Propofol administration leads to a significant decrease of STN neuronal activity. Thus, it may interfere with MER identification of the STN borders. However, activity returns to baseline shortly after administration stops. Therefore, propofol can be safely used until shortly before MER for DBS.

No abstract

We report the extradural administration of low-dose morphine in 10 ml of 10% dextrose (2-3 mg) to 98 adult patients with various types of acute and chronic pain. Extradural morphine injections were given either via a Tuohy needle (single or repeat injection) or via an extradural catheter. Pain relief was evaluated by subjective scoring and by the subsequent need for systemic analgesics. In 56% of patients, pain relief was considered good or excellent, in 24% it was fair, and in 20%, poor. The best results were after surgery and trauma and in patients with advanced peripheral vascular disease. The analgesia of each dose of extradural morphine lasted for 8 h (mean range 4-36 h). There was no motor, sensory or sympathetic blockade and no respiratory or haemodynamic complications. Dizziness and vomiting occurred in two patients, and urinary retention for about 12 h in three.

An inverse correlation between postischemic gastrointestinal motility and the length of intestinal ischemia was found in an animal model. Intestinal ischemia was caused without concurrent laparotomy and for a predetermined time period (ischemia time) by pulling on an external nylon thread that was threaded through a double-lumen catheter. This catheter was passed into the abdominal cavity to encircle the superior mesenteric artery. Gastrointestinal motility was determined by the introduction of a color-marked meal into the animal's stomach and the measurement of the proportionate length of the small bowel filled with it (transit index). This simple and reliable animal model can also be used for the evaluation of techniques and pharmacological manipulations aimed at modulation of the effects of intestinal ischemia on intestinal motility and its consequences.

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.

No abstract

We report the extradural administration of low-dose morphine in 10 ml of 10% dextrose (2-3 mg) to 98 adult patients with various types of acute and chronic pain. Extradural morphine injections were given either via a Tuohy needle (single or repeat injection) or via an extradural catheter. Pain relief was evaluated by subjective scoring and by the subsequent need for systemic analgesics. In 56% of patients, pain relief was considered good or excellent, in 24% it was fair, and in 20%, poor. The best results were after surgery and trauma and in patients with advanced peripheral vascular disease. The analgesia of each dose of extradural morphine lasted for 8 h (mean range 4-36 h). There was no motor, sensory or sympathetic blockade and no respiratory or haemodynamic complications. Dizziness and vomiting occurred in two patients, and urinary retention for about 12 h in three.

The effect of volume loading in 20 patients with clinical and bacteriological evidence of generalized sepsis was studied. The patients were divided into two groups according to their response to volume loading. Group A included 9 patients in whom the initial pulmonary capillary wedge pressure (PWP) was lower than the central venous pressure (CVP). In this group the intravenous administration of 5089 + 409 ml/24 hr fluids was accompanied by a significant rise in blood pressure from 94.4 ± 9.3 mm Hg to 118.9 ± 6.3 mm Hg with no significant change in pulse rate or CVP. PWP rose from 5.7 ± 1.8 to 10.0 ± 1.4. The rise in cardiac output from 8.0 ± 1.3 liter/ min to 9.7 ± 1.1 liter/min was not statistically significant.Group B included 11 patients in whom the initial PWP was higher than the CVP. In this group, signs of fluid overloading appeared after administration of 3151 ± 540 ml/24 hr. There was no significant change in blood pressure, pulse rate, CVP, PWP or cardiac output. Urine output was adequate in both groups. This volume load did not affect pulmonary oxygenating capacity (PaO2/F102) and effective lung compliance in both groups, but the maintenance of an unchanged oxygenating capacity necessitated an increase in PEEP in some patients.