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Biomedical subjects

S Strandgaard

Publications and source records attributed to S Strandgaard.

At least 37 records · Page 2Linked to original sources
PubMed1988

Can differences in cerebral and coronary autoregulation and O2-extraction explain why antihypertensive treatment prevents stroke but not myocardial infarction?

It is proposed that the failure of current antihypertensive treatment to reduce the incidence of coronary heart disease in patients with hypertension is due to severe, possibly irreversible restriction of coronary vascular reserve in the deeper layers of the left ventricle. Contrary to the heart, the brain can maintain a normal oxidative metabolism when the blood pressure is lowered, by extracting more oxygen from the blood. The brain is thus better suited than the heart to take advantage of the beneficial effect of antihypertensive treatment in terms of protection against hypertensive organ damage. This hypothesis is supported by studies of cerebral and coronary autoregulation and the J-shaped relation between death from myocardial infarction and treated diastolic blood pressure now reported from a number of studies.

Cerebrovascular Circulation↗
PubMed1987

Why does antihypertensive treatment prevent stroke but not myocardial infarction?

It is proposed that differences in autoregulatory reserve and blood oxygen extraction potential between the coronary and cerebral circulations explain why antihypertensive treatment effectively protects patients against stroke but has failed to reduce the increased incidence of myocardial infarction associated with hypertension. In the brain, oxygen extraction from the blood can be increased if blood pressure falls below the lower limit of autoregulation. In the coronary circulation, however, oxygen extraction is nearly maximum at rest, and lowering of blood pressure by antihypertensive therapy can lead to myocardial ischaemia.

Antihypertensive Agents↗
PubMed1987

Cerebrospinal fluid creatine kinase isoenzyme BB levels do not predict the clinical outcome in patients unconscious following cardiac resuscitation.

It has recently been claimed that an increase in creatine kinase isoenzyme BB(CK-BB) in cerebrospinal fluid (CSF) is well correlated with the cerebral outcome in patients resuscitated after cardiac arrest. Twenty-one such patients consecutively admitted from outside this hospital participated in the study. The patients were divided into two groups: 6 survivors and 15 nonsurvivors. The median CSF-CK-BB value was 5 U/L among nonsurvivors and below detection limit among survivors (NS). However, the predictive value of a positive test is limited, since only 6 of 15 nonsurvivors (40%) had an increase in CSF-CK-BB (predictive value of positive test = 67%). The predictive value of a negative test is limited, since 3 of 6 survivors (50%) showed no rise in CSF-CK-BB (predictive value of negative test = 25%). No relationship between cerebral dysfunction and CSF-CK-BB values was revealed. Thus, CSF-CK-BB does not predict the clinical outcome in patients resuscitated after cardiac arrest.

Creatine Kinase↗
PubMed1987

The renal handling of sodium and water is not affected by the standard-dose cisplatin treatment for testicular cancer.

Renal clearances of 51Cr-EDTA, lithium, sodium and potassium were measured before and after each of four consecutive treatment series with cisplatin in 15 men with testicular cancer. Since lithium is reabsorbed like sodium and water in the proximal tubules, but not reabsorbed to any measurable degree in the remainder of the nephron, lithium clearance equals the amount of fluid delivered from the end of the proximal straight segment to the thin descending limb of the loop of Henle. From the clearances of lithium and sodium, distal tubular reabsorption can be calculated. Lithium clearance and all other parameters of glomerular filtration and renal sodium handling remained normal throughout the study (with the exception of a fall in fractional sodium excretion after the first treatment series). Plasma magnesium declined during all four treatment periods, signifying renal magnesium wasting.

Adult↗
PubMed1986

Hypertension in renal allograft recipients may be conveyed by cadaveric kidneys from donors with subarachnoid haemorrhage.

Evidence for hypertension was sought retrospectively in the necropsy records of 37 cadaveric kidney donors who had died of subarachnoid haemorrhage and 41 donors who had died of head injury, cerebral tumour, or (in a few instances) other causes. Mean relative heart weight in the donors with subarachnoid haemorrhage was 0.58 (1 SD = 0.09)% and in the other donors 0.52 (0.09)% (p less than 0.01), a difference unexplained by any factor other than a comparatively higher blood pressure in the donors who had died of subarachnoid haemorrhage. Blood pressure was analysed over 72 months after renal transplantation in 23 recipients with normal or near normal graft function and no evidence of chronic rejection or graft artery stenosis. Twelve patients who had received kidneys from donors with subarachnoid haemorrhage had consistently higher systolic blood pressures (p less than 0.004) and needed more antihypertensive treatment (p less than 0.0004) than the 11 recipients of kidneys from donors who had died of head injury or cerebral tumour. These observations suggest that cadaveric kidneys from donors dying of subarachnoid haemorrhage may induce or sustain hypertension after transplantation.

Adult↗
PubMed1986

Effects of sulindac and naproxen in patients with chronic glomerular disease.

Eight patients with chronic glomerulonephritis were treated with either naproxen or sulindac in an open randomized study to observe their effects on the urinary excretion of prostaglandins and renal function. Both drugs were given for 7 days. Naproxen caused a decrease (p less than 0.01) of 80% in prostaglandin PGE2 and decrease (p less than 0.01) of 55% in prostaglandin PGF2 alpha. Sulindac caused a decrease (p = 0.01) of 37% in PGE2 and a decrease (p less than 0.05) in PGF2 alpha of 13%. The decrease in urinary excretion of prostaglandins were greater (p less than 0.05) during the naproxen treatment. Naproxen caused a decrease (p less than 0.05) in 24-hour creatinine clearance of 14 ml/min, an increase (p less than 0.05) in plasma urea of 1.0 mmol/l, an increase (p less than 0.05) in plasma potassium of 0.4 mmol/l and a decrease (p less than 0.01) in 24-hour urinary excretion of albumin of 11 mumol. Sulindac did not change any of these parameters significantly. In conclusion, sulindac affects renal prostaglandin synthesis to a significantly minor degree than naproxen and contrary to naproxen it does not influence the renal function in patients with chronic glomerular disease.

Adult↗
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↗