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Biomedical subjects

E Kraft

Publications and source records attributed to E Kraft.

At least 73 records · Page 4Linked to original sources

Influence of prostaglandin precursors and synthesis inhibitors in vascular bed perfused without a pump.

The present investigation was coducted to examine the role of endogenous prostaglandin (PG) on blood flow and arenergic responses in the paw vasculature perfused without a pump. The PG precursors, arachidonic acid and dihomo-gamma-linolenic acid, given i.a. caused only small increments in paw blood flow which were much less than that caused by PGE2 and PGE1. The i.a. administration of the PG synthesis inhibitors, indomethacin, meclofenamate and naproxen, caused a decrease in paw blood flow and increase in vascular resistance, whereas eicosa-5,8,11,14-tetraynoic acid had no significant effect. Vasoconstrictor responses evoked by norepinerphrine were unaffected after administration of indomethacin or eicosa-5,8,11,14-tetraynoic acid, whereas slight potentiation of the response to sympathetic nerve stimulation was obtained after indomethacin. These results suggest that in the cutaneous vascular bed of the paw, endogenous PG decreases the vascular resitance, but plays only a minor adrenergic modulating role, and then only on the response to adrenergic nerve stimulation.

5,8,11,14-Eicosatetraynoic Acid↗

Diabetic osteopathy of the foot and ankle.

Neuropathic osteopathy of the foot and ankle is almost always due to underlying diabetes mellitus. The "Charcot joint," or destructive type, affects the ankle or tarsal area, and the "bone absorption," or mutilating type, usually affects the forefoot. If both types are present in the feet, it is almost certain that the patient is a diabetic. While these findings are usually seen in patients with long-standing, poorly controlled diabetes, they may be the first indication of diabetes.

Ankle↗

Influence of histamine H1- and H2-receptor blockers on sympathetic vasodilator and vasoconstrictor responses in canine paw.

1 Vasodilator responses to histamine, bradykinin and sympathetic nerve stimulation were elicited in the perfused paw of dogs treated with bretylium (15-20 mg/kg) and atropine. The H2-receptor blocking agent, burimamide, when administered in the dose of 5 mg/kg intravenously and 4 mg intra-arterially did not depress significantly these vasodilator responses. The subsequent administration of tripelennamine in the dose of 2.5-5 mg/kg intravenously and 4 mg intra-arterially produced a significant blockade of the response to histamine and reduced the sustained vasodilator response to nerve stimulation. 2 In guanethidine-treated dogs, tripelennamine administered in the same dose following burimamide produced a blockade of the response to histamine comparable to that in the bretylium experiments, but decreased only the sustained vasodilator response to stimulation at 1 Hz. When the order of administration of the antihistamines was reversed in another group of guanethidine-treated dogs, tripelennamine had only a slight blocking effect on the response to histamine and did not affect the responses to nerve stimulation. Burimamide exerted a significant blocking effect on the response to histamine, but not to nerve stimulation. Another H2-receptor blocking agent, metiamide, when given after tripelennamine, also had a marked blocking effect on the response to histamine and almost abolished the vasodilator response to 4-methylhistamine, an H2-agonist. Nevertheless, even in the presence of this profound histamine blockade, the sustained vasodilator response to nerve stimulation remained unchanged. 3 In another group of experiments vasoconstrictor responses to exogenous noradrenaline and sympathetic stimulation were initially depressed by burimamide and later returned to control values. Tripelennamine increased these responses by its uptake blocking action. 4 It is concluded that the sustained vasodilator response is not antagonized by a specific antihistaminic action. The decrease in the sustained vasodilator response produced by antihistamines is produced attributable to potentiation of a residual adrenergic vasoconstricotr effect not completely blocked by bretylium.

Animals↗

Neurogenic disorders of the foot in diabetes mellitus.

Neurogenic disorders of the foot in diabetics have been found with increasing frequency in recent years, Therefore, familiarity with the spectrum of roentgen findings appears essential. Significant changes include Charcot joints of the tarsus (destructive type), and bone absorption of the forefoot (multilating type). Charcot joints have been observed in 11 patients, bone absorption in 12, and a combination of both types in 3. This combination strongly suggests a diabetic neuropathy. Pathogenesis and differential diagnosis are briefly discussed.

Arthropathy, Neurogenic↗