We localized the sites of vasodilation of inhaled nitric oxide (NO), a selective pulmonary vasodilator, and sodium nitroprusside (SNP) in isolated rat lungs. The sites were determined by analyzing the arterial, venous, and double-occlusion data with a two-resistor (small arteries and veins) three-capacitor (large arteries, large veins, and capillaries) model of the pulmonary vascular bed. Inhaled NO (170 and 670 ppm) and SNP (22.5 and 45.0 micrograms) decreased the small-artery resistance by 7.4 +/- 1.6, 17.2 +/- 2.2, 14.2 +/- 2.8, and 21.4 +/- 3.4% and the small-vein resistance by 13.5 +/- 3.2, 20.3 +/- 3.4 (SNP of 22.5 micrograms not significant), and 9.3 +/- 3.3%, respectively, in blood-perfused lungs (n = 12). Similar results were observed in Krebs-perfused lungs (n = 12). Capillary compliance was unaffected by inhaled NO and SNP. SNP increased the large-artery capacitance by 40.0 +/- 8.6 and 69.3 +/- 9.7%, whereas inhaled NO had no effect. SNP increased the large-vein capacitance by 31.0 +/- 8.7 and 48.0 +/- 10.7%, whereas inhaled NO had no effect in blood-perfused lungs. However, in Krebs-perfused lungs inhaled NO and SNP (45.0 micrograms only) increased the large-vein capacitance by 43.3 +/- 11.9, 41.4 +/- 14.2, and 44.2 +/- 11.0%. In conclusion, in blood-perfused isolated rat lungs inhaled NO and SNP dilate small-resistance arteries and veins, whereas SNP but not inhaled NO dilates larger capacitance arteries and veins. Furthermore, blood appears to prevent the downstream vasodilation by inhaled NO on larger capacitance pulmonary veins.

Administration, Inhalation↗

PubMed1994

Direct effects of intravenous anesthetics on pulmonary vascular resistance in the isolated rat lung.

We determined the direct effects of thiopental, ketamine, midazolam, etomidate, and propofol on pulmonary vascular resistance (PVR), the relationship of the direct effects to the baseline PVR, and the possible interaction with functional endothelium. The intravenous anesthetics were injected randomly into 1) endothelium-intact isolated rat lungs which were either unconstricted or constricted with angiotensin II (n = 10), and 2) lungs with endothelial injury produced by electrolysis (n = 10). In endothelium-intact lungs thiopental (0.5 and 5.0 mg/kg) and etomidate (3.0 mg/kg) significantly (P < 0.05) increased PVR by 3% +/- 1%, 30% +/- 7%, and 29% +/- 5%, respectively. Ketamine (3.0 and 100 mg/kg) and propofol (20 mg/kg) significantly (P < 0.05) decreased the PVR by 6% +/- 1%, 15% +/- 1%, and 8% +/- 1%, respectively. Midazolam (0.3 and 3.0 mg/kg) and smaller doses of etomidate (0.3 mg/kg) and propofol (2.0 mg/kg) did not affect PVR. These responses did not vary with the baseline PVR over a twofold range. The effects of thiopental, ketamine, etomidate, and midazolam were not altered by endothelial injury. In contrast to the vasodilation produced by propofol in normal lungs, propofol (20 mg/kg) significantly (P < 0.05) increased the PVR by 8% +/- 2% after endothelial injury. In conclusion, this study demonstrates that thiopental and etomidate are direct pulmonary vasoconstrictors, ketamine and propofol are direct pulmonary vasodilators, and midazolam has no direct effects in the isolated rat lung. Further, these effects on pulmonary vasculature do not vary with baseline PVR, and only propofol appears to have endothelium-dependent effects.

Anesthesia, Intravenous↗

PubMed1994

Comparison of the force required for dural puncture with different spinal needles and subsequent leakage of cerebrospinal fluid.

An in vitro model was used to determine the force required to pierce bovine dura with a range of new spinal needles and to measure the subsequent leakage rate of cerebrospinal fluid (CSF). A significantly greater force was required to pierce the dura with pencil-point style needles compared to Quincke needles of the same size. Quincke needles caused a greater loss of CSF than their pencil-point equivalents. The results suggest that there is not likely to be a significant reduction in postdural puncture headache (PDPH) using a 27-gauge pencil-point needle compared to a 25-gauge needle that may be easier to use. Different makes of the same design and gauge of needle showed significant differences in the amount of CSF leakage, which may influence the clinician's choice of needle.

Anesthesia, Epidural↗

PubMed1994

Yet another source of needlestick injury: a case of needle packaging not up to scratch?

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Drug Packaging↗

PubMed1994

Inhaled nitric oxide selectively decreases pulmonary vascular resistance without impairing oxygenation during one-lung ventilation in patients undergoing cardiac surgery.

BACKGROUND: Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigated whether inhaled NO decreases pulmonary vascular resistance (PVR) while preserving hypoxic pulmonary vasoconstriction and whether it maintains or improves oxygenation in patients during one-lung ventilation. METHODS: In supine cardiac surgical patients with a normal mean pulmonary artery pressure (PAP) (< 25 mmHg, n = 10) or a moderately elevated PAP (25-35 mmHg, n = 10), one-lung ventilation was established with 80% oxygen and 20% nitrogen followed by the same gas mixture containing 20 ppm NO for 6 min. RESULTS: Inhaled NO decreased (P < 0.05) PAP from 30 +/- 2 to 27 +/- 2 mmHg in the patients with moderate pulmonary hypertension. Likewise, PVR decreased (P < 0.05) from 266 +/- 10 to 205 +/- 8 dyn.s.cm-5. The PAP and PVR did not change significantly after NO inhalation in the patients without pulmonary hypertension. All other hemodynamic variables remained unchanged after inhalation of NO in both groups. In the patients with pulmonary hypertension, the PAP and PVR returned to baseline after discontinuation of inhaled NO. Inhaled NO did not significantly change the arterial oxygen tension or venous admixture in either group of patients. Ventilation, airway pressure, tidal volume, and lung compliance also were unaffected by inhaled NO. CONCLUSIONS: This study demonstrates that 20 ppm inhaled NO is a selective pulmonary vasodilator in patients with moderate pulmonary hypertension secondary to cardiac disease who are undergoing one-lung ventilation. In contrast to what would be expected with intravenous vasodilators that inhibit hypoxic pulmonary vasoconstriction, inhaled NO does not increase the venous admixture or impair oxygenation.

Cardiac Surgical Procedures↗

PubMed1993

Pain and the paramedian approach to epidural catherisation.

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Catheterization, Peripheral↗

PubMed1993

A comparison of keyed and non-keyed vaporizer filling modes and volatile agent wastage.

Two hundred and forty bottles of enflurane were collected after their contents had been emptied into vaporizers equipped with keyed or non-keyed filling ports. The volume of agent remaining, the residual volume, was measured. There was a greater (p < 0.001) residual volume in 'empty' bottles which had been used to fill keyed compared with non-keyed enflurane vaporizers. Five hundred and fifty two bottles of isoflurane were also collected after they had been used to fill keyed vaporizers. There was no significant difference between the residual volume remaining in bottles of isoflurane and enflurane used to fill keyed fillers; however, the difference was statistically significant if the residual volume was expressed as a proportion to the volume of agent contained in the full bottle. The results show that volatile anaesthetic agent wastage is increased by the use of keyed fillers. Isoflurane wastage caused by utilisation of keyed fillers could be reduced by a factor of 2.5 by supplying isoflurane in 250 ml rather than 100 ml bottles.

Anesthesia, Inhalation↗