The influence of induced hypotension and spine distraction on canine spinal cord blood flow.

Deliberate hypotension is used in scoliosis surgery to reduce the need for blood transfusion and to improve operating conditions. There are concerns, however, that hypotension may decrease spinal cord blood flow (SCBF) and thereby predispose the spinal cord to ischemic injury, particularly when it is distracted during Harrington instrumentation. In a canine model, the mean arterial pressure (MAP) was reduced to 50% of the normotensive value with sodium nitroprusside and halothane to study its effects, with and without spinal distraction, on spinal cord blood flow measured by the hydrogen clearance technique. The induction of systemic hypotension resulted in a significant decrease in spinal cord blood flow from 15.7 +/- 1.1 ml/min/100 g (control) to 10.7 +/- 4.7 ml/min/100 g. This initial decrease in spinal cord blood flow returned to normotensive values by 35 minutes following the induction of hypotension, suggesting an autoregulatory effect. This indicates that the induction of deliberate hypotension to half its normotensive mean arterial pressure is associated with a significant decrease in spinal cord blood flow that returns to normotensive levels by 35 minutes. One and two centimeters of longitudinal distraction applied during systemic hypotension did not reduce spinal cord blood flow when it was applied at least 45 minutes after the hypotension was induced. Thus, when longitudinal stretch of a magnitude approximating that used clinically during Harrington instrumentation is applied in the presence of systemic hypotension, the normal SCBF is not reduced when the autoregulating system is functioning.(ABSTRACT TRUNCATED AT 250 WORDS)

Urban hypothermia.

A case is reported of a 23-year-old man who became hypothermic within 4 hours of exposure. Full physical recovery occurred within 5 hours of an asystolic cardiac arrest using simple rewarming techniques.

Acebutolol and oral surgery: plasma levels following a single oral dose.

Twenty eight patients were randomly allocated into treatment or placebo groups. The treatment group received a single 400 mg oral dose of acebutolol, the placebo group an identical inert prepation. A blood sample from each patient was subsequently analysed for plasma concentrations of acebutolol and diacetolol, and the electrocardiogram was continuously monitored for changes of rate and rhythm. The plasma concentrations of acebutolol and diacetolol were all above the previously reported minimum levels for effective dysrhythmia control and the nine patients in whom irregularities of rhythm occurred were all in the placebo group. One patient in the treatment group, who was 58 years old, required intravenous injection of atropine for bradycardia and hypotension after induction of anaesthesia. It is suggested that in patients with small body weights and in those patients over 50 years of age the predmedication dose of acebutolol should be reduced to 200 mg.