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Biomedical subjects

S Strandgaard

Publications and source records attributed to S Strandgaard.

At least 91 records · Page 5Linked to original sources
PubMed1985

Complete remission in pure red cell aplasia after plasmapheresis.

A 17-year-old girl with a severe pure red cell aplasia (PRCA) and an appropriate elevation of erythropoietin titres was treated successfully with plasmapheresis, during which plasma was exchanged with human albumin and Ringer lactate. Before this treatment, therapeutic attempts with prednisolone, oxymetholone and infusions with fresh frozen plasma had all been without effect. Bone marrow culture studies revealed an inhibitory activity against BFU-E in the plasma, an activity which could not be demonstrated after the plasmapheresis. 22 months after the plasmapheresis the patient is still healthy without any medication. This case adds additional evidence for the presence of a pathogenetic erythroid inhibitory factor in the plasma of some patients with PRCA.

Adolescent↗
PubMed1984

Effects of captopril on cerebral blood flow in normotensive and hypertensive rats.

Cerebrovascular effects of the angiotensin converting enzyme inhibitor captopril were examined in normotensive and hypertensive rats. Cerebral blood flow was measured with the intracarotid 133xenon injection method in halothane-anesthetized animals. The blood-brain barrier permeability of captopril (determined with an integral-uptake method) was negligible, the permeability-surface area product in most brain regions being 1 X 10(-5) cm3/g per second, that is, three to four times lower than that of sodium ion. When administered into the cerebral ventricles to bypass the blood-brain barrier, captopril had no effect on cerebral blood flow: furthermore, cerebral blood flow autoregulation (studied by raising and lowering blood pressure) was identical to that in controls. In contrast, when given intravenously, captopril had a marked effect on cerebral blood flow autoregulation--both the lower and upper limits of autoregulation being shifted to a lower pressure (by about 20 to 30 and 50 to 60 mm Hg, respectively), and the autoregulatory range was shortened by about 40 mm Hg. This effect may be ascribed to inhibition of converting enzyme in the cerebral blood vessels rather than within the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebrovascular aspects of converting-enzyme inhibition I: Effects of intravenous captopril in spontaneously hypertensive and normotensive rats.

The cerebrovascular effects of converting enzyme inhibition were examined in normotensive and hypertensive rats. Cerebral blood flow was measured using the intracarotid 133xenon injection method in halothane/nitrous oxide anaesthetized animals. The main finding was that following intravenous administration of captopril (10 mg/kg), cerebral blood flow autoregulation was markedly altered. Although cerebral blood flow was unchanged from baseline levels, both the lower and upper limits of autoregulation were reset to lower mean arterial pressure and the autoregulatory plateau shortened. The lower limit was shifted 20-30 mmHg, the upper limit 50-60 mmHg, and the plateau shortened by 20-40 mmHg. The effect was interpreted as being a consequence of compensatory autoregulatory constriction of small resistance vessels in the brain following captopril-induced dilatation of large resistance vessels. It was inferred that locally produced angiotensin II might play a role in the resistance of large cerebral arteries.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebrovascular aspects of converting-enzyme inhibition II: Blood-brain barrier permeability and effect of intracerebroventricular administration of captopril.

The blood-brain barrier permeability to captopril, and the cerebrovascular effects of intracerebroventricular administration of captopril, were studied in normotensive Wistar rats. The blood-brain barrier permeability-surface area product (PS), determined by an integral-uptake method, was about 1 X 10(-5) cm3/g/s in all brain regions studied. This was three to four times lower than the simultaneously determined PS of Na+ and Cl-, both of which are known to have very low blood-brain barrier permeability. Cerebral blood flow, determined by the intra-arterial 133xenon injection method, was unaffected by intracerebroventricular administration of 100 micrograms captopril. Furthermore the lower limit of cerebral blood flow autoregulation during haemorrhagic hypotension was also unaffected, being in the mean arterial pressure range (50-69 mmHg) in both controls and captopril-treated rats. It was concluded that the blood-brain barrier permeability of captopril was negligible and that inhibition of the brain renin-angiotensin system has no effect on global cerebral blood flow. The cerebrovascular effects of intravenously administered captopril (a resetting to lower pressure of the limits and range of cerebral blood flow autoregulation) are probably exerted via converting enzyme on the luminal surface of cerebral vessels.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Converting enzyme inhibition and autoregulation of cerebral blood flow in spontaneously hypertensive and normotensive rats.

The cerebrovascular effects of the converting enzyme inhibitor captopril were examined after intravenous or intracerebroventricular administration in normotensive and hypertensive rats. Cerebral blood flow (CBF) was measured using the intracarotid 133xenom method in halothane/nitrous oxide anaesthetised animals. Captopril given either way did not influence the absolute value of CBF. The main finding, however, was that following intravenous administration of captopril at a dose of 10 mg/kg, both the lower pressure limit of CBF autoregulation were shifted to lower pressure and the autoregulatory plateau shortened. The lower limit was shifted 20-30 mm Hg, the upper limit 50-60 mm Hg, and the autoregulatory plateau consequently shortened by 20-30 mm Hg. In contrast to the marked effects of intravenous captopril, intracerebroventricular captopril was without effect on CBF autoregulation. The effect of intravenous captopril was thus probably mediated by converting enzyme in the cerebrovascular endothelium.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Visual disturbances and occipital brain infarct following acute, transient hypotension in hypertensive patients.

In four hypertensive patients, acute lowering of blood pressure by therapeutic or diagnostic procedures caused visual disturbances ranging from transient visual hallucinations to severe, long-lasting visual impairment. These symptoms were associated with occipital lobe cerebral infarcts that tended to occur in the border zones between the major cerebral arteries. The infarcts may be seen as the combined result of a "watershed" effect during acute hypotension and the presence of structural hypertensive vascular adaptation. When a hypertensive patient complains of visual disturbances during acute blood pressure lowering, the pressure should be allowed to settle at a level somewhat above normal.

Adult↗
PubMed1983

Necrotizing vasculitis in athymic rats with infarct kidney hypertension.

Infarct kidney hypertension was induced in congenital athymic nude rats and in their haired normal littermates. In both groups a significant and similar elevation of blood pressure was observed. The mesenteric vessels were studied histologically five, 12 and 20 days after operation. Necrotizing vasculitis with and without perivascular inflammatory reactions was found in mesenteric arteries and arterioles in six out of six athymic and in six out of 11 control rats. In sham operated athymic rats and in haired littermates neither hypertension nor vasculitis was observed. These observations indicate that the thymus play no role in the pathogenesis of acute hypertensive vascular disease.

Animals↗
PubMed1983

Effect of diazoxide-induced hypotension on cerebral blood flow in hypertensive rats.

The effect on cerebral blood flow of acute diazoxide-induced hypotension was studied in rats with renal and spontaneous hypertension. Diazoxide (5 mg/kg, i.v. bolus), caused arterial pressure to fall rapidly to that of normotensive rats, i.e. c. 75 mmHg. There was a concomitant fall in cerebral blood flow of about 35% (P less than 0.01) in renal hypertensive rats and 25% (P less than 0.05) in spontaneously hypertensive rats; the greater fall in flow in the former corresponded to a greater drop in pressure. Flow remained at these reduced levels during a 2 h observation period. Histological examination revealed small areas of ischaemic damage in the brains of five of the twelve animals. In control hypertensive rats not given diazoxide, cerebral blood flow and blood pressure were stable during a 2 1/2 h period and there was no evidence of ischaemic damage to the brains. The diazoxide-induced reduction in cerebral blood flow was interpreted as being secondary to a blood pressure fall to below the lower limit of cerebral blood flow autoregulation. No evidence was found of direct effects on the cerebral circulation such as seen with ganglionic blockers, alpha-blockers and cerebral vasodilators.

Animals↗
PubMed1983

Cerebrovascular effects of the converting enzyme inhibitor captopril.

The effect of captopril on cerebral blood flow (CBF) and its autoregulation was studied in spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Wistar rats. CBF was measured by the intracarotid 133Xe injection method. In one study 1 and 10 mg/kg captopril respectively were given intravenously to SHR and WKY. This caused the blood pressure to fall transiently below the lower blood pressure limit of CBF autoregulation; nonetheless CBF remained normal during captopril induced hypotension. In a second study it was shown with an integral uptake method that captopril is a very poor penetrator of the blood-brain barrier. In a third study captopril was instilled intracerebroventricularly in Wistar rats without any effect on CBF or its autoregulation. Thus when given intravenously, but not intracerebroventricularly captopril caused cerebral vasodilatation during acute hypotension.

Animals↗
PubMed1982

[Hypotension].

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Humans↗
PubMed1982

Cerebral blood flow in rats with renal and spontaneous hypertension: resetting of the lower limit of autoregulation.

The effect of chronic hypertension on cerebral blood flow (CBF) was studied in anaesthetised rats. CBF was measured with the intracarotid 133Xe injection method. Rats with spontaneous and renal hypertension were compared with normotensive controls. The lower limit of autoregulation was determined during controlled haemorrhage. In the normotensive rats, CBF remained constant until mean arterial pressure (MAP) had decreased to the range of 50-69 mm Hg. Thereafter, CBF decreased with each further decrease in MAP. In both types of hypertensive rats, CBF remained constant until MAP had decreased to the range of 70-89 mm Hg. Thus, a 20-mm Hg shift of the lower limit of CBF autoregulation was found in both spontaneous and renal hypertensive rats. A neuropathological study revealed ischaemic brains lesions in half of the hypertensive rats following hypotension, whereas only a single lesion was found in one of six normotensive rats. No ischaemic brain lesions were found in a control study in which CBF was shown to be stable over a 21/2-h period. In conclusion, hypertensive rats showed a shift of the lower limit of CBF autoregulation as well as an increased susceptibility to ischaemic brain damage during hypotension. These findings presumably reflect hypertensive structural changes in the cerebral circulation.

Animals↗