage was noted on any lung surface by the surgeon on gross observation. We conclude that clinical transesophageal echocardiography, even at field levels a little greater than the reported thresholds for lung hemorrhage in laboratory animals, did not cause surface lung hemorrhage apparent on gross observation. These negative results support the conclusion that the human lung is not markedly more sensitive to ultrasound exposure than that of other mammals.

Adult↗
PubMed1997

Skeletal muscle function, oxygenation and biochemistry in an endotoxemic model of SIRS.

We have developed a reproducible low-dose endotoxin model which is useful for the investigation of early SIRS. The data confirm that organ function cannot be inferred from whole animal data (e.g. SVR vs. MVR). Thus, the study of SIRS at the organ and cellular level is essential. Decreased skeletal muscle oxygen consumption with 4 Hz exercise in early SIRS may be related to depletion of physiologic reserves, especially microcirculatory reserves, as suggested by decreased myoglobin saturation and decreased energy charge. Using this model, we will investigate whether organ dysfunction in SIRS is due to oxygen-limited cellular ATP production or impaired cellular metabolism.

Animals↗
PubMed1995

Determination of myoglobin saturation of frozen specimens using a reflecting cryospectrophotometer.

This report describes a method and instrumentation for determining myoglobin (Mb) oxygen saturation in skeletal muscle. Canine gracilis is frozen in situ using a liquid N2-cooled copper block. Transverse section surfaces of frozen unstained muscle are observed at -110 degrees C using a microspectrophotometric system. The Mb saturation is determined using epi-illumination and a four-wavelength optical method. A special aperture permits illumination of a 20-microns-square area, and the radius of the catchment volume is estimated to be approximately 60 microns, with the strongest signal arising from the central region. The equibestic wavelengths used were 546.6, 570.5, and 584.1 nm. The method was validated using the nonlinear multicomponent analysis method of Lübbers. End-point (0 and 100% saturation) calibration was set using ischemic and adenosine-treated highly oxygenated muscles, respectively. The effects of hemoglobin (Hb) and metmyoglobin (metMb) signal contamination were evaluated experimentally and by computer-mixing simulations. Mb saturation determinations adjacent to large vessels are to be avoided. MetMb and capillary Hb do not interfere with the determination. The reproducibility of the method is estimated to be +/- 5%.

Animals↗
PubMed1993

Resistance to O2 diffusion in anemic red muscle: roles of flux density and cell PO2.

Normal and anemic dog gracilis muscles were compared at equal O2 uptake rates (VO2) to locate the principal site of resistance to diffusive O2 transport. Anemia halved the hematocrit and the number of red blood cells per square millimeter of muscle cross section. Flow doubled in anemia, and flow times arterial O2 content, PO2 of effluent blood, and O2 extraction per red blood cell were approximately the same as control. Nevertheless, intracellular PO2 was significantly lower in anemia. At any instant the aggregate red blood cell surface area for O2 release was about half normal. Because the flux (VO2) was the same as control, the driving force for diffusion from red blood cell to myocyte should have doubled. An estimate of the total driving force from red blood cell to mitochondria was greater in anemia. This increase was much less than a factor of 2 because lower intracellular PO2 increases myoglobin-facilitated diffusion, thus decreasing resistance inside the myocyte. The role of myoglobin and the coupling of convective to diffusive transport are discussed. We conclude that the principal resistance to O2 diffusion lies outside the myocyte.

Anemia↗
PubMed1992

Interaction of blood flow, diffusive transport and cell metabolism in isovolemic anemia.

1) High blood flow can compensate for half-normal hematocrit, leaving the rate at which O2 is offered to the capillaries unchanged. Nevertheless, intracellular PO2 is lower in anemia, indicating impaired diffusive transport. 2) Anemia increases O2 flux per red cell and decreases functional capillary surface area. These changes increase flux density and the extracellular component of resistance to diffusive O2 transport, in accord with current theory (Federspiel and Popel, 1986; Groebe, 1990; Hellums, 1977). 3) Maintenance of diffusive flux in presence of anemia required a larger delta PO2 between Hb and Mb, and higher intracellular O2 conductance brought about by greater Mb-facilitated diffusion. Both compensations depend on lower PmbO2. 4) PmbO2 and creatine charge fall with increasing VO2 and ATP demand. These responses, as well as adaptive changes in redox help maintain VO2 in the presence of a lower O2 drive on electron transport. 5) Greater engagement of reserves of both transport and metabolism limits the range of aerobic performance in anemia. 6) The match between the transcapillary and mitochondrial O2 fluxes depends on interaction of transport and metabolism as a system.

Anemia↗
PubMed1992

O2 transport and its interaction with metabolism; a systems view of aerobic capacity.

This commentary demonstrates that VO2max depends, in part, on diffusive O2 transport; exercise hyperemia is necessary but not sufficient. Experiments and new mathematical models place the principal site of resistance to O2 diffusion between the surface of a red cell and the sarcolemma. The large drop in PO2 over this short distance is caused by high flux density and absence of heme protein O2 carrier in this region. PO2 gradients within red myocytes are shallow at high VO2 because myoglobin acts as O2 carrier and PO2 buffer. At high VO2 cell PO2 is less than 5 torr, the myoglobin P50. Low cell PO2 relative to blood PO2 is essential to a) maintain the driving force on diffusion as capillary PO2 falls, and b) to increase myoglobin-facilitated diffusion and the overall O2 conductance. O2 per se does not limit mitochondrial ATP production under normal circumstances because the low O2 drive on electron transport is compensated by greater phosphorylation and redox drives. These metabolic adaptations support transcapillary diffusion by defending VO2 at the low cell PO2 required to extract O2 from blood. Thus aerobic capacity is a distributed property, dependent on the interaction of transport and metabolism as a system.

Adenosine Triphosphate↗
PubMed1991

Intracellular PO2 in individual cardiac myocytes in dogs, cats, rabbits, ferrets, and rats.

Myoglobin (Mb) saturation in individual subepicardial myocytes was determined by cryospectroscopy in dogs, cats, ferrets, rabbits, and rats. Mb saturation within 800 microns of the epicardium is not affected by quick freezing or absorption of light by cytochromes. The PO2 in equilibrium with Mb (PMbO2) was calculated from the Mb oxydissociation curve. The minimum PMbO2 found among the 1,000 cells examined was 2.5 Torr, at least five times the critical PO2 for cytochrome turnover in myocardium. The maximum PMbO2 found was about one-half that in subepicardial venules, suggesting a large change in PO2 between capillaries and the cytosol. PMbO2 was the same in right and left ventricles and was unchanged by moderate hemodynamic stress. Median PMbO2 was remarkably uniform among species (range, 4.3-7.0 Torr in 20 animals), even though left ventricular work per minute varied approximately 200-fold, heart rate about fivefold, and arterial O2 content about twofold. Relatively uniform Mb saturation below venous PO2 should accelerate release of O2 from capillaries, promote Mb-facilitated O2 diffusion, and minimize diffusive O2 shunting.

Animals↗
PubMed1991

Arteriovenous oxygen diffusion shunt is negligible in resting and working gracilis muscles.

Distribution of O2 within and among arterioles and venules was determined in dog and rat gracilis muscles with a cryospectrophotometric method. Saturation in 40-microns arterioles was not demonstrably different from saturation in the aorta even when flow was abnormally low. Arterioles greater than 40 microns ran parallel to venules. Measurements and a mathematical model indicate that diffusive shunting is negligible for typical separation distances between arterioles and venules. Most separation distances were greater than 30 microns. In some venule segments less than 15 microns from an arteriole, saturation within 10 microns of the wall facing the arteriole was higher than at other locations within the venule. However, saturation in the population of venules did not increase with venule diameter, and mean venular saturation was not different from saturation in effluent blood. We make the following conclusions: 1) a small arteriovenous diffusive O2 flux exists in postural muscles; 2) contribution of this flux to O2 mass balance is negligible; 3) O2 diffusivity of the arteriolar wall and surrounding tissue in vivo cannot be much higher than O2 diffusivity determined in vitro; and 4) effluent PO2 closely approximates mean end-capillary PO2.

Animals↗
PubMed1990

Effect of tachycardia on intracellular PO2 and reserves of O2 transport in subendocardium of mouse left ventricle.

Intracellular PO2 (PmbO2) was determined by cryospectrophotometry in individual cardiac myocytes. The rate of progression of the freezing front was sufficient to trap the O2 distribution across the wall of the mouse left ventricle. The transmural PmbO2 distribution was uniform despite moderate tachycardia. Maximal heart rate produced a small but statistically significant transmural O2 gradient but no hypoxic myocytes in subendocardium. Reserves of diffusive as well as convective transport contribute to maintenance of aerobic metabolism during tachycardia.

Animals↗
PubMed1990

Determination of microvascular oxyhemoglobin saturations using cryospectrophotometry.

Although a four-wavelength method for cryospectrophotometric measurement of intravascular oxyhemoglobin (HbO2) saturations has previously been described, the relationship between experimental measurements and theory has not been clearly detailed. The current work utilizes an empirical relationship between HbO2 saturation measurements and reflected light oximetry, which is consistent with the two-flux theory of Kubelka and Munk (Z. Tech. Phys. 11a: 593-603, 1931). To obtain linear, concentration-independent calibration curves, the theoretical results require that 1) the complex function relating optical density, scattering, and absorption can be linearly approximated over the range of scattering and absorption coefficients used; and 2) the scattering coefficient is independent of wavelength. Incident light cannot easily be measured using reflection spectroscopy, which precludes the determination of isosbestic points. Therefore, equibestic wave-length pairs were used at which optical density differences were invariant with saturation. This allows numerous wavelength sets over the range 540-600 nm to be selected, rather than the limited choices of isosbestic wavelengths. Finally, the effects of freeze rate, freeze depth, Hb concentration, and vessel diameter are each discussed in terms of their influence on experimental measurements.

Animals↗
PubMed1990

Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2.

The necessity for defining hypoxia as O2-limited energy flux rather than low partial pressure is explored from a systems perspective. Oxidative phosphorylation, the Krebs cycle, glycolysis, substrate supply, and cell energetics interact as subsystems; the set point is a match between ATP demand and aerobic ATP production. To this end the transport subsystem must match the transcapillary and mitochondrial O2 fluxes. High transcapillary O2 flux requires intracellular PO2 in the range 1-10 Torr. In this range the O2 drive on electron transport must be compensated by adaptive changes in the phosphorylation and redox drives. Thus the metabolic subsystem supports diffusive O2 transport by maintaining O2 flux at intracellular partial pressures required for O2 release from blood. Since responses to stress are distributed according to the state of the entire system, several simultaneous metabolic measurements, including intracellular PO2 (or a known direction of change in intracellular PO2) and the O2 dependence of a measurable function are required to judge the adequacy of O2 supply. ATP demand and aerobic capacity must also be evaluated, because the hypoxic threshold depends on the ratio of ATP demand to aerobic capacity. The application and limitation of commonly used criteria of hypoxia are discussed, and a more precise terminology is proposed.

Adenosine Triphosphate↗
PubMed1989

Precapillary O2 loss and arteriovenous O2 diffusion shunt are below limit of detection in myocardium.

1. Mean intracellular PO2 is much lower than mean venous PO2 in subepicardium. 2. The drop in Hb saturation between aorta and terminal arterioles is within the 5% error of our method. 3. Arteriolar O2 has no effect on saturation in paired countercurrent venules in myocardium. 4. Saturation in coronary venules is independent of venule diameter and indistinguishable from saturation in macroscopic epicardial veins. 5. Since diffusive O2 shunting is negligible and PO2 is approximately linearly related to saturations over the observed range, mean coronary venous PO2 should closely approximate mean-end capillary PO2. 6. O2 mass transport from blood to tissue requires a steep PO2 gradient between the capillary and the surface of a tissue cell.

Animals↗
PubMed1989

Anatomical determinants of O2 flux density at coronary capillaries.

Calculations indicate that the PO2 in plasma falls to zero approximately 3 microns from an erythrocyte at O2 consumption (VO2) characteristic of myocardium (Federspiel, W.A., and A. Popel, Microvasc. Res. 32: 164-189, 1986). We measured distances between individual red cells along capillaries in rat hearts rapidly frozen in situ. Cell spacing varied widely even in branches of the same capillary. Plasma gaps between red cells were divided into two populations, those less than 5 microns and those greater than 5 microns. Mean gap lengths were 2.1 and 16.5 microns, respectively. Although the number of long plasma gaps was underestimated, gaps greater than 5 microns accounted for one-third of observed capillary length. Frozen muscles were also viewed in cross section. Because the depth of penetration of light was approximately equal to 3 microns, counts of red cell-containing capillary profiles in cross section depend on cell spacing as well as on number of cell-containing flow paths. Counts varied markedly with arterial O2 partial pressure, indicating that the capillary surface area functional for O2 transport changes in response to stress. The adaptive role of change in O2 flux density (flux per area) is discussed in light of new knowledge of tissue O2 gradients.

Animals↗
PubMed1988

Intracellular PO2 in long axis of individual fibers in working dog gracilis muscle.

Dog gracilis muscles were frozen in situ during twitch contraction at 25-100% of aerobic capacity. O2 saturation of myoglobin (Mb) was determined from spectrophotometric measurements along individual fibers. Intracellular PO2 was calculated from the oxymyoglobin dissociation curve. At all work rates, long lengths of fibers were found in which saturation and PO2 were within the 4% error of measurement. During work at approximately 25% of aerobic capacity, Mb functioned at high saturation on the shallow slope of its dissociation curve. Consequently PO2 was poorly buffered. Although the range of saturation was small, PO2 varied up to 15 Torr along a fiber, and gradients up to 0.3 Torr/micron were observed. In contrast, at high O2 consumption (VO2), Mb functioned on the steep slope of its dissociation curve. Therefore gradients in intracellular PO2 along the axis of a myocyte were small (less than 0.05 Torr/micron) despite large gradients in Mb saturation (up to 0.5%/micron). Changes in intracellular PO2 over hundreds of microns did not reflect the large drop in intracapillary PO2 between arterioles and venules. Because intracellular PO2 is low and relatively uniform in the long axis of a fiber, the driving force for release of O2 from blood is dominated by intravascular PO2 in working red muscle.

Animals↗