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Background: Patients with drug allergies are commonplace in anaesthetic practice. We investigated the incidence and nature of drug 'allergies' reported by surgical patients attending a hospital pre-admission clinic, and went on to ascertain to what degree drug allergies recorded in the records influenced drug prescribing during the patients' hospital stay and determine whether any adverse events occurred in relation to drug prescribing in this population., Methods: Patients attending for anaesthetic assessment at a Pre-Admission Clinic over a 30 week period were questioned concerning drug allergies. Medical records of these patients were then examined after their hospitalization to assess medications prescribed during that period., Results: Of 1260 patients attending the Pre-admission clinic during the study period 420 (33.4%) claimed to have a total of 644 individual drug 'allergies'. The most common agents implicated were antibiotics (n=272), opioid analgesics (n=118) and NSAIDs (n=62); the most common form of these reactions were dermatological (n=254) and nausea and vomiting (n=124). There were 41 self-reports specifically of anaphylaxis and a further 61 where there was significant respiratory system involvement., Conclusions: The majority of the self-reported allergies were in fact simply accepted adverse effects of the drugs concerned. The patients' reported drug 'allergy' history was generally well respected by anaesthetists and other medical staff. There were 13 incidents, mainly involving morphine, where patients were given a drug to which they had claimed a specific allergy. There were 101 incidents in 89 patients where drugs of the same pharmacological group as that of their allergic drug were used. There were no untoward reactions in 84 patients who had claimed a prior adverse reaction to penicillin who were given cephalosporins. There were no sequelae from any other events. While anaesthetists generally respected patients self-reported 'allergies', more attention needs to be paid to the accurate recording of patients' events and a clear distinction should be made both in medical records and to the patient between true drug allergy and simple adverse drug reactions.

Unlabelled: The aim of this study was to test the hypothesis that halothane interferes with the myogenic response to an increase in intraluminal pressure. Myogenic responsiveness refers to the intrinsic property of vascular smooth muscle to dilate and then constrict in response to an increase in intraluminal pressure, in an attempt to maintain vessel diameter. Vessel segments taken from the rabbit central ear artery were cannulated, pressurized to 60 mm Hg, and perfused with and suspended in Krebs solution. After exposure to extraluminal l-norepinephrine, vessels contracted to an initial diameter (Di) and were subjected to intraluminal pressure increases to 100 mm Hg. Myogenic reactivity was assessed by measurement of the extent of dilatation after the pressure increase from Di to a maximal diameter (Dm) and then the constriction and recovery (against the pressure increase) to a final (Df) diameter. Myogenicity was further assessed by determining the rate of return of the vessel diameter (angle of recovery) and vessel recovery (defined as Dm - Df/Dm - Di) and expressed as a percentage. Myogenicity was determined before and after exposure to halothane in concentrations of between 1-5%. Halothane significantly attenuated the myogenic response at all concentrations studied. The effect of halothane was maximal at a concentration of 5% where there was virtual abolition of the myogenic response with recovery assessed at 6+/-2.7% (SEM), compared with control (98+/-2.5%, P < 0.05). The angle of recovery was likewise attenuated. These data suggest that halothane, in a dose-dependent manner, attenuates myogenicity in the isolated rabbit ear artery preparation., Implications: Blood pressure is controlled partially by the myogenic response. This refers to the capacity of arteries to dilate and then constrict in response to pressure increase. Using arteries from rabbits, we have shown that administration of halothane reduces or abolishes this response. This observation may be a contributing factor to hypotension caused by halothane.

The myogenic response is the tendency of certain vessels, most notably small arteries and arterioles, to constrict in response to an increase in intravascular pressure. The effects of propofol on the myogenic response of the isolated pressurized rabbit ear artery were studied in segments preconstricted either with norepinephrine or 5-hydroxytryptamine and subjected to pressure increases from 60 to 100 mm Hg applied either rapidly (jumps over 500 ms) or slowly (ramps over 120 s). In the control experiments the preconstricted vessels initially dilated, then rapidly returned toward their initial diameter. In response to pressure ramps, vessels slowly dilated, but closely retained their resting diameter. Administration of propofol (1.6 x 10(-4) to 1.6 x 10(-3) M) resulted in dilation of the constricted vessels. With pressure jumps vessels had a reduced capacity to recover their initial diameters, and with pressure ramps vessels dilated to greater diameters. When the concentration of vasoconstrictor was increased to antagonize the propofol-induced dilation the myogenicity was not restored. This attenuation of myogenicity, distinct from the drug's vasodilator effect may represent a further mechanism by which anesthetic agents can affect cardiovascular function.

To determine if accidental intraarterial injection of propofol results in vascular damage, the effect of bolus administration of propofol on vascular smooth muscle and the endothelium was investigated using the isolated rabbit ear artery. Ear artery segments, removed from urethane anesthetized rabbits, were perfused with Krebs solution (1 ml.min-1) and pressurized to 60 mmHg before being constricted with extraluminal norepinephrine (1.8-4.2 x 10(-6) M). The external diameter of the vessel was measured by an array of light-dependent diodes. Functional responsiveness was determined by the degree of constriction to norepinephrine and the subsequent dilatation of the artery to intraluminal acetylcholine (2 x 10(-6) M) and glyceryl trinitrate (2 x 10(-6) M), and by the myogenic reactivity to a pressure increase from 60 to 100 mmHg. These responses were measured before and after perfusion with 1% propofol for 120 s. Administration of propofol did not result in any vasoactivity nor did it increase the sensitivity to norepinephrine. Vessels maintained their capacity to dilate to both agents, while the myogenic activity was unaffected. Histologic examination of the propofol exposed vessels showed no changes to smooth muscle structure, and the endothelial layer remained intact.

Teaching gastrointestinal physiology to preclinical medical students presents problems in finding suitable practical exercises to demonstrate the physiology of gastric acid secretion. In our course, students measure their own gastric secretory activity by the use of nasogastric tubes. Gastric secretion can be stimulated by insulin-induced hypoglycemia or by pentagastrin, a synthetic gastrin analogue. The time course of the secretory responses, i.e., volume, acid output, and pH, are followed by collecting control and poststimulatory secretions into 15-min samples. The effect of antiulcer drugs, such as cimetidine, can be easily studied in such experiments. The results of these experiments are very reproducible, allowing year-to-year comparisons of treatments. Examples of results of various experimental protocols are shown. We believe this to be a useful class exercise not only because of the excellent results it yields but because of the experience and insights it produces.

Ear artery segments removed from urethane-anaesthetized rabbits were mounted, perfused with Krebs solution, and pressurized before constriction with extraluminal noradrenaline. Vessel diameter was measured using a diode array mounted above the artery. After the degree of dilatation in response to intraluminal acetylcholine and glyceryl trinitrate was measured, vessels were perfused for 120 s with solutions of either 2.5-10% thiopentone or isotonic sodium carbonate in saline of matched pH. Administration of thiopentone solutions in all concentrations resulted in destruction of endothelial cells. The dilatation of vessels to glyceryl trinitrate and their myogenic reactivity was unaltered. Isotonic solutions of sodium carbonate (pH 10.6) had no effect on either endothelial cell function or direct vasodilatation. These data show that administration of thiopentone removes arterial endothelial cells, while vascular smooth muscle function is essentially unaltered.