DRUG‐INDUCED CHANGES IN CAPILLARY FILTRATION COEFFICIENT AND BLOOD FLOW IN THE INNERVATED SMALL INTESTINE OF THE ANAESTHETIZED CAT

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Abstract
1 A modification of the Folkow Technique for simultaneous measurement of blood flow and capillary filtration coefficient (CFC) in the cat jejunum is described. The modification retained the sympathetic innervation of the preparation, and in the present experiments, drugs were administered intravenously. 2 There is evidence that CFC is a cardiovascular quantity independent of blood flow or regional vascular resistance in these preparations. Low doses of drugs may affect CFC without altering the blood pressure, blood flow, or heart rate. 3 Under control conditions the CFC, a measure of functional exchange vessel area, was lower than previously reported for similar, but denervated preparations. 4 α-Adrenoceptor stimulation with phenylephrine (1.0 μg kg−1 min−1, i.v.) caused a fall of 75–85% from control values of CFC with concomitant rises in blood pressure of 0–15% and falls in blood flow of 10–40%. The heart rate rose by 0–15%. Phentolamine (0.5–2.0 mg/kg, i.v.) caused a rise in CFC and a slight fall in vascular resistance, and blocked the effects of phenylephrine on this tissue. 5 β-Adrenoceptor stimulation with isoprenaline (0.2 μg kg−1 min−1, i.v.) caused a rise in CFC of 75–110%, a fall in blood pressure of 0–10%, a rise in blood flow of 10–60% and a rise in heart rate of up to 35%. Propranolol caused a transient rise in CFC when injected i.v. in a dose of 0.1 mg/kg, which was adequate to block the effects of isoprenaline. 6 Angiotensin (25–100 ng kg−1 min−1, i.v.) caused falls in CFC of up to 100% and rises in vascular resistance. Aminophylline (0.2–0.4 mg kg−1 min−1, i.v.) caused rises in CFC of up to 200% with falls in vascular resistance. 7 Histamine (0.01 to 1.0 μg kg−1 min−1, i.v.) had little effect on vascular resistance, but 10 and 40 μg kg−1 min−1 caused falls in vascular resistance. Doses up to and including 10 μg kg−1 min−1 caused falls in CFC, but the higher doses, or smaller doses after histaminase inhibition caused rises in CFC. α-Adrenoceptor blockade reversed the fall in CFC caused by small doses of histamine, to a rise. Mepyramine completely blocked the effects of histamine on these preparations. 8 5-Hydroxytryptamine (33–100 μg kg−1 min−1, i.v.) caused a rise in vascular resistance and a fall in CFC of up to 85%. These effects were blocked by methysergide (250 μg/kg, i.v.). 9 Rises in CFC indicate an increase in functional exchange vessel area in the tissue, and falls in CFC a decrease in the area available for vascular exchange. These changes are examined against the possibility of the drugs causing reflex adjustments in sympathetic tone, of systemic deactivation of intravenously administered drugs, and of drug effects on vascular permeability.