Hypokalemia and Ventricular Arrhythmias in Acute Myocardial Infarction

ABSTRACT Thirty-seven patients with a supine systolic blood pressure >160 and/or a diastolic blood pressure >95 mmHg were enrolled in the study and treated for 6 months with prazosin and 6 months with metoprolol (in random order). Neither the systolic nor the diastolic blood pressures differed after the two types of treatment (median difference 0/0 mmHg). The mean and median differences in serum cholesterol, however, were 0.4 and 0.3 mmol/l respectively, which were 9 and 5% of the pretreatment values. The corresponding differences in the atherogenic index (in which cholesterol in high density lipoproteins is integrated) were 10 and 8% of the pretreatment values. This difference in the metabolic response to the two drugs at the same blood pressure level is most probably of importance in the long-term prevention of ischaemic heart disease, for which high levels of serum cholesterol and atherogenic index are major risk factors.     

Obstetric Vacuum Extraction

A brief historical review of vacuum extraction, indications for use, safety considerations, mode of action, delivery technique, and discussion of nursing implications is presented. Safety and effectiveness of vacuum extraction are supported by the results of a comparative study done at Mount Sinai Medical Center in which 256 vacuum extractions and 300 randomly selected forceps deliveries were performed. Indications for use, clinical status before application, maternal complications, and immediate neonatal complications are analyzed and discussed.     

Evidence for bicarbonate-dependent lithium reabsorption in dog kidneys

To examine whether lithium is reabsorbed along a transcellular or a paracellular route, experiments were performed in anesthetized volume-expanded dogs under conditions of constant glomerular filtration rate (GFR). Ouabain, in doses inhibiting about 80 % of Na,K-ATPase, and ethacrynic acid, another inhibitor of transcellular NaCl reabsorption, did not inhibit lithium or bicarbonate reabsorption. Lithium reabsorption increased in proportion to plasma concentration of lithium (P_Li) up to 12 mM, suggesting a passive transport of lithium. During ouabain administration acetazolamide halved bicarbonate reabsorption, the main driving force for paracellular reabsorption, and halved the reabsorption of lithium. The reabsorbate concentration of lithium, calculated from data obtained before and after acetazolamide infusion, was almost equal to P_Li. Mannitol, which reduces paracellular osmotic transport without affecting bicarbonate reabsorption, reduced lithium and chloride reabsorption in the same proportion as acetazolamide (r=0.87). Combined acetazolamide and mannitol administration reduced fractional lithium reabsorption to 0.09±0.02. These data indicate that lithium is not actively transported but reabsorbed passively along a paracellular route by osmotic forces provided by transcellular NaHCO₃ reabsorption.     

Luminal and basolateral uptake and degradation of insulin in the proximal tubules of the dog kidney

In order to determine the major routes of insulin degradation in the body, insulin was labelled with a ‘trapped’ or ‘residualizing’ label: [¹²⁵I]tyramine-cellobiose ([¹²⁵I]TC) and injected intravenously in dogs. In contrast to conventional iodine-labelled insulin (¹³¹I-insulin), the [¹²⁵I]TC-insulin allows measurements of total uptake in specific organs in vivo because the radioactive degradation products do not leave the cells. One h after the injection of trace doses, the amount of radioactivity recovered in the kidney from [¹²⁵I]TC-insulin was nine times higher than when conventional [¹³¹I]insulin was used. In the blood, the amount of acid-precipitable radioactivity was the same for both labelled preparations, indicating similar clearance rates. A comparison of the uptake of insulin in filtering vs. non-filtering (ureter-occluded) kidneys indicated that the uptake of insulin is twice as high through the luminal than through the basolateral cell membrane; after 60 min, 8.9 ± 0.8% of the injected [¹²⁵I]TC-insulin dose remained in the filtering kidney and 3.2 ± 0.2% of the dose was accumulated in the contralateral kidney, with occluded ureter but normal blood perfusion. In both filtering and non-filtering (ureter-occluded) kidneys, the subcellular distributions of [¹²⁵I]TC-insulin were studied after various times by isopycnic sedimentation in sucrose gradients. No difference between peritubular and tubular uptake was discernible. The intracellular transport was rapid, leading to accumulation of radioactive label in dense lysosomes within 10 min.     

Haemodynamic conditions for renal PGE2 and renin release during α- and β-adrenergic stimulation in dogs

Constriction of the renal artery and infusion of an α-adrenergic agonist induce autoregulated vasodilation and increase prostaglandin E₂ (PGE₂) and renin release. The enhancement of renin release during autoregulated vasodilation might be mediated by prostaglandins. To examine this hypothesis, experiments were performed in three groups of anaesthetized dogs. In six dogs constriction of the renal artery to a perfusion pressure below the range of autoregulation raised renin release from 2 ± 1 to 27 ± 6 μg AI.min^-1 and PGE₂ release from 1 ± 1 to 10 ± 2 pmol. min^-1. After administration of indomethacin (10 mg. kg^-1 b. wt), PGE₂ release was effectively blocked and constriction of the renal artery raised renin release only from 0.1 ± 0.1 to 6 ± 1 μg AI.min^-1. During subsequent continuous infusion of a β-adrenergic agonist, isoproterenol (0.2 μg. kg^-1.min^-1), constriction of the renal artery raised renin release from 0.1 ± 0.1 to 52 ± 11 μg AI.min^-1, although there was no rise in PGE₂ release. In six dogs, intrarenal infusion of phenylephrine, an α adrenergic agonist, increased PGE₂ and renin release before, but not after, indomethacin administration. In six other dogs, phenylephrine infused during isoproterenol infusion increased renin release equally before and after indomethacin administration. Thus the enhancing effect of constricting the renal artery or infusing an α-adrenergic agonist is not dependent upon prostaglandins. We propose that autoregulated dilation enhances renin release whether the stimulatory agent is a prostaglandin or a β-adrenergic agonist.