Tissue oxygen measurement and 31P magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia.

Muscle tissue oxygen tension was measured by a polarographic oxygen fine-needle probe, and inorganic phosphate and creatine phosphate spectra were recorded using magnetic resonance spectroscopy in patients with chronic low back pain and in patients with fibromyalgia. Results were compared with healthy controls. The tissue oxygen tension was markedly higher in those with tense muscles than in normal subjects. Magnetic resonance spectra for inorganic phosphate were higher in patients demonstrating muscle contraction, and intracellular pH was shifted in the alkaline direction in cases with increased muscle tension. Results show that hypoxia is not the result of increased muscle tension, as was thought previously, but results from oversupply of oxygen demanded by the muscle, leading to increased capillary perfusion and rising oxygen tension.

Monitoring cerebral oxygenation: experimental studies and preliminary clinical results of continuous monitoring of cerebrospinal fluid and brain tissue oxygen tension.

Cerebral ischaemia is considered to be the central mechanism leading to secondary brain damage in patients with severe head injury. It would therefore seem appropriate to monitor cerebral oxygenation in these patients. The possibilities of continuous monitoring of brain tissue and CSF oxygen tension as parameters for cerebral oxygenation were evaluated. In experimental studies the influence of changed oxygen offer and decreased cerebral perfusion pressure on CSF and brain tissue pO2 were investigated. Fast changes in CSF pO2 were observed in response to decreasing oxygen offer. Slower changes were noted in response to hypo- and hyperventilation. An autoregulatory mechanism regulating CSF pO2 is postulated. Reducing cerebral perfusion pressure decreased both brain tissue and CSF pO2, but in the reperfusion phase after complete ischaemia a dissociation occurred between brain tissue and CSF pO2, CSF pO2 being restored, but brain tissue pO2 remaining low or even decreasing further. From these studies it is concluded that both CSF pO2 and brain tissue pO2 reflect changes in cerebral oxygenation caused by changes in oxygen offer as well as by changes in cerebral blood flow. Brain tissue pO2 is also sensitive to oxygen demand from the tissue. Preliminary studies of continuous monitoring of brain tissue pO2 in patients with severe head injury are reported.

pO2-profiles in human muscle tissue as indicator of therapeutical effect in septic shock patients.

Automatically stepwise driven pO2 electrodes were transcutaneously inserted into muscle tissue of severely ill septic shock patients. The pO2 profile was plotted from 200 individual measurements registered during 5 minutes and a histogram plotted for documentation. Arterial and venous blood gases, cardiac output, systemic and pulmonary vascular resistance were measured continuously on-line. In septicemia multiple drug schemes are suggested all intending to increase oxygen supply to the tissue and to improve oxygen demand/supply mismatch. So far the attending physician is bound to conclude and continue respectively change the treatment scheme according to the above described macrophysiological parameters. Perfusion distribution and local inhomogenities of tissue oxygen supply remain undetected. In the described study pretreatment pO2 profiles in musculus quadriceps femoris were obtained and measurements repeated in intervals of 10 minutes after start of pharmacological treatment. The changes of pO2 profiles of 20 patients, monitored in such a way over days and weeks, were carefully correlated to the described cardiocirculatory parameters and blood gas analyses. Dopamine was used to improve cardiac function and tissue oxygen supply as well. The investigations show that resulting changes of cardiovascular and blood gas parameters do not always indicate that tissue oxygen supply has really improved. On the other hand there was never an improvement in tissue oxygen supply when no changes of the other parameters had occurred. It is advised to add as a further diagnostic parameter tissue pO2 measurements to get insight if improvement in cardiac and pulmonary function really has the intended effect of improvement of tissue oxygen supply.

[Tissue pO2 measurement in taut back musculature (m. erector spinae)]. / Gewebe-pO2-Messung in der verspannten Rückenmuskulatur (m. erector spinae).

Measurements with polarographic needle probes in fibromyalgic muscles (mm. erectores spinae) revealed an elevated mean tissue-pO2. The total mean tissue-pO2 in the patient group was significantly higher than that in the control group. Greater pathological tension in fibromyalgic muscles increases the mean tissue-pO2. The distribution of local tissue-pO2 values was normal; there was no evidence of small hypoxic areas in the muscle. The elevated tissue-pO2 in fibromyalgic muscles could either be explained by an increase in local blood flow or by disturbance of oxygen-utilization of the muscle cells. The mean tissue-pO2 in patients treated with NSAD was lower than in patients without this treatment. Myogelosises (i.e., circumscript tautness in muscles, that, contrary to fibromyalgic muscles, do not relax under general anesthesia) showed low tissue-pO2 values and even hypoxia in the core. In myogelosises, pain could be hypoxic in nature. However, in fibromyalgic muscles no evidence for hypoxia or hypoxia-related pain could be found.

[Monitoring the oxygen supply of skeletal muscle and total oxygen uptake in coronary surgery interventions]. / Uberwachung der Sauerstoffversorgung des Skelettmuskels und der Gesamtsauerstoffaufnahme bei koronarchirurgischen Eingriffen.

In patients undergoing aortocoronary bypass operations, extensive monitoring is used for early recognition of complications that may decrease the oxygen supply of body organs. However, none of the parameters usually monitored during open-heart surgery yield information on the state of oxygen supply to a certain organ. Particularly during and after extracorporeal circulation (ECC), undetected organ hypoxia may occur and lead to an increase in postoperative complications. In order to study whether functionally significant changes in oxygen supply to skeletal muscle occur during extracorporeal circulation, in 14 patients undergoing aortocoronary bypass operations pO2 histograms from local pO2 values in resting skeletal muscle were monitored. Intra- and postoperatively, whole-body oxygen uptake (VO2) and pO2 histograms of skeletal muscle were simultaneously measured to determine whether the observed decrease in VO2 during cooling of the patient or the increase in VO2 during rewarming was reflected in the distribution of tissue pO2 in skeletal muscle. PATIENTS AND METHODS. Fourteen patients (aged 42 to 68; 12 male, 2 female) scheduled for 2-4 aortocoronary venous bypass grafts were studied. Measuring periods of 6 min were undertaken after induction of anesthesia (1), after thoracotomy (2), during ECC (3), after ECC (2), and every hour postoperatively up to 5 h. The following data were measured during each period: pO2 histograms of the biceps brachii muscle using a pO2 histograph VO2 using open indirect calorimetry; arterial (a. radialis) and venous (v. cava superior) blood gases, acid-base balances, and blood pressures; venous lactate (v. cava superior); muscle and rectal temperatures. RESULTS. During ECC mean muscle pO2 in all 14 patients decreased from 25 to 14 mmHg. In 7 of 14 patients pO2 values between 0 and 5 mmHg had the highest incidence (left-shifted pO2 histograms). After ECC mean muscle pO2 increased to the same value observed before ECC (25 mmHg). During the first 3 h postoperatively an intermediate decrease in mean muscle pO2 (range 23%-46%) occurred in each patient. Stable values above 20 mmHg were reattained 4 h postoperatively. The postoperative increase in individual VO2 was correlated to the increase in body temperature (r = 0.84); in 5 patients with severe shivering, VO2 was markedly increased (up to 130% compared to the last intraoperative value).(ABSTRACT TRUNCATED AT 400 WORDS)

The effect of dopamine on muscle PO2 in healthy volunteers and intensive care patients.

The effect of systemic dopamine administration (2-10 micrograms kg-1 min-1) on the Po2 distribution (histograms) and the mean Po2 in the m. vastus lateralis of m. quadriceps femoris in nine healthy volunteers and seven critically ill patients has been studied with a newly developed bedside measuring procedure. Dopamine initially raised mean muscular Po2 in both groups. In the volunteers, mean muscular Po2 thereafter decreased gradually but still remained slightly elevated after 30 min of dopamine infusion. This increase in muscle oxygenation could be abolished by the administration of a dopamine antagonist (metoclopramide). In the patients, the initial dopamine-induced increase of Po2 was significantly slower and reached a plateau within 30 min. The results are discussed with special attention given to the data available on the action of dopamine on given peripheral circulation.