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Acute postburn edema: Role of strongly negative interstitial fluid pressure
232
ABSTRACTS
and ire, decreased -20% in HiOx with constant-pressure perfusion, regardless of Hct. In the constant-flow protocol, leg VO, in HiOx was maintained by the anemic animals and actually increased in the normocythemic group. We conclude that HiOx directly affected vascular smooth muscle to cause flow restriction and maldistribution. Constant flow offset these effects, but the increased limb 00, may have been a toxic effect. Anemia appeared to exaggerate the microcirculatory maldistribution caused by HiOx. (Reprinted with permission.) Hyperoxia and Moderate Hypoxia Fail to Affect lnspiratory Muscle Fatigue in Humans. Ameredes BT, Clanton TL.
Normal human subjects (n = 7) breathing 21% O2 (normoxia), 13% O2 (hypoxia), or 100% 0, (hyperoxia) performed repeated maximal inspiratory maneuvers (inspiratory duration = 1.5 s, total breath duration = 3.5 s) on an “isoflow” system, which delivered a constant mouth flow (1.25 or 1 l/s) while maintaining normocapnia (5.5% end-tidal CO&. Respective mean arterial 0, saturation values (ear lobe oximetry) were 98 2 1, 91 lr 4 (Ps 0.01). and 99 + 1% (NS). Maximal mouth pressure (Pm) was measured during inspirations at rest and during a IO-min fatigue trial, and the Pm measurements obtained during the fatigue trials were fit to an exponential equation. The parameters of the equation included the time constant (r), which describes the rate of decay of Pm from the initial pressure (Pi) to the asymptote, or “sustainable” pressure (Ps). The mean fraction of Pm remaining at the end of the fatigue trials (Ps/Pi) was 63 * 5%. No significant differences in Pi, Ps, or r were observed between Or treatments. This suggests that fatigue of the inspiratory muscles in normal humans occurs by a mechanism that is insensitive to changes in blood O2 content that occur during inspiration of O2 in the range of 13-100%. (Reprinted with permission.) Blood
Flow
and Evoked
Koehler
in Sheep.
RW,
Am J Physiol256:H779,
et al.
Potentials
RC, Backofen
Response
During
Acute Postburn Edema: tial Fluid Pressure. Lund
Role of Strongly
Negative
T, Wiig H, Reed RK.
Intersti-
Am J Physiol
255:H1069,1988. J
Appl Physiol66:894, 1989.
Cerebral
>65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO, (Reprinted with permission.)
Interstitial fluid hydrostatic pressure (P,) was measured with micropipettes during the acute edema generation that followed thermal skin injury in rats. Intradermal Pk was reduced from normal level of - 1 mmHg to very negative values after thermal injury. The strongly negative Pk reflects a tissue imbibition pressure created by the thermal injury. The magnitude and duration of this pressure was dependent on the extent of the injury and the availability of fluid. After in vivo injury to 10 and 40% of the total body surface area (TBSA), mean intradermal Pir was temporarily reduced to - 20 and - 3 1 mmHg, respectively. Intravenous fluid infusion resulted in a rapid return of P,r to slightly positive values. Fluid available for transfer from the circulation was reduced by inducing the injury after killing the animal (postmortem injury) and even more by the subcutaneous insertion of a plastic barrier; this led to more pronounced reductions in Pir to average minimum values of -95 and - 135 mm Hg, respectively. Our data show that increased tissue imbibition pressure and increased net filtration pressure (tissue mechanisms) are responsible for a major part of the acute fluid shifts into thermally injured skin. Vascular mechanisms (permeability changes and intravascular pressure) are involved in the postburn edema development but are clearly less important than hitherto believed. (Reprinted with permission.)
Cushing
JE. McPherson
1989.
We determined how alterations in systemic hemodynamits, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of 0, (CMRO*), and brain electrical conductive function, as assessedby somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was ~50 mmHg. CMROz fell when CBF fell >30-40%. Mean aortic pressure and cardiac output increased when CBF fell >40%, ie., at approximately the level at which CMRO, fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMR02. SEP latency did not increase unless CBF fell >55-65%, corresponding to a 2030% reduction of CMROI. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of
Hypoxanthine and Lactate Concentrations in Lambs During Hypoxic and Stagnant Hypoxia. Moss M, Kurzner s, Razlog
Y, et al. Am J Physiol255H53,
1988.
To determine the suitability of plasma hypoxanthine as a marker of tissue hypoxia, we studied the relationship of arterial plasma hypoxanthine and blood lactate concentrations to the cumulative O1 deficit during hypoxemia and low cardiac output (hypoxic and stagnant hypoxia, respectively). Eight intact, chronically catheterized lambs were studied using ketamine sedation. Comparable reductions in 0, transport and consumption were produced with each form of hypoxia. Lactate was linearly related to O2 deficit during both forms of hypoxia, although the slope of the regression was greater for low cardiac output (0.049) than hypoxemia (0.032). Hypoxanthine was linearly related to cumulative 0, deficit only during low cardiac output. During hypoxemia, hypoxanthine concentration initially increased but plateaued with further increases in 0, deficit. The discrepancy in response of hypoxanthine was most likely caused by differences in the rate of elimination between stagnant and hypoxic hypoxia. We concluded that plasma hypoxanthine concentraton was not a reliable marker for tissue hypoxia because it
ABSTRACTS
and ire, decreased -20% in HiOx with constant-pressure perfusion, regardless of Hct. In the constant-flow protocol, leg VO, in HiOx was maintained by the anemic animals and actually increased in the normocythemic group. We conclude that HiOx directly affected vascular smooth muscle to cause flow restriction and maldistribution. Constant flow offset these effects, but the increased limb 00, may have been a toxic effect. Anemia appeared to exaggerate the microcirculatory maldistribution caused by HiOx. (Reprinted with permission.) Hyperoxia and Moderate Hypoxia Fail to Affect lnspiratory Muscle Fatigue in Humans. Ameredes BT, Clanton TL.
Normal human subjects (n = 7) breathing 21% O2 (normoxia), 13% O2 (hypoxia), or 100% 0, (hyperoxia) performed repeated maximal inspiratory maneuvers (inspiratory duration = 1.5 s, total breath duration = 3.5 s) on an “isoflow” system, which delivered a constant mouth flow (1.25 or 1 l/s) while maintaining normocapnia (5.5% end-tidal CO&. Respective mean arterial 0, saturation values (ear lobe oximetry) were 98 2 1, 91 lr 4 (Ps 0.01). and 99 + 1% (NS). Maximal mouth pressure (Pm) was measured during inspirations at rest and during a IO-min fatigue trial, and the Pm measurements obtained during the fatigue trials were fit to an exponential equation. The parameters of the equation included the time constant (r), which describes the rate of decay of Pm from the initial pressure (Pi) to the asymptote, or “sustainable” pressure (Ps). The mean fraction of Pm remaining at the end of the fatigue trials (Ps/Pi) was 63 * 5%. No significant differences in Pi, Ps, or r were observed between Or treatments. This suggests that fatigue of the inspiratory muscles in normal humans occurs by a mechanism that is insensitive to changes in blood O2 content that occur during inspiration of O2 in the range of 13-100%. (Reprinted with permission.) Blood
Flow
and Evoked
Koehler
in Sheep.
RW,
Am J Physiol256:H779,
et al.
Potentials
RC, Backofen
Response
During
Acute Postburn Edema: tial Fluid Pressure. Lund
Role of Strongly
Negative
T, Wiig H, Reed RK.
Intersti-
Am J Physiol
255:H1069,1988. J
Appl Physiol66:894, 1989.
Cerebral
>65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO, (Reprinted with permission.)
Interstitial fluid hydrostatic pressure (P,) was measured with micropipettes during the acute edema generation that followed thermal skin injury in rats. Intradermal Pk was reduced from normal level of - 1 mmHg to very negative values after thermal injury. The strongly negative Pk reflects a tissue imbibition pressure created by the thermal injury. The magnitude and duration of this pressure was dependent on the extent of the injury and the availability of fluid. After in vivo injury to 10 and 40% of the total body surface area (TBSA), mean intradermal Pir was temporarily reduced to - 20 and - 3 1 mmHg, respectively. Intravenous fluid infusion resulted in a rapid return of P,r to slightly positive values. Fluid available for transfer from the circulation was reduced by inducing the injury after killing the animal (postmortem injury) and even more by the subcutaneous insertion of a plastic barrier; this led to more pronounced reductions in Pir to average minimum values of -95 and - 135 mm Hg, respectively. Our data show that increased tissue imbibition pressure and increased net filtration pressure (tissue mechanisms) are responsible for a major part of the acute fluid shifts into thermally injured skin. Vascular mechanisms (permeability changes and intravascular pressure) are involved in the postburn edema development but are clearly less important than hitherto believed. (Reprinted with permission.)
Cushing
JE. McPherson
1989.
We determined how alterations in systemic hemodynamits, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of 0, (CMRO*), and brain electrical conductive function, as assessedby somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was ~50 mmHg. CMROz fell when CBF fell >30-40%. Mean aortic pressure and cardiac output increased when CBF fell >40%, ie., at approximately the level at which CMRO, fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMR02. SEP latency did not increase unless CBF fell >55-65%, corresponding to a 2030% reduction of CMROI. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of
Hypoxanthine and Lactate Concentrations in Lambs During Hypoxic and Stagnant Hypoxia. Moss M, Kurzner s, Razlog
Y, et al. Am J Physiol255H53,
1988.
To determine the suitability of plasma hypoxanthine as a marker of tissue hypoxia, we studied the relationship of arterial plasma hypoxanthine and blood lactate concentrations to the cumulative O1 deficit during hypoxemia and low cardiac output (hypoxic and stagnant hypoxia, respectively). Eight intact, chronically catheterized lambs were studied using ketamine sedation. Comparable reductions in 0, transport and consumption were produced with each form of hypoxia. Lactate was linearly related to O2 deficit during both forms of hypoxia, although the slope of the regression was greater for low cardiac output (0.049) than hypoxemia (0.032). Hypoxanthine was linearly related to cumulative 0, deficit only during low cardiac output. During hypoxemia, hypoxanthine concentration initially increased but plateaued with further increases in 0, deficit. The discrepancy in response of hypoxanthine was most likely caused by differences in the rate of elimination between stagnant and hypoxic hypoxia. We concluded that plasma hypoxanthine concentraton was not a reliable marker for tissue hypoxia because it