Summary Celatiri solutions o j various kinds have been used as intruvenous infusions since the Key wordsCntnplicwtions; anaphylactoid reactions. in/ravenous infusion; gelati ti solu ti ons. HistoryOnce the acceptability of intravenous fluid infusions had been cstablished around the turn of' the century. clinicians had to decide which solutions were the most beneficial and the debate on this issue continues today.' Crystalloid prcparations were readily available and inexpensive but they remained within the intravascular compartment only transiently before they were excreted or lost to the interstitial fluid spaces. Following Starling's concept that plasma volume is regulated by the oncotic pressure,* attempts were made to find a suitable colloid solution. Human plasma was suitable, but was scarce and expensive. Of the artificial preparations, the vegetable colloids such as acacia, pectin and gum arabic enjoyed a ~o g u e~,~ and were used for a time in the management of hypoproteinaemic states. e.g. the nephrotic ~y n d r o r n e .~ They gradually fell into disuse when a variety of unwanted side effects came to light; these included agglutination and interference with hepatic Gelatin. a macromolecular protein found in mammals. had potential as a colloidal solution.It was inexpensive, readily available, could be stored over long periods without degradation and seemed to possess low antigenic properties. It was thought that enzymatic pathways in man could split the compound to yield rnolccules which could be excreted or metaboliscd. However, gelatin also possessed the disadvantages of a high viscosity in solution, due to the molecular weight of 100 000, and preparations tended to gclate at lower temperatures. The first reports of the use in man of gelatin solutions appeared in 1915, when transfusion of blood was both difficult and potentially dangerous. It was realised then that salt solutions of

The cardiovascular responses to tracheal intubation using a jibreoptic bronchoscope or Macintosh laryngoscope were compared in twenty in-patients and twenty day-stay patients. Within these groups patients were randomly allocated to direct laryngoscopic or jibreoptic bronchoscopic intubation. Arterial blood pressure, heart rate and arterial oxygen saturation were recorded before induction and at one-minute intervals untilfour minutes after intubation. In both groups both laryngoscopic and bronchoscopic intubation resulted in a significant rise in blood pressure and heart rate. At no stage was there a significant difference in mean blood pressure in either group, or in heart rate in the day-stay patients, betl'v'een the different methods of intubation. In the in-patients mean heart rate was signijicantly higher in those patients intubated with the bronchoscope at three and four minutes after intubation. Time taken for intubation was significantly longer in those patients intubated with the bronchoscope. In no patient did the arterial oxygen saturation fall below 98%.

This study was performed to determine the effects of various doses of succinylcholine on resting tension and evoked twitch height at the masseter and adductor pollicis muscles in children. Twenty patients, aged 3-10 yr, ASA physical status I or II, were randomly assigned to receive succinylcholine 0.15, 0.25, 0.50 or 1.00 mg.kg-1, during halothane-nitrous oxide anaesthesia. Supramaximal train-of-four stimulation was applied simultaneously to the ulnar nerve and the nerve to the masseter. Transducers recorded force at the jaw and the thumb. Maximum blockade of the first twitch (T1) and maximum resting tension change were measured. Potency of succinylcholine at the two muscles was estimated by linear regression of the logit transformation of T1 versus log dose. The relationship between resting tension change and log dose was established by linear regression. The masseter muscle was more sensitive to succinylcholine than the adductor pollicis with an ED95 of 0.28 +/- 0.02 (mean +/- SEM) vs 0.44 +/- 0.05 mg.kg-1 (P less than 0.05). Onset of neuromuscular blockade was faster at the masseter, and recovery occurred simultaneously in both muscles. A dose-related increase in resting tension was observed in both muscles, but its magnitude was five times greater at the masseter. With succinylcholine, 1 mg.kg-1, this increase was 51.6 +/- 16.8 g at the masseter and 9.1 +/- 2.3 g at the adductor pollicis. Tension returned to baseline within 1-2 min.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of intravenously administered ethanol and morphine on pain threshold, reaction time, motor skills and short-term memory were investigated, and the ability of naloxone to reverse any changes was studied. Morphine (loading dose 0.2 mg/kg with an infusion of 0.004 mg/kg per min) and ethanol (loading dose 0.75 ml/kg with an infusion of 0.0025 ml/kg per min) produced a similar increase in pain threshold of 6.3 (s.e.m. = 1.5, n = 8) pain units and 7.7 (s.e.m. = 1.9, n = 8) pain units, respectively. Naloxone 0.015 mg/kg produced a significant reduction in pain threshold in the morphine group, but not in the ethanol group, and there was a significant difference between the groups following naloxone (P less than 0.05, t-test, 7 d.f.). Ethanol produced a significantly greater deterioration in motor skills than did morphine (P less than 0.05, t-test, 7 d.f.) and performance in both groups was improved following naloxone (P less than 0.05, t-test, 7 d.f.). There was no significant change in the other modalities studied. It is concluded that the reversal of ethanol effects by naloxone is probably due to a non-specific analeptic action rather than blockade of opioid receptors.

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