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Biomedical subjects

M Wareing

Publications and source records attributed to M Wareing.

24 records · Page 2Linked to original sources

Drug induced otalgia due to mesalazine and sulphasalazine.

A case of left otalgia in a patient suffering from longstanding ulcerative colitis is reported. The patient was treated for an exacerbation of his disease with courses of mesalazine and sulphasalazine during which time he developed otalgia. The otalgia disappeared with cessation of the drugs. It is concluded that in the absence of any other head and neck cause that the otalgia was a complication of the drug therapy.

Aminosalicylic Acids↗

Estimated potassium reflection coefficient in perfused proximal convoluted tubules of the anaesthetized rat in vivo.

1. As yet there is no definitive description of the mechanism and route by which K+ reabsorption is achieved in the proximal convoluted tubule (PCT). We have assessed the contribution of convective K+ transport to net potassium ion flux (JK) by estimating the reflection coefficient of K+ (sigma K) in the proximal tubule of anaesthetized rats previously prepared for in vivo microperfusion. 2. Alterations in the luminal concentration of the impermeant solute raffinose in single-perfused (lumen only) and double-perfused (lumen and capillaries) PCTs were found to change fluid reabsorption in a predictable fashion. 3. Net potassium ion flux (JK) in single- and double-perfused tubules was significantly correlated with net fluid flux (Jv), suggesting that convective K+ transport may be a significant factor in overall K+ transport by the PCT. 4. Estimates of sigma K in single- and double-perfused tubules were very similar (0.14 +/- 0.06 and 0.13 +/- 0.05, respectively), even though K+ diffusion was not strictly controlled in the former group. The maximum effect of 'pseudo-solvent' drag in double-perfused tubules was estimated to give a sigma K of 0.40. This low value for sigma K suggests that true convection/solvent drag may be an important driving force for the reabsorption of K+ from the PCT of the rat.

Anesthesia↗

Effect of barium on potassium diffusion across the proximal convoluted tubule of the anesthetized rat.

The role of diffusion in transepithelial potassium flux and the importance of potassium channels in the luminal cell membrane to this process were examined by applying a luminal microperfusion technique to surface tubules in kidneys of anesthetized rats. Potassium concentration gradients were applied by altering the concentration of KCl in perfusates. To some perfusates, 2 mmol/l BaCl2 was added to block potassium channels in the luminal cell membrane. The mean applied potassium concentration gradient was highly predictive of net potassium transport in the absence of any change in fluid reabsorption, with an apparent potassium permeability of 22 x 10(-5) cm/s. Thus potassium transport in the proximal tubule may have an important diffusive component. Luminal barium significantly reduced the concentration of potassium in collected fluid under conditions of net potassium secretion, although a substantial barium-insensitive potassium permeability was also observed. However, the site of action of luminally applied barium is uncertain in proximal tubule, since barium was reabsorbed by the tubule at a rate of 13.6 pmol.mm-1.min-1. We conclude that diffusion is a significant driving force for potassium reabsorption in proximal tubule and that most diffusive potassium transport occurs via a barium-insensitive route, possibly the paracellular pathway.

Animals↗

Effect of formate and oxalate on fluid reabsorption from the proximal convoluted tubule of the anaesthetized rat.

1. It has recently been suggested that both formate and oxalate may be involved in the reabsorption of chloride from the proximal convoluted tubule (PCT). Reabsorption is achieved via a mechanism coupling Na(+)-H+ exchange to Cl(-)-anion exchange thus facilitating net NaCl transport. This possible mechanism was investigated further by observing the effect of luminal addition of formate and oxalate on proximal tubule transport in anaesthetized rats, previously prepared for in vivo microperfusion. 2. Addition of formate (0.25 mmol l-1) to the luminal perfusate resulted in a significant stimulation of fluid reabsorptive rate. 3. Oxalate was found to have a concentration-dependent effect on fluid reabsorption. Luminal oxalate concentrations below 0.05 mmol l-1 stimulated fluid reabsorption, while an oxalate concentration of 0.5 mmol l-1 inhibited fluid reabsorption. 4. The presence of formate (0.25 mmol l-1) and oxalate (0.001 mmol l-1) in the same luminal perfusate stimulated fluid reabsorption from the proximal tubule lumen, but the effects of formate and oxalate were not additive. 5. The removal of bicarbonate from the luminal perfusate and its replacement with phosphate had no significant effect on fluid reabsorptive rate. An alteration in perfusate pH was also ineffective. Addition of oxalate at high and low pH failed to stimulate fluid reabsorption compared with pH-matched control perfusions. 6. The experimental data suggest the involvement of both formate and oxalate in the reabsorption of NaCl from the proximal tubule lumen, though their influence may not be exerted through the same mechanisms.

Absorption↗

Pharmacokinetics and pharmacological effects of neostigmine in man.

1 The pharmacokinetics of neostigmine was studied in six patients during the reversal of neuromuscular block induced by tubocurarine chloride. The effect of the drug on neuromuscular function was simultaneously assessed by electromyography. 2 Neostigmine was rapidly eliminated from plasma after intravenous administration. The decline in the plasma concentration of the drug was invariably resolved into two exponential components. The fast disposition (distribution) half-life of the drug was invariably less than 1 min; the slow disposition (elimination) half-life ranged from 15.4--31.7 min. 3 Neostigmine usually increased the amplitude of the compound muscle action potential and diminished electromyographic decrement within 2 min of intravenous injection. The pharmacological effect of neostigmine was usually maximal between 7 and 15 min. There was an inverse relationship between the plasma concentration of the drug and the facilitation of neuromuscular transmission. 4 Red cell acetylcholinesterase activity was almost completely inhibited within 2--3 min of intravenous injection of neostigmine. Enzyme activity recovered to approximately 28% of control values by 30 min and to 55% by 60 min.

Acetylcholinesterase↗