The present study explored the hypothesis that a prolonged 8 weeks exposure to a high fructose intake suppresses adrenergic and angiotensin II (Ang II)-mediated vasoconstriction and is associated with a higher contribution of α1D-adrenoceptors. A total of thirty-two Sprague–Dawley rats received either 20 % fructose solution (FFR) or tap water (control, C) to drink ad libitum for 8 weeks. Metabolic and haemodynamic parameters were assessed weekly. The renal cortical vasoconstrictor responses to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined in the presence and absence of BMY7378 (α1D-adrenoceptor antagonist). FFR had increased blood pressure, plasma levels of glucose, TAG and insulin. FFR expressed reduced renal vascular responses to adrenergic agonists and Ang II (NA: 50 %, PE: 50 %, ME, 65 %, Ang II: 54 %). Furthermore in the C group, the magnitude of the renal cortical vasoconstriction to all agonists was blunted in the presence of the low or high dose of BMY7378 (NA: 30 and 31 %, PE: 23 and 33 %, ME: 19 and 44 %, Ang II: 53 and 77 %), respectively, while in the FFR, vasoconstriction was enhanced to adrenergic agonists and reduced to Ang II (NA: 8 and 83 %, PE: 55 %, ME, 2 and 177 %, Ang II: 61 and 31 %). Chronic high fructose intake blunts vascular sensitivity to adrenergic agonists and Ang II. Moreover, blocking of the α1D-adrenoceptor subtype results in enhancement of renal vasoconstriction to adrenergic agonists, suggesting an inhibitory action of α1D-adrenoceptors in the FFR. α1D-Adrenoceptors buffer the AT1-receptor response in the renal vasculature of normal rats and fructose feeding suppressed this interaction.

Accurate bedside assessment of the ratio of pulmonary to systemic flow (Qp/Qs ratio, referred to as “the flow ratio” or “the ratio”) plays an important role in the management of many congenital heart defects, especially the complexes unified by univentricular atrioventricular connections. Arterial oxygen saturation can be a misleading measure of the ratio, and may not reflect derangements until they are quite large. Theoretical analysis suggests that systemic venous oxygenation may be a better indicator of the ratio. To examine this, we created a widely patent atrial septal defect in neonatal piglets (weight =4–6.5 kg, n=6). Snares aruond the aorta and pulmonary trunk were adjusted to alter the flow ratio from 0.1 to 6.5. Venous oxygen saturations, measured in the mid-inferior caval vein, were at a maximum at a ratio about 1, and declined rapidly with increases or decreases in the ratio beyond a limited range. The venous oxygen saturation was found to vary much more than arterial oxygen saturation, with arterial oxygen saturation only falling when the ratio dropped below 0.5. Oxygen delivery (Oxygen Content x Cardiacoutput) was found to parallel closely systemic venous oxygen saturation, and was at a maximum at the same ratio that produced a maximum value of systemic venous oxygen saturation. The study suggests that systemic venous oxygen saturation provides a better estimate than does systemic arterial oxygen saturationof the flow ratio and oxygen delivery. Interventions that maximize systemic venous oxygen saturation should maximize oxygen delivery, and determination of systemic venous oxygen saturation should be a helpful addition in managing children with a number of congenital heart defects.

Summary

Background and objective: We have evaluated the effects of propofol and its relationship with K+ channels on human isolated umbilical vessels. Methods: Umbilical vessel rings were suspended in isolated organ baths containing Krebs–Ringer solution. In the first series of experiments the effect of propofol (10−9–10−4M) was examined in a concentration-dependent manner on umbilical vessels precontracted with KCl (60 mmol). In the second series, these effects were studied in the presence of tetraethylammonium. Results: A mild contraction was produced by low dose propofol in both precontracted umbilical artery and umbilical vein segments. 10−4M propofol caused significant relaxation in both umbilical artery and umbilical vein. The relaxation response was significantly reduced by the addition of 10−1 M tetraethylammonium. Conclusion: These results suggested that the responses of propofol on KCl-induced contractions of both umbilical artery and vein were dose dependent, and this effect involved Ca2+ activated K+ channels.

The aim of this study was to determine which anaesthetic and vasoconstrictor preparations UK Otorhinolaryngologists use for rhinological surgery, with particular reference to cocaine and adrenaline. The incidence and types of adverse reactions to cocaine were also recorded.

A postal survey of all BAO-HNS consultant members was performed. Of the 360 consultant surgeons included in the survey, the majority still use peri-operative cocaine on a regular basis, 66 per cent use cocaine and adrenaline together and more than 40 per cent use cocaine in paediatric patients. Sixteen per cent of respondents did not use cocaine. Only 11 per cent of surgeons had experienced cocaine toxicity in their patients, with only one recorded case of mortality.

Most surgeons in the UK use cocaine because of the superior operative field it provides and because they consider it to be safe even with adrenaline. The actual incidence of adverse reactions to cocaine is low, with serious complications being less common than the risks from general anaesthesia. Cocaine remains a valuable agent in the armamentarium of the rhinologist.

Background and objective: Cardiovascular and mental stress in dental patients with phobias about dentistry may be reduced by propofol sedation. We tested the hypothesis that even low doses of propofol may have effects on body temperatures in male volunteers.

Methods: Six healthy male volunteers were given propofol over 28 min with the following infusion rates: 8 mg kg−1 h−1 for the first 3 min, 4 mg kg−1 h−1 for the next 10 min, and 2 mg kg−1 h−1 for the final 15 min. Body temperatures were measured at five locations: tympanic membrane, forehead, forearm, dorsum of the hand and fingertip. Thermoregulatory vasoconstriction was evaluated using the forearm minus fingertip temperature gradient.

Results: Tympanic membrane and forehead temperatures began to decrease at 10 and 20 min, respectively, after the start of the propofol infusion, and reached a minimum at 30 min (tympanic −0.5 ± 0.2°C) and 40 min (forehead −0.6 ± 0.2°C), respectively. Peripheral skin temperatures showed an increase between 10 and 30 min in the forearm and fingertip and between 20 and 30 min in the dorsum of the hand. After 30 min, a decrease in peripheral skin temperatures was observed. The forearm minus fingertip temperature gradient changed from negative to positive after 40 min, and increased continuously thereafter (baseline −0.3 ± 0.4°C, 90 min: 6.5 ± 1.6°C).

Conclusions: A low dose of propofol impairs tonic thermoregulatory vasoconstriction and induces heat redistribution from the core to the periphery.

Topical vasoconstriction using four to 10 per cent cocaine is widely used for nasal surgery. A number of techniques are being used with equally satisfactory results. Here we describe a novel method of topical application of cocaine for nasal surgery. The method is simple, cheap and effective.