Since its development more than twenty years ago, non-invasive near-infrared-spectroscopy (NIRS) has been widely used to monitor cerebral oxygenation. Despite of its growing number of users, the diagnostic value of near-infrared spectroscopy still remains unclear, especially in case of acute brain injury and long-term neuromonitoring, necessary during intensive care therapy. To evaluate quality and sensitivity of NIRS measurements compared to invasive ICP-, CPP- and regional brain tissue--pO2 (p(ti)O2) monitoring, 31 patients, suffering from severe brain injury due to subarachnoid hemorrhage or severe head injury, were studied. NIRS measurements were only possible in 80% (using the INVOS oximeter) and in 46% (using the CRITIKON monitor), while good data quality was obtained in 100% from ICP, CPP and p(ti)O2. Major reasons for the failure of NIRS measurements were: (1) a wet chamber between sensor and skin, (2) galea hematoma or (3) subdural air after craniotomy. Different tests were performed to compare the sensitivity of regular oxygen saturation (NIRS) with the sensitivity of invasively determined p(ti)O2. Only induced hyperoxia (FiO2 = 1.0) revealed a significant correlation between both parameters (r = 0.67, p < 0.01). Lower or no correlation was found after changing paCO2 and administration of mannitol. The high failure rate and the limited sensitivity does not make the clinical use of near-infrared spectroscopy suitable as a part of neuromonitoring after acute brain injury at the present time.

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Charge-pulse experiments were performed on giant algal cells of Valonia utricularis. If the tonoplast and plasmalemma in series are charged to voltages of the order of 10mV, the decay of the initial voltage with time can be described by the sum of two or three exponential relaxations. It is not possible to explain the exponential decay of the voltage by two RC-circuits in series (e.g. tonoplast and plasmalemma), because this would lead to unreasonable values for the specific capacities of the two membranes. The exponential relaxations might be attributable to the transport of mobile negative charges present in both membranes, possibly as a part of a transport system. From an analysis of the experimental results in terms of the proposed model, the translocation rate constant k and the total surface density N t of the mobile charges in one membrane could be evaluated. On average k is of the order of 600sec 1 and N~ is about 5 x 10-12molcm 2 (average turgor pressure 1.6bar). The transport properties of the mobile charges within the tonoplast and plasmalemma were studied as a function of different parameters such as external pH, glutardialdehyde, electrical breakdown and turgor pressure. When the pH is lowered from 8.2 to 4 or 5 the mobile charges disappear completely, presumably as the result of protonation of the anionic groups. This pH effect was found to be completely reversible. Electrical breakdown causes a reversible disappearance of the relaxation with the longer half-time due to the decrease in membrane resistance. The value of the electrical breakdown voltage determined by injection of charge pulses of 300-psec duration into the cell is pH-independent and therefore is consistent with the mobile charge model and with results previously reported (U. Zimmermann & R. Benz, J. Membrane Biol. 53:33-43, 1980). Addition of glutardialdehyde leads also to a disappearance of the mobile charges probably due to cross-linkage. Increase of the turgor pressure from 0.05 bar to 2 bar results in an increase in k by a factor of 2 and in N~ by about 30 %. The increase in k is in reasonable agreement with that expected on the basis of the assumed compressibility of the membranes. The elastic compressive modulus perpendicular to the membrane plane calculated from the pressure dependence of the translocation rate constant k is in very good agreement with that derived from electrical breakdown experiments (14 and 13bar, respectively). The presence of charges within the membranes as well as the compressibility of the membranes are discussed in terms of a possible turgor-pressure-sensing mechanism.

Using a pressure probe, turgor pressure was directly determined in leaf-mesophyll cells and the giant epidermal bladder cells of stems, petioles and leaves of the halophilic plant Mesembryanthemum crystallinum. Experimental plants were grown under non-saline conditions. They displayed the photosynthetic characteristics typical of C-plants when 10 weeks old and performed weak CAM when 16 weeks old. In 10 week old plants, the turgor pressure (P) of bladder cells of stems was 0.30 MPa; of bladder cells of petioles 0.19 MPa, and of bladder cells of leaves 0.04 MPa. In bladder cells from leaves of 16 week old plants, marked changes in turgor pressure were observed during day/night cycles. Maximum turgor occurred at noon and was paralleled by a decrease in the osmotic pressure of the bladder cell sap. Similar changes in the cell water relations were observed in plants in which traspirational water loss was prevented by high ambient relative humidity. Turgor pressure of mesophyll cells also increased during day-time showing macimum values in the early morning. No such changes in turgor pressure and osmotic pressure were observed in bladder and mesophyll cells of the 10 week old plants not showing the diurnal acid fluctuation typical of CAM.

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