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Biomedical subjects

B Ljunggren

Publications and source records attributed to B Ljunggren.

At least 109 records · Page 6Linked to original sources
PubMed1984

Aneurysmal subarachnoid hemorrhage--historical background from a Scandinavian horizon.

The historical background of aneurysmal subarachnoid hemorrhage is depicted with emphasis in the Scandinavian contribution to improvements in the treatment. It is concluded that an aneurysmal subarachnoid hemorrhage with all certainty was the cause of death of the prospective King of Sweden, Charles August, in the year 1810. Despite advances in management and surgical treatment of this devastating disease the outcome in this important patient--which led to a new royal dynasty in Sweden--would certainly have turned out as fatal today as became the case 174 years ago.

England↗
PubMed1984

Characterization of the prostanoid receptors and of the contractile effects of prostaglandin F2 alpha in human pial arteries.

The contractile and relaxant effects of various prostanoids were studied on isolated human pial arteries. Contractions were elicited with the following order of potency: U46619 approximately equal to U44069 greater than PGB2 greater than PGF2 alpha greater than PGE2 approximately equal to PGD2 approximately equal to PGF1 alpha greater than or equal to TXB2, indicating that prostanoid-induced contractions probably are mediated by a thromboxane-sensitive receptor. Relaxation of PGF2 alpha-contracted arteries was induced with the order of potency: PGE2 greater than PGE1 greater than PGD2 approximately equal to PGD1. Vessels contrated by K+ were relaxed only by PGE1. Since PGI2 was previously found to be more potent than all the prostanoids tested in the present study, relaxant responses are probably mediated via a PGI2-sensitive receptor. The role of free extracellular and cellularly bound calcium for the contractile effects of PGF2 alpha and K+ were estimated by incubating the arteries for various times in calcium-free medium containing 10(-5) M EGTA. Incubation for 5-10 min abolished K+-induced contractions, whereas after 40 min of incubation PGF2 alpha still induced contractions that reached 70% of control. The PGF2 alpha-induced contraction was biphasic in 8 out of 10 preparations. The second phase could be eliminated by increasing the EGTA-concentration to 10(-4) M, as well as by nifedipine pretreatment. In calcium-free, high K+ medium calcium-induced contractions were elicited at lower concentrations in the presence of PGF2 alpha. The results suggest that PGF2 alpha-induced contractions in human pial arteries are relatively independent of free extracellular calcium. PGF2 alpha may promote trans-membrane influx of calcium, as well as release calcium from seemingly superficially located cellular stores.

Calcium↗
PubMed1984

Early aneurysm operation and outcome in two remote Scandinavian populations.

The Kuopio University Clinic is the neurosurgical referral center for a population of 930,000 inhabitants in central Finland while the Lund University Clinic is the neurosurgical referral center for a population of 1.46 million inhabitants in southern Sweden. The incidence of aneurysmal subarachnoid hemorrhage (SAH) is approximately 19/100,000/year in central Finland and approximately five/100,000/year in southern Sweden. During the calendar year 1982, 69 patients with a ruptured supratentorial aneurysm were admitted in Lund, and 71 such patients were admitted in Kuopio. Thirty-nine patients in neurological Grades I to III (according to Hunt and Hess) underwent early aneurysm operation in Lund, and 46 such patients were operated on within a week after SAH in Kuopio. In the combined series of 85 Grade I to III patients with aneurysm operation within a week after rupture, 78% made a good recovery; the morbidity rate was 14%, and the mortality rate was 8%.

Adult↗
PubMed1984

Outcome in 60 consecutive patients treated with early aneurysm operation and intravenous nimodipine.

Sixty consecutive patients with a ruptured supratentorial aneurysm underwent operation during the acute stage, 56 of them within 72 hours after the first bleed, one on the 4th day, and three on the 5th day. Six patients were classified preoperatively in Hunt and Hess neurological Grade I, 39 in Grade II, 11 in Grade III, and four in Grade IV or V. Nine patients had severe intracerebral hematomas, and one patient had a subdural hematoma. After the aneurysm was clipped, nimodipine was applied to the exposed arterial segments in a 2.5 X 10(-5)M solution for 10 minutes. Subsequently, all patients received a continuous intravenous nimodipine infusion (2 mg/hr) for 7 to 12 days, followed by oral treatment (270 mg/day). Forty-six patients (77%) made a good neurological recovery; the morbidity rate was 22%, and mortality rate 1.5%. Of the 45 patients in good condition (Grades I to II) preoperatively, 38 (84%) made a good neurological recovery. Two patients (3% of the total series) developed a typical picture of cerebral ischemic dysfunction of delayed onset with subsequent fixed neurological deficits. The results favor the opinion that early operative intervention is beneficial in patients in good condition rather than delaying surgery, and indicate that nimodipine provides an additional anti-ischemic effect. The appearance and severity of late angiographic vasospasm did not seem to be affected by nimodipine.

Adult↗
PubMed1984

Fatal connective tissue disease with antinuclear antibodies following PUVA therapy.

Antinuclear antibodies with a nucleolar staining pattern appeared in a psoriasis patient during PUVA therapy. No antinuclear antibodies were found after the termination of PUVA but they reappeared one year later together with symptoms consistent with a connective tissue disease. The course was fatal and the clinical and the laboratory investigations suggested a scleroderma-like syndrome.

Antibodies, Antinuclear↗
PubMed1984

Studies on photohemolysis with special reference to demethylchlortetracycline.

Hemolysis induced by ultraviolet radiation as well as demethylchloretetracycline (DMCT) phototoxicity have been investigated in a model using human red blood cells. Total hemolysis for UV-B and UV-C was obtained with 8.3 and 1.9 J/cm2 respectively. DMCT was shown to have pronounced hemolytic properties causing 88% hemolysis at 50 micrograms/ml and 72 J/cm2 of UV-A. No increased hemolysis rate was seen in combination with UV-B. Several factors influencing the results were studied such as incubation time, UV-A dose, drug concentration and different methods for hemoglobin detection. Photohemolysis is an accurate tool for demonstrating DMCT phototoxicity.

Chlorpromazine↗
PubMed1983

Experimental studies on the mechanism of benoxaprofen photoreactions.

Benoxaprofen (BP), a non-steroidal antiphlogistic drug causing skin and nail photoreactions, has been evaluated for photoactivity using three experimental techniques. In vivo in the mouse, BP was phototoxic in doses of 25 mg/kg in combination with UV-A 54J. The phototoxic potency could be confirmed in vitro with the Candida albicans test. In vitro, using photohemolysis, BP showed a dose-dependent activity causing 40% hemolysis at a concentration of about 25 micrograms/ml with UV-A. Also, small UV-B doses caused red cell lysis with a moderate BP concentration. Pre-irradiation experiments showed that UV-A, but not UV-B, photoproducts could account for some of the activity. The action spectrum of BP photoactivity lies mainly in the UV-A, but may also extend into UV-B. Compared with chlorpromazine in vivo and in vitro, and with doxycycline in vivo, BP showed intermediate phototoxic activity.

Animals↗
PubMed1983

Variations between individuals in cerebrovascular responsiveness.

1. Despite extensive research no explanation has been put forward to account for the fact that cerebral arterial spasm complicates the course of disease of many but not all patients suffering from rupture of an intracranial aneurysm. Although vasoactive material in hemorrhagic cerebrospinal fluid (CSF) most probably is of major importance in the pathophysiology of delayed cerebral vasospasm, recent studies have failed to demonstrate a correlation between CSF vasoconstrictor activity and the development of delayed cerebral vasospasm. 2. In the present study the reactivity of isolated human pial arteries to various vasoactive agents [prostaglandin F2 alpha, noradrenaline, serotonin, human plasma and CSF from patients with aneurysmal subarachnoid hemorrhage (SAH)] was investigated. 3. There was a very marked variability in the spectrum of responses between arteries from different individuals with regard to the contractile responses to plasma, hemorrhagic CSF and amines. On the other hand, the contractions produced by prostaglandin F2 alpha and potassium were consistent. 4. The markedly individual profile in terms of reactivity toward vasoactive substances emphasizes the importance of a human cerebral vessel wall factor and may explain the capricious occurrence of cerebral vasospasm after aneurysmal SAH.

Adult↗
PubMed1983

Prostaglandin metabolism and prostacyclin in cerebral vasospasm.

1. Contractions of isolated human pial arteries, induced either by exposition to hemorrhagic cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage and cerebral vasospasm or by exposition to noradrenaline, were markedly augmented after preincubation of the vessel segments with the cyclooxygenase inhibitor indomethacin, while serotonin-induced contractions were unaffected. 2. Prostacyclin relaxed human pial arteries contracted by either PGF2 alpha, noradrenaline, serotonin or hemorrhagic CSF. The same though less marked effects were obtained with 6-keto-PGE1. 3. The results support the contention that an intact vascular prostacyclin synthesis is important for the maintenance of a normal cerebrovascular tone, and that disturbances of the prostaglandin metabolism may be a prerequisite for the development of arterial spasm after aneurysmal subarachnoid hemorrhage. Tentatively. 4. a prostacyclin deficiency may be involved in the pathogenesis of delayed cerebral vasospasm after subarachnoid hemorrhage.

Alprostadil↗
PubMed1983

Responses of isolated feline and human cerebral arteries to prostacyclin and some of its metabolites.

The effects of prostacyclin (PGI2) were studied in isolated cat basilar and middle cerebral arteries and in human pial arteries. In feline vessels with low resting tension, PGI2 had a contractile effect that reached a maximum of 132% (basilar artery) and 23% (middle cerebral artery) of the potassium-induced (127 mM) contraction. In potassium-contracted feline vessels, PGI2 caused a further contraction. When these vessels were contracted by PGF2 alpha, PGI2 induced relaxation, which was most marked in the middle cerebral artery. PGI2 consistently relaxed the middle cerebral artery contracted by the prostaglandin endoperoxide analogue U-44069, whereas the basilar artery was almost unaffected. In human pial arteries with low resting tension, PGI2 had no effects in concentrations below 10(-6) M, whereas higher concentrations induced contractions. In potassium-contracted (35 or 127 mM) preparations, PGI2 in concentrations below 10(-6) M produced relaxation; in higher concentrations further contraction was induced. Human pial arteries contracted by PGF2 alpha, U-44069, noradrenaline, or 5-hydroxytryptamine consistently relaxed in response to PGI2 (less than 10(-6) M). The PGI2 metabolite 6-keto-PGE1 had effects similar to those of PGI2, but proved to be less potent on human pial vessels. 6-Keto-PGF1 alpha was ineffective, whereas 6,15-diketo-PGF1 alpha had minor relaxant effects. The results suggest that consideration must be given to regional as well as species differences concerning the cerebrovascular effects of PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Effects of topical application of a calcium antagonist (nifedipine) on feline cortical pial microvasculature under normal conditions and in focal ischemia.

Cat cortical arterioles and venules were exposed in vivo to the Ca2+ antagonist nifedipine under normal conditions and in focal ischemia. Topical application of nifedipine caused a marked, concentration-dependent arteriolar dilatation. The dilatatory responses increased significantly with decreasing arteriolar size. Perivenular microapplication of nifedipine invariably caused dilatation that was less pronounced but more long-lasting than that on the arteriolar side. Arterioles, which constricted after middle cerebral artery occlusion, invariably dilated following nifedipine application. These dilatatory responses were transient but could be repeated, and on some occasions were accompanied by a return of flow in vessels in which stasis had been present. The results suggest that nifedipine is able to dilate cerebral vessels both under normal conditions and when contracted during focal ischemia.

Animals↗
PubMed1983

Are the vascular effects of naloxone attributable to the preservatives methyl- and propylparaben?

In vitro, the Nalonee preparation of naloxone caused a concentration-dependent relaxation of human pial cortical arteries contracted by potassium, noradrenaline, serotonin, prostaglandin F2 alpha (PGF2 alpha), and haemorrhagic cerebrospinal fluid, or inhibited contractions elicited by these agents. However, the preservatives in the Nalonee preparation, methyl- and propylparaben, had similar effects. Pure naloxone alone had no effect on potassium or PGF2 alpha-induced contractions. It is suggested that the relaxant effects on vascular smooth muscle of Nalonee can be attributed to the alkylparabens rather than to naloxone. The pronounced relaxations induced by the alkylparabens had a rapid onset, and they were stable and could easily be cleared after rinsing.

Arteries↗