Hyperpolarizing action of cromakalim on the rat aorta

Cromakalim alone at 1 microM had no effect and at 10 microM hyperpolarized the rat aorta. The rat aorta was depolarized by KCl (20 mM), noradrenaline (0.3 microM) and 5-hydroxytryptamine (1 microM). In the presence of depolarization with KCl, noradrenaline or 5-hydroxytryptamine, cromakalim at 1 and 10 microM hyperpolarized the rat aorta. Thus the antispasmogenic actions of modest concentrations of cromakalim is compatible with potassium channel opening.     

Maternal deaths from neurological complications of hypertensive crises in pregnancy

Fourteen maternal deaths from eclampsia or severe pre-eclampsia where disturbed cerebral function, as evidenced by prolonged unconsciousness, was given as the main cause of death are reviewed. Prolonged duration of seizures, hypotensive/hypoxic episodes, cerebral oedema and intracranial haematomas were most frequently identified as causative agents in the development of cerebral dysfunction. Failure to maintain an airway and iatrogenically induced hypotension were the two most important contributory factors to the patients' deaths. Management recommendations to prevent this type of maternal death are given.     

Repair of left ventricular aneurysm. Changes in ventricular mechanics, hemodynamics, and oxygen consumption.

Anteroapical left ventricular aneurysms were produced in 23 sheep by coronary arterial ligation. Plication of the aneurysm does not change stroke volume or cardiac output and does not significantly change left ventricular oxygen consumption from the preoperative value of 5.1 +/- 2.6 ml/100 gm per minute. Plication, however, does increase left ventricular end-systolic elastance from 3.2 +/- 0.9 to 4.4 +/- 1.5 mm Hg/mm (p = 0.005). In nine of these sheep the midsagittal plane of the left ventricle was imaged by means of an array of sonomicrometry crystals before and after plication of the aneurysm. Regional wall stresses at end-systole and end-diastole and changes in diastolic function were calculated for anterior and posterior ventricular walls in the border zone adjacent to the aneurysm and in more basilar myocardium remote from the infarct. Plication significantly reduced end-systolic wall stresses and systolic stress integrals in the posterior border zone and remote myocardium, but it did not significantly change anterior wall systolic stresses or stress integrals. Plication also decreased diastolic stretching of border zone myocardium. Plication of anteroapical left ventricular aneurysm produced a shorter, more spherical ventricle and removed the dyskinetic segments but altered deformation (strain) in both circumferential and longitudinal directions. The changes in ventricular wall geometry and deformation provide an explanation for the increased ventricular end-systolic elastance and unchanged stroke volume observed after aneurysm plication.