The aims of this work were: (1) to establish a technique for the sampling of human tracheobronchial mucus not contaminated by saliva or topical anesthesia, and (2) to measure its viscoelastic properties. After local anesthesia of the hypopharynx by topical application of 4% xylocaine, a double-sleeve microbiology specimen brush was introduced into a flexible bronchoscope placed in the trachea. The brush was left in direct contact with the bronchial mucosa for 20 to 30 s to allow mucus to collect on it. The mucus sample was then scraped from the brush and immediately covered with paraffin oil. Its viscoelastic properties were determined by the magnetic microrheometer technique. Excluding the time to anesthetize, the whole procedure took less than 1 min (thus minimizing the effect of cough) and resulted in sufficient mucus for rheologic analysis in approximately 90% of trials, i.e., 2.1 +/- 1.5 (SD) mg. Mucus specimens were collected from 20 fasting healthy nonsmoking subjects; 17 of them returned for a second collection several days later. Values for mucus mechanical impedance (vector sum of elasticity and viscosity) at 1 rad/s were: Control 1, 141 +/- 41 (SE); Control 2, 155 +/- 58 dyn/cm2. There was a large variation in mucus viscoelasticity, both between subjects (CV, 130%) and within the same subject (CV, 55%) on different days. In 7 subjects, mucus samples were collected 15 min after intravenous injection of 0.6 mg atropine. Viscoelasticity in these samples was 708 +/- 147 dyn/cm2, a value significantly different from Control 1 (p less than 0.05) and Control 2 (p less than 0.05) values.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this work was to determine whether the nonadrenergic, noncholinergic, inhibitory nervous system can be reflexly activated in humans by laryngeal stimulation. The stimulation was achieved with a cytology brush passed through a bronchoscope previously introduced transnasally and positioned just above the epiglottis. In one series of experiments, subjects were premedicated with beta-adrenergic and cholinergic blockers, and bronchoconstriction was induced by histamine inhalation. The results showed that mechanical irritation of the vocal cords with the cytology brush produced a sharp, short-lasting (less than 1 min) decrease in RL from (mean +/- SE) 6.8 +/- 2.1 to 4.8 +/- 1.5 cm H2O.L-1.s, and in the absence of parasympathetic blockade, laryngeal irritation produced a fall in RL from (mean +/- SE) 9.0 +/- 3.7 to 5.4 +/- 2.0 cm H2O.L-1.s (p less than 0.0001) (ANOVA). This decrease in RL was independent of the slight cough produced by laryngeal stimulation and reflects a change in lower and not upper airway resistance. Adequacy of the beta-adrenergic and cholinergic blockade was checked with an intravenous infusion of isoproterenol and inhaled methacholine, respectively. In 2 subjects, the fall in RL was abolished by a block of the superior laryngeal nerves and direct local anesthesia of the vocal cords. We conclude that mechanical irritation of the larynx produces a partial reversal of histamine-induced bronchoconstriction that is mediated through nervous pathways that are neither beta-adrenergic nor cholinergic in origin. We suggest that this decrease in bronchoconstriction is modulated by the nonadrenergic, noncholinergic, inhibitory nervous system.

The aim of this work was to determine if the nonadrenergic noncholinergic nervous system can be reflexly activated in asthmatic patients by stimulating the vocal cords. The stimulation was produced by a cytology brush passed through a bronchoscope previously introduced transnasally and positioned just above the epiglottis. The subjects were premedicated with cholinergic blockers, and bronchoconstriction was induced by inhalation of histamine. In 11 experiments performed on six patients, vocal cords stimulation resulted in a decreased RL from 8.4 +/- 1.0 to 6.3 +/- 0.8 cm H2O.L-1.s (mean +/- SE) (p less than 0.01). To assess the possible contribution of circulating catecholamines to this decrease, plasma epinephrine and norepinephrine levels were measured in six experiments, before and 30 s, 1, 3, and 5 min after the stimulation. Pulmonary resistance fell from 10.0 +/- 1.3 to 7.6 +/- 0.9 cm H2O.L-1.s (mean +/- SE) (p less than 0.05) 30 s and to 7.9 +/- 0.9 cm H2O.L-1.s (p less than 0.05) 60 s after stimulation. Epinephrine and norepinephrine levels increased slightly but not significantly throughout the experiment. We conclude that in asthmatic patients, as in normal subjects, stimulation of the vocal cords produces a reflex decrease in histamine-induced bronchoconstriction which is modulated by the nonadrenergic noncholinergic nervous system.

A case of villous adenoma of the colon with hyponatremia, hypovolemia, and syncope is presented. The correct diagnosis was delayed because of the prevailing idea that villous adenomas are associated with hypokalemia. The patient recovered fully after surgical removal of one of the largest villous adenomas reported in the literature. Sodium loss may be the dominant feature of this syndrome. Villous adenoma has to be included among the causes of hyponatremia.

1. To test whether cystic fibrosis (CF) altered the kinetics and dynamics of oral salbutamol, 11 patients with CF (19‐33 years old; five females; FEV1: 37 +/‐ 12% of predicted value) and 10 healthy volunteers (20‐41 years old; five females; FEV1: 99 +/‐ 14% of predicted value) received orally 4 mg salbutamol. 2. The estimated pharmacokinetic parameters of salbutamol in patients with CF were identical to those in healthy subjects. For instance, peak plasma concentrations of salbutamol were 10.5 +/‐ 2.6 (mean +/‐ s.d.) and 10.2 +/‐ 2.9 ng ml‐1 (NS), and the area under salbutamol plasma concentrations as a function of time (AUC (0, 7 h)) was 43.0 +/‐ 9.3 ng ml‐1 h and 43.3 +/‐ 12.7 ng ml‐1 h (NS) in CF patients and in healthy subjects, respectively. Since on a mg kg‐1 dose basis, CF patients received a dose 28% greater than healthy subjects, this lack of differences implies a decrease in the amount of salbutamol absorbed, or alternatively, an increase in both clearance and volume of distribution of salbutamol. 3. Salbutamol did not elicit bronchodilation in CF patients, but increased heart rate from 77 +/‐ 2 to 103 +/‐ 3 beats min‐1 (P < 0.05). 4. Salbutamol decreased plasma potassium concentrations from 4.5 +/‐ 0.1 to 3.8 +/‐ 0.1 mmol l‐1 in the CF group (P < 0.05) and from 4.1 +/‐ 0.2 to 3.4 +/‐ 0.1 mmol l‐1 in the controls (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

During thoraco-abdominal aortic aneurysmectomy, the aorta is replaced from the left subclavian artery to the aortic bifurcation. We wished to describe the haemodynamic events occurring during clamping and unclamping of the thoracic aorta and the metabolic changes associated with the interruption of organ perfusion beyond the left subclavian artery. MethodsWe studied I I patients (58-77 years) undergoing thoracoabdominal aortic aneurysm resection without the use of cardiopulmonary bypass. All patients had normal left ventricular systolic function. No patient had angina.Diazepam, fentanyl, pancuronium, air/O2 anaesthesia was used, An arterial line, a Swan-Ganz catheter and a left double lumen endobronchial tube were inserted. The left lung was collapsed to facilitate surgical exposure. Immediately prior to the application of the thoracic aortic cross-clamp, sodium nitroprusside was infused in an attempt to eliminate excessive hypertension at the time of cross-clamp. This was continued for the duration of the cross-clamp (mean 72 minutes) to maintain systolic arterial pressures between 150-200 mmHg. An IV infusion of five per cent sodium bicarbonate was given to achieve a serum b/carbonate of 30-35 nunol.L-~ prior to unclamping of the aorta. ResultsHaemodynamic results (Table I) Cross-clamping of the thoracic aorta produced an immediate increase in mean arterial blood pressure (MAP). This reverted hack to preclamp levels with removal of the clamp, Mean pulmonary artery pressure (MPAP) increased significantly with clamp application and this increase persisted after removal of the clamp. There was no significant change in either systemic vascular resistance (SVR) or pulmonary vascular resistance (PVR). Cardiac indices (CI) were not affected by clamp application but increased significantly after clamp removal. Both the central venous (CVP) and pulmonary capillary wedge pressures (PCWP) increased with clamp application and these changes persisted after clamp removal.Metabolic results (Table 11) An average of 791 mmol of sodium bicarbonate (range 240-1545 mmol) was infused during the time of crossclamp. Unclamping of the aorta with re-establishment of circulation to liver, gut, and kidneys produced an acid wash out, resulting in a highly significant drop in pH (p < 0.001) and plasma bicarbonate. PCO2 rose significantly Catecholamine release may influence the haemodynamic response to anaesthetic induction with narcotics in patients with coronary disease. 1 Previous studies have yielded conflicting results regarding serum catecholamine responses to narcotic anaesthesia.~-4 We have noted unexplained, potentially deleterious, increases in heart rate (HR) and arterial pressure (AP) in occasional patients during induction with high-dose fentanyl. 5 Therefore we tested the hypothesis that catecholamine release accompanies anaesthetic induction with potent narcotics. MethodsInstitutional approval was obtained and all patients gave informed consent. Thirty-three patients with preoperative left ventricular ejection fraction >0.50...