11. |
- Ljunghall, S, et al.
(författare)
-
Clinical studies of calcium metabolism in essential hypertension
- 1987
-
Ingår i: European Heart Journal. - 1522-9645. ; 8:Suppl. B, s. 37-44
-
Tidskriftsartikel (refereegranskat)abstract
- Many factors can ultimately lead to an increased blood pressure and it is a generally accepted view that an increase in the active tension of arterioles reflects an increase of the free calcium concentration in the cytosol of the vascular smooth muscle cells. Only recently, however, has the possibility been considered that blood pressure regulation could be influenced by calcium homeostasis. A background for these studies has been provided by the epidemiological observations which link hypertension to a low dietary intake of calcium as well as experimental studies in animals, mostly rats, which have demonstrated that various disturbances of calcium metabolism are related to a raised blood pressure. This review is focused on clinical studies of a possible association between systemic calcium metabolism and the regulation of blood pressure.
|
|
12. |
- Swedberg, Karl, 1944, et al.
(författare)
-
Central haemodynamic and antiplatelet effects of iloprost--a new prostacyclin analogue--in acute myocardial infarction in man.
- 1987
-
Ingår i: European heart journal. - 0195-668X. ; 8:4, s. 362-8
-
Tidskriftsartikel (refereegranskat)abstract
- In 14 patients with acute myocardial infarction, a 24-hour Iloprost infusion was started with a mean delay of 309 +/- 22 minutes from onset of symptoms. Patients were haemodynamically monitored with a pulmonary artery catheter and an arterial cannula. The dose of Iloprost was 1-4 ng kg-1 min-1 and titrated according to blood pressure and systemic vascular resistance. When 2.0-4.0 ng kg-1 min-1 of Iloprost were infused, 5 out of 10 patients required dose reduction due to hypotension, nausea or both. However, in all patients the infusion period was completed as planned. Acute reductions of systolic blood pressure and vascular resistance were seen, whereas stroke volume increased and heart rate remained unchanged. The infusion of Iloprost caused profound inhibition of ADP-induced platelet aggregation but no significant changes in plasma values for platelet-specific proteins or thromboxane B2 were recorded. It is concluded that it was possible to safely administer Iloprost over 24 hours in the early phase of acute myocardial infarction and profound anti-aggregatory effects were observed. These findings should be evaluated in a controlled study.
|
|