Frequency-dependent effective hydraulic conductivity of strongly heterogeneous media.

The determination of the transport properties of heterogeneous porous rocks, such as an effective hydraulic conductivity, arises in a range of geoscience problems, from groundwater flow analysis to hydrocarbon reservoir modeling. In the presence of formation-scale heterogeneities, nonstationary flows, induced by pumping tests or propagating elastic waves, entail localized pressure diffusion processes with a characteristic frequency depending on the pressure diffusivity and size of the heterogeneity. Then, on a macroscale, a homogeneous equivalent medium exists, which has a frequency-dependent effective conductivity. The frequency dependence of the conductivity can be analyzed with Biot's equations of poroelasticity. In the quasistatic frequency regime of this framework, the slow compressional wave is a proxy for pressure diffusion processes. This slow compressional wave is associated with the out-of-phase motion of the fluid and solid phase, thereby creating a relative fluid-solid displacement vector field. Decoupling of the poroelasticity equations gives a diffusion equation for the fluid-solid displacement field valid in a poroelastic medium with spatial fluctuations in hydraulic conductivity. Then, an effective conductivity is found by a Green's function approach followed by a strong-contrast perturbation theory suggested earlier in the context of random dielectrics. This theory leads to closed-form expressions for the frequency-dependent effective conductivity as a function of the one- and two-point probability functions of the conductivity fluctuations. In one dimension, these expressions are consistent with exact solutions in both low- and high-frequency limits for arbitrary conductivity contrast. In 3D, the low-frequency limit depends on the details of the microstructure. However, the derived approximation for the effective conductivity is consistent with the Hashin-Shtrikman bounds.

[The significance and cost of preoperative laboratory screening in young healthy patients in a public hospital in Israel].

UNLABELLED: We evaluated the clinical significance and cost of routine preoperative laboratory screening in young healthy patients in a public hospital. Three hundred consecutive young (aged 18-40 years), healthy (ASA I) patients undergoing minor elective surgical procedures were enrolled in this prospective study. A preoperative test was considered to be significant if its result lead to a new diagnose or to cancellation of surgery. The lab tests revealed only one new diagnosis. None of the procedures were cancelled. The total cost of the lab tests was NIS 114,000. Of this amount, NIS 104,000 could have been saved if the tests were ordered as required by the patients medical history and physical examination and not performed routinely. CONCLUSION: This study suggests that routine preoperative laboratory screening is not recommended prior to minor, elective surgery in young, healthy patients.

Labetalol-induced hypotension decreases blood loss during uncontrolled hemorrhage.

In a model of uncontrolled hemorrhagic hypotension (UCHH) in rats, we examined whether blood loss or blood chemistry were affected by (1) deliberate, controlled hypotension induced with labetalol (L) or sodium nitroprusside (SNP) and (2) intravenous (iv) fluid therapy. Two hours of UCHH was induced by resecting the distal 25% of the tail. L or SNP was infused with the aim of decreasing MAP to 50 mmHg. In the groups receiving iv fluid, 3 ml of 0.9% saline was given for each 1 ml of blood loss. L decreased blood loss (2.8+/-2.0 and 3.0+/-1.9 ml, respectively, in the groups not receiving and receiving iv fluid) compared to the groups not given hypotensive drugs (6.3+/-4.1 and 13.5+/-6.6 ml). SNP did not decrease blood loss (5.7+/-4.7 and 11.0+/-6.2 ml), increased serum potassium (5.0+/-0.6 and 5.8+/-0.4 mEq l(-1)), and with accompanying iv fluid administration decreased hematocrit, worsened acidosis, and increased mortality. In this model of 2 h of UCHH in rats, hypotension to MAP of 50 mmHg with L but not with SNP decreased blood loss.

Neuroprotective effects of NPS 846, a novel N-methyl-D-aspartate receptor antagonist, after closed head trauma in rats.

OBJECT: The authors sought to determine whether 3,3-bis (3-fluorophenyl) propylamine (NPS 846), a novel noncompetitive N-methyl-D-aspartate receptor antagonist, alters outcome after closed head trauma in rats. METHODS: The experimental variables were: presence or absence of closed head trauma, treatment with NPS 846 or no treatment, and time at which the rats were killed (24 or 48 hours). The NPS 846 (1 mg/kg) was administered intraperitoneally at 1 and 3 hours after closed head trauma or sham operation. Outcome measures were the neurological severity score (NSS), ischemic tissue volume, hemorrhagic necrosis volume, and specific gravity, water content, and concentrations of calcium, sodium, potassium, and magnesium in brain tissue. The following closed head trauma-induced changes in the injured hemisphere (expressed as the mean +/- the standard deviation) were reversed by NPS 846: decreased specific gravity of 1.035 +/- 0.006 at 24 hours was increased to 1.042 +/- 0.004; the decreased potassium level of 0.583 +/- 0.231 mg/L at 48 hours and at 24 hours was increased to 2.442 +/- 0.860 mg/L; the increased water content of 84.7 +/- 2.6% at 24 hours was decreased to 79.8 +/- 2%; the increased calcium level of 0.592 +/- 0.210 mg/L at 24 hours was decreased to 0.048 +/- 0.029 mg/L; and the increased sodium level of 2.035 +/- 0.649 mg/L was decreased to 0.631 +/- 0.102 mg/L. Administration of NPS 846 also lowered the NSS (improved neurological status) at 48 hours (7 +/- 3) and caused no significant changes in ischemic tissue or hemorrhagic necrosis volumes in the injured hemisphere at 24 or 48 hours. CONCLUSIONS: In this model of closed head trauma, NPS 846 improved neurological outcome, delayed the onset of brain edema, and improved brain tissue ion homeostasis.

0.45% saline and 5% dextrose in water, but not 0.9% saline or 5% dextrose in 0.9% saline, worsen brain edema two hours after closed head trauma in rats.

UNLABELLED: In this study, we examined the effect of four i.v. fluids (250 mL/kg) on blood glucose and osmolality and brain tissue specific gravity after closed head trauma (CHT) in rats. CHT was delivered at Time 0; blood was sampled at 60 min; fluid infusion began at 75 min and ended at 105 min. Blood was again sampled at 105 and 120 min, and brain tissue specific gravity was determined at 120 min. Five groups (one control and four fluid-treated groups) received CHT, and five other groups (one control and four fluid-treated) did not (n = 9 in each group). 0.45% saline (1/2 NS) and 5% dextrose in water (D5W) accentuated the decrease of brain tissue specific gravity (1.0366 +/- 0.0025 and 1.0368 +/- 0.0028, respectively; mean +/- SD) caused by CHT (1.0395 +/- 0.0036), but 5% dextrose in 0.9% saline (D5NS) and 0.9% saline (NS) did not (1.0431 +/- 0.0042 and 1.0389 +/- 0.0049, respectively). In addition, 1/2 NS decreased blood osmolality (248 +/- 6 mOsm/L), D5W increased blood glucose (1095 +/- 173 mg/dL), D5NS increased blood osmolality (350 +/- 5 mOsm/L) and glucose (1695 +/- 76 mg/dL), and NS caused no significant change. We conclude that administering hypoosmolar i.v. fluids after CHT causes a significant worsening of cerebral edema 2 h after CHT. IMPLICATIONS: We previously reported worse neurological outcome and/or mortality after closed head trauma in rats when 5% dextrose in water or 0.45% saline was given i.v. compared with 0.9% saline or 5% dextrose in 0.9% saline. The present results and our previous findings indicate that worsening of outcome after closed head trauma in rats may be caused more by edema formation than by hyperglycemia.

Brain edema, hemorrhagic necrosis volume, and neurological status with rapid infusion of 0.45% saline or 5% dextrose in 0.9% saline after closed head trauma in rats.

We previously reported that in rats with closed head trauma (CHT), intravenous (IV) administration of 0.25 mL/g of 5% dextrose solution (D5W) increased blood glucose (G), decreased blood sodium (Na), caused no change in blood osmolality (Osm), increased brain edema (BE), and worsened neurological severity score (NSS) and mortality rate (MR). D5W in 0.9% saline (D5NS) is isonatremic and hyperosmolar with respect to blood and may avoid the problems reported with D5W. The present study compared the effects of 0.25 mL/g of D5NS or 0.45% saline (0.45 S) after CHT in rats. In 11 groups of rats, the three experimental variables were CHT (yes or no), IV fluid (none, D5NS, or 0.45 S), and time of death (4 or 24 h). D5NS or 0.45 S was given IV at 1 h after surgical preparation with or without CHT, and experimental values were determined at 1, 2, 4, and 24 h. D5NS decreased BE at 4 h compared with the untreated group, increased Osm (380 +/- 2 mOsm/kg) and G (1278 +/- 199 mg/dL), decreased Na (131 +/- 2 mEq/L) in blood, and caused no significant change in hemorrhagic necrosis volume (HNV), NSS, or MR. 0.45 S increased MR (50%) at 24 h, decreased Osm (270 +/- 5 mOsm/kg) and Na (123 +/- 1 mEq/L) in blood, and caused no significant change in G, BE, HNV, or NSS. We conclude that after CHT in rats, D5NS decreased BE without changing NSS or MR. 0.45 S increased MR and significantly altered blood chemistries.

Influence of closed head injury on isoflurane MAC in the rat.

We designed the present study to determine whether the minimum alveolar concentration (MAC) for isoflurane is decreased after closed head trauma (CHT) in rats and, if so, whether the decrease of MAC is related to the severity of neurological impairment following CHT. Isoflurane MAC was determined in 36 Sprague-Dawley rats. Then, at time = 0 h, animals were grouped. Group 1 (n = 8) received no CHT, group 2 (n = 14) received moderate CHT, and group 3 (n = 14) received severe CHT. Neurological severity score (NSS, 0 = no deficit and 25 = maximal impairment) and MAC were determined at 1, 4, 24, and 48 h. In groups 1 and 2, isoflurane MAC at 1, 2, 24, and 48 h (1.0-1.1 +/- 0.8-1.2%, median +/- range) was not significantly different from baseline (1.0-1.1 +/- 1.0-1.1%). In group 3, isoflurane MAC at 1, 2, 24, and 48 h (0.4 +/- 0.2-0.5%) was decreased as compared to baseline (1.1 +/- 1.0-1.1%). In group 2, NSS at 1 h was 18 +/- 11-21 and improved by 48 h to 9 +/- 4-15. In group 3, NSS at 1 h was 24 +/- 22-25 and was not significantly different from NSS at 48 h (24 +/- 24-25). Thus, moderate CHT does not significantly alter isoflurane MAC, whereas severe CHT equivalent to a Glasgow Coma Scale score of 3 to 6 significantly decreases isoflurane MAC.