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Biomedical subjects

E Kraft

Publications and source records attributed to E Kraft.

At least 55 records · Page 3Linked to original sources
PubMed1983

[Therapy and prognosis of 300 primary extrahepatic bile duct cancers].

A total of 300 patients (66% women, 34% men) had carcinoma of the bile ducts; 64% were located in the gallbladder and 36% in the bile ducts. In 77.3% the carcinomas had metastasized or were conglomerate tumors, while in 22.7% a curative resection was performed. In 35.3% a palliative operation or resection was indicated. An exploratory laparotomy was performed in 42%, but 75% of the patients died within 6 months. After 1 year 10.2% had survived. After curative resection 46 patients survived on the average over 17.6 months, while 12 patients survived an average of 5.1 years.

Adenocarcinoma↗
PubMed1981

Pharmacological evaluation in conscious dogs of factors involved in the renal vasodilator effect of captopril.

The objective of this study was to examine the roles of the blockade of formation of angiotensin II and prostaglandins in the renal vasodilator effect of captopril in conscious salt-replete dogs. Blood pressure was recorded from an indwelling catheter and renal blood flow (RBF) was measured with an electromagnetic flowmeter and an implanted flow probe. Plasma renin activity was measured by radioimmunoassay. The effect of captopril (0.2 mg/kg i.v.) on RBF was compared in dogs given either saralasin (0.5 micrograms/kg min i.a.) or indomethacin (5mg/kg i.v.) with that in dogs given saline vehicle. Control plasma renin activity in these groups of animals before drug treatment ranged from 0.74 to 1.18 ng of angiotensin 1 per ml/hr. Captopril decreased blood pressure from 102 +/- 4 to 92 +/- 4 mm Hg (P less than .01) and increased RBF from 278 +/- 23 to 345 +/- 29 ml/min (25%) (P less than .01) in saline vehicle-treated animals. In the presence of intrarenal infusion of saralasin, captopril did not increase RBF but decreased blood pressure slightly. Captopril still increased RBF by 18% in indomethacin-treated dogs. These results suggest that the renal vasodilator effect of captopril in conscious salt-replete dogs is mainly due to the blockade of angiotensin II formation. Furthermore, the renin-angiotensin system appears to have an influence on renal vascular tone even under these basal conditions.

Angiotensin I↗
PubMed1980

Interrelationship between renal prostaglandin E, renin, and renal vascular tone in conscious dogs.

PGSI cause renal vasoconstriction in furosemide- and low-salt-treated dogs, but not in untreated normotensive dogs, and this effect is closely related to their control PRA. PGSI cause a lesser degree of renal vasoconstriction in 2-kidney 1-clip Goldblatt hypertensive dogs which does not correlate with their control PRA. PGSI abolish PG modulation of the renin-angiotensin system, and this effect appears to account for the increased renal vascular tone induced in furosemide- and low-salt-treated dogs.

Animals↗
PubMed1979

Did Röntgen discover the X ray by himself?

The historical background of the discovery of the x ray and some of Lenard's claims to priority are discussed. There is no doubt that the x ray is the sole discovery of Wilhelm Conrad Röntgen.

Famous Persons↗
PubMed1979

Blockade by saralasin of adrenergic potentiation induced by renin-angiotensin system.

Participation of the renin-angiotensin system in the potentiation of responses to adrenergic nerve stimulation in the pump-perfused dog paw was studied during suprarenal aortic constriction. Vasoconstrictor responses in the paw were elicited by norepinephrine injected intra-arterially and by sympathetic nerve stimulation in a control session and during suprarenal aortic constriction (cephalad to the origin of one or two renal arteries). Aortic constriction decreased renal blood flow by approximately 50% and increased systemic blood pressure and plasma renin activity. The vasoconstrictor responses to norepinephrine and nerve stimulation were not significantly affected when the constriction was cephalad to only one renal artery, but there was a 31% increase in the response to stimulation at 5 Hz during aortic constriction above two renal arteries. There was an approximate 2-fold greater increase in plasma renin activity during the latter than in the former case. Saralasin administered intra-arterially to the paw reversed the adrenergic potentiating effect of aortic constriction. These results indicate that when the renin-angiotensin system is activated by restricting renal blood flow, sufficient circulating endogenous angiotensin is formed to cause a moderate adrenergic potentiating effect in the canine cutaneous circulation of the paw.

Angiotensin II↗
PubMed1977

Adrenergic potentiation by angiotensin II in isolated canine cutaneous arteries: effect of bathing media and calcium.

Contractions were elicited by field stimulation and norepinephrine in canine cutaneous arteries in Krebs-bicarbonate and Krebs-Tris media and the effect of angiotensin II, 1 x 10(-7) M, on these responses was determined. The absolute magnitude of the field stimulation responses was much greater in the bicarbonate buffer. Angiotensin caused potentiation in both media of the responses to field stimulation and norepinephrine. In Triss buffer with 5 mM calcium the responses to field stimulation and norepinephrine were greater than in 2.5 mM calcium, however; the degree of potentiation caused by angiotensin was similar at both calcium concentrations. The angiotensin potentiating effect in vitro appears to involve a postsynaptic action of the polypeptide which is not affected by alteration of calcium concentration or the medium.

Angiotensin II↗