To determine whether magnesium sulphate could induce controlled hypotension, reduce choroidal blood flow, provide a ‘dry’ operative field and could be compared with sodium nitroprusside in the recently raised issue of the use of hypotensive anaesthesia in eye surgery, i.e. for choroidal tumour surgery as the choroid is the most fragile and vascular structure in the eye.

Forty adult patients undergoing choroidal melanoma resection and anaesthetized with 2.5 mg kg−1 propofol, followed by a constant infusion of 120 μg kg−1 min−1, and remifentanil 1 μg kg−1, followed by a continuous infusion of 0.25 μg kg−1 min−1, were randomly assigned to two groups to receive either magnesium sulphate or sodium nitroprusside.

Controlled hypotension was achieved at the target systolic pressure of 80 mmHg within 107 ± 16 and 69 ± 4.4 s for magnesium sulphate and sodium nitroprusside, respectively. Choroidal blood flow decreased by 24 ± 0.3% and 22 ± 3.3% for magnesium sulphate and sodium nitroprusside, respectively. Controlled hypotension was sustained in both groups throughout surgery, and the surgical field rating decreased in a range of 80% in both groups. Sodium nitroprusside decreased pH and increased PaCO2. There were no postoperative complications in any of the groups.

Magnesium sulphate controlled hypotension, reduced intraoperative pressure and provided good surgical conditions for choroidal melanoma resection with no need for additional use of a potent hypotensive agent in adults.

This study was carried out to clarify the effect of the combination of acute hypervolaemic haemodilution and hypotensive anaesthesia induced with sevoflurane on human middle cerebral artery flow velocity using transcranial Doppler ultrasonography.

Thirty patients who were maintained with N2O–O2–sevoflurane anaesthesia undergoing hip surgery were randomly divided into two groups (no controlled hypotension group, Group A, and controlled hypotension group, Group B). Haemodilution was produced by acute preoperative infusion of 1000 mL of hydroxyethylstarch without removing blood in both groups. Mean arterial pressure was maintained at approximately 95 mmHg in Group A and at 55 mmHg for 80 min by increasing the inspired concentration of sevoflurane in Group B. Middle cerebral artery flow velocity was measured before haemodilution, after haemodilution, 80 min after starting hypotension, and 60 min after recovery from hypotension.

Middle cerebral artery flow velocity significantly increased in both groups after haemodilution; by 28%, in Group A, P < 0.05 vs. before haemodilution and by 30% vs. before haemodilution in Group B, P < 0.05). During controlled hypotension, it decreased towards the pre-haemodilution value (P < 0.05 vs. after haemodilution).

Sevoflurane-induced hypotension to a mean arterial pressure of 55 mmHg would reduce middle cerebral artery flow that had been increased by acute hypervolaemic haemodilution, such as haematocrit value of 26%, whereas it could preserve the flow in pre-haemodilution condition during normocapnia.

Atrial and brain natriuretic peptide, synthesized by cardiac myocytes, are mediators secreted secondary to cardiac volume expansion and increased filling pressure. The study was designed to assess serum concentration of atrial and brain natriuretic peptide in patients undergoing endonasal sinus surgery receiving controlled hypotension.

We studied 45 patients without cardiovascular history, scheduled for elective endonasal sinus surgery. Patients were allocated to one of three groups: controlled hypotension was induced either by using esmolol (n = 15) or sodium nitroprusside (n = 15) with a mean arterial pressure of 50–55 mmHg. In the control group (n = 15), mean arterial pressure was adjusted to 70–80 mmHg. Atrial and brain natriuretic peptides were measured preoperatively (T1), at the end of surgery (T2), 2 h (T3), 24 h (T4) and 48 h (T5) postoperatively.

Preoperative atrial and brain natriuretic peptide plasma levels were within normal ranges and similar between all groups. Patients treated with esmolol (atrial natriuretic peptide: 2.46 ± 0.75 μg mL−1; brain natriuretic peptide: 4.34 ± 3.06 μg mL−1) and sodium nitropusside (atrial natriuretic peptide: 2.48 ± 0.92 μg mL−1; brain natriuretic peptide: 4.49 ± 3.21 μg mL−1) showed significantly lower concentrations of atrial and brain natriuretic peptide at T2 and T3 compared with controls (atrial natriuretic peptide: 5.31 ± 2.32 μg mL−1; brain natriuretic peptide: 13.26 ± 8.98 μg mL−1, P < 0.01) as well as a reduction in blood loss and duration of surgery.

Controlled hypotension decreases the release of natriuretic peptides in cardiovascular healthy patients. This effect may be contributed to by changes in cardiac filling pressure due to lower systemic resistance and diminished perfusion pressure.