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The syndrome of inappropriate ADH secretion (SIADH), also termed ''syndrome of inappropriate antidiuresis (SIAD)'', is an often unrecognized cause of hypotonic hyponatremia, arising from ectopic release of ADH in lung cancer or as a side effect of various drugs. In SIADH, hyponatremia results from selectively impaired water excretion by the kidney, whereas the external Na+ balance is normally regulated. Despite the increase in total body water, only a slight reduction of urine output and modest edema are usually seen. Renal function and acid-base balance are generally preserved, while subclinical neurological impairment may occasionally become life-threatening, when hyponatremia has an abrupt onset. The major clinical variants of SIADH are reviewed here, with particular emphasis on causes, iatrogenic complications and hospital-acquired hyponatremia. Effective treatment of SIADH is based on water restriction, hypertonic saline plus loop diuretics, or aquaretics. Worsening of hyponatremia may result from parenteral isotonic fluid administration, emphasizing the importance of an early diagnosis and careful follow-up of these patients.

Background: Bicarbonate therapy for metabolic acidosis can cause tissue hypercapnia. We tested the hypothesis that CO2 retention is initially confined to blood and that tissue hypercapnia is consequent to blood hypercapnia., Design: prospective study., Setting: general Intensive Care Unit in an University Hospital., Patients: ten patients, aged 34-84, undergoing fixed mechanical ventilation for stroke, respiratory failure, polytrauma, or coma and presenting fairly stabilized circulatory condition were included in the study providing that definite exclusion criteria were absent. Sodium bicarbonate, 0.08, 0.17, and 0.25 mEq/kg, was infused in 5 minutes during stages A, B, and C. During each stage, before and after bicarbonate infusion, heart rate, arterial pressure, central venous pressure, and PetCO2 were registered and arterial and central venous haemogasanalysis were performed. CO2 output was measured during and after bicarbonate infusion and total CO2 output over basal values was calculated., Results: Heart rate, arterial pressure, central venous pressure did not change in any stage, while PetCO2 increased in all. Following bicarbonate infusion, pH increased more in venous than in arterial blood and was significantly affected by the amount of bicarbonate infused. In arterial blood both PCO2 and total CO2 content (TCO2) increased. In venous blood PCO2 did not change while TCO2 increased so that arterial-venous rl CO2 difference was unaffected. CO2 output changed in no patient but two during stage A, and increased by 0.54 +/- 0.16 mL/kg during stage B and by 1.18 +/- 0.26 mL/kg during stage C so that 14.5 +/- 4.3 and 21.2 +/- 4.7% of given bicarbonate was released as CO2 through the lungs. CO2 output increased after a latency that was significantly shorter during stage C (145 +/- 51 sec) than during stage B (226 +/- 53 sec)., Conclusions: Since arterial-venous TCO2 difference was unaffected and haemodynamic parameters were stable, the conclusion is drawn that CO2 and bicarbonate did not diffuse out of vascular compartment during this study. However CO2 and bicarbonate diffusion out of blood would have occurred if bicarbonate infusion had continued, because CO2 excess was released through the lungs after a latency and extended after the infusion. Consequently, tissue hypercapnia during bicarbonate infusion could probably be prevented by improving CO2 release through the lungs, i.e. by hyperventilating the patient.

Plasma and red cell acid-base equilibrium was studied in 14 healthy subjects following the induction of acidosis by means of i.v. acetazolamide. It was found that changes in red cell values were significantly less marked than those in plasma.

The Authors studied the effects of e.v. Salbutamol evaluating the acute "in vivo" variations of acid-base and hydro-electrolitic balance in 16 chronic obstructive lung patients undergoing e.v. drug administration, and also ionic variations "in vitro" of venous blood samples incubated and tonometrated with the drug. The results "in vivo" do not show variations of acid-base equilibrium (paO2, paCO2, pH, HCO3-); whereas diminution of haematocrit (Ht), rise of urinary osmolarity and variations of hydro-electrolitic balance (Na+, K+, Cl-) are demonstrated. The results "in vitro" do not show considerable variations on ionic assessment. These data, according to the other latest result, indicate the possible role of haemodilution. We think that the explanation of these phenomena could be a modification of renal water and electrolytes reabsorption, likely under the influence of antidiuretic hormone (ADH), stimulated in the hypothalamus and activated also by the beta-stimulant drug at tubular cell receptors.

Fluorocarbonates are organic compounds capable of carrying oxygen and surrendering it to tissues by means of biological sound modalities. Experimentation of an emulsion consisting of perfluorotripropylamine and perfluorodecaline (Fluosol DA 20%) as a blood substitute is reported. Acute (Ht less than 1%) and chronic morphological (Ht = 15%) studies were performed on rats, and a semi-acute biochemical and morphological protocol (Ht = 21%) was experimented in pigs. The first signs of altered cerebral electrical activity occurred at Ht = 2% in the acute experiments, and death due to respiratory arrest took pace at Ht = 0.5%. In the semiacute and chronic experiments, widespread infiltration of fluorocarbonic micelles was noted on histological and electron microscope lung and liver preparations.

The Authors studied lung mechanics, acid-base balance parameters, arterial blood pressure and pulse rate in five different groups of chronic obstructive lung disease patients, undergoing e.v. different bronchodilators. The drug were: 1. group: 500 gamma of orciprenalina; 2. group: 500 gamma of idrossi-fenil-orciprenalina; 3. group: 200 gamma of salbutamolo; 4. group: 100 gamma of trimetochinolo; 5. group: 500 gamma of terbutalina. The comparative analysis of bronchodilators, their cardiovascular effects and on acid-base balance indicate that mainly salbutamol and trimetochinol have negligeable adverse effects.

The Authors have studied in a homogeneous group of rabbits the variations of intraocular pressure and of aqueous humour pH caused by instillation of timolol maleate at different concentrations. In the animals treated with drug concentration of 0,25% and 0,5% a constant reduction of IOP has been observed in comparison with controls, associated to acidification of aqueous humour: no evidence of this correlation it seems to be at low doses of timolol. Further studies are in course to indicate an eventual action of intermediate substances in the mechanism of IOP depression caused by timolol.

The in vitro effect of diuretics, osmotic pressure and acidity of the medium on red cell volume was examined. The results showed that:1) diuretics lead to a reduction in volume;2) this reduction is enhanced at higher concentrations; 3) the effect is more noticeable in more diluted blood; 4) a decrease in volume is also displayed by cells whose volume has been increased by hypo-osmotic solutions; 5) this effect is not apparent when cell volume is reduced to the minium by hypersmotic solutions;6) the effect of the pH value is only felt in the case of extreme variations.

Plasma and red cell acid-base balance were studied in 13 patients with metabolic alkalosis and 14 healthy subjects following the infusion of bicarbonate. Differences between the plasma and red cell patterns suggested that application of the results of plasma determinations to the body as a whole could be the cause of serious inaccuracies. Since the changes noted occurred in different combinations according to whether alkalinisation was acute or not, it is felt that cell response to a fall in (H+) varies in relation to the time available for compensation.

A previously described method was used to induce haemorrhagic shock in the rabbit by removing 40% of the circulating mass. This had been previously established as 2.6 +/- 0.5 kg-1 by a radioisotopic technique. Survivals were determined 1 and 2 weeks later after treatment with 40 mg/kg-1 6-MPD and vascular refilling with 3.5% gelatine equal to the amount removed. The blood gas analysis and EAB findings suggested that haemorrhagic shock includes both a fast and a slow physiopathological stage, and that the results of treatment are strictly linked to the time of its commencement. Metabolic acidaemia and respiratory alkalosis was constant, and all the controls died within 2 days, 6-MPD was not able to normalise the EAB, but ensured 100% survival at 2 weeks. Gelatin brought the lab data close to normal, but only ensured 100% survival at 2 weeks if given immediately after the removal of blood.

Malignant hyperthermia may appear during surgery. It has at least three features: 1) an anesthesiological trigger, usually the association of halothane and succinylcholine; 2) rapid increase in body temperature; 3) widespread muscle hypertonia. The literature is reviewed in an assessment of the physiopathological mechanism underlying the syndrome, with particular reference to the part played by calcium. Experimental data are cited and their similarity with the clinical, laboratory, anatomical, and histopathological picture in man is discussed. A detailed account is also given of two personal cases. Lastly, questions associated with the prevention and treatment of malignant hyperthermia are examined.