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In the early phase of asymptomatic left ventricular dysfunction, neurohumoral systems are activated and are closely associated with the deterioration of left ventricular function and the progression into symptomatic heart failure. Congestive cardiac failure is characterized by an increasing activation of the sympathetic nerve activity, the renin angiotensin aldosterone system, vasopressin and endothelin. Together with a reduced endothelial formation of NO, the activation of neurohumoral systems leads to vaso-construction and retention of sodium and water, and by this, to a deterioration of cardiac function. On the other side, systems are activated like prostaglandins, ANP, BNP, dopamine and bradykinin, which act as vasodilators and increase natriuresis and diuresis. In the early phase of cardiac failure, natriuretic and vasodilator mechanisms are able to counteract vasoconstrictor factors, preventing by this unfavorable effects on left ventricular function.
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A 2-hour period of regional hypotension at 30-35 mmHg in the feline small bowel was produced by partial occlusion of the superior mesenteric artery. In one series of animals the sympathetic fibres in the splanchnic nerves were stimulated bilaterally at 6 Hz throughout the hypotension. In another group of animals no such stimulation was performed on the denervated intestinal segments. A mucosal damage was observed in both series and it was graded histologically according to Chiu et al. (1970). The two groups were also compared as regards the magnitude of the blood pressure fall occurring during the first hour after the period of intestinal hypotension. No statistically significant difference could be demonstrated between the two series of experiments with regard to mucosal damage or blood pressure fall. It is hence concluded that sympathetic nervous activity does not contribute to any measurable extent to the development of mucosal damage and cardiovascular deterioration observed in connection with regional intestinal hypotension. The explanation for this is discussed.
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The effects of 6-hydroxydopamine (6-OHDA) on the isolated portal vein and caudal artery of the rat were studied to investigate the possibility of producing in vitro adrenergic denervation of these blood vessels. Loss of nerve function was determined by field stimulation of the nerves, using short pulses, and by 3H-norepinephrine (NE) uptake. Addition of 6-OHDA produced contractions of both veins and arteries. Two hours after treatment with 6-OHDA, the contractile responses of the caudal arteries and portal veins to field stimulation were reduced to undetectable levels. At this point, the vessels were unable to take up 3H-NE and incubation of the preparations with l-NE failed to restore the contractile responses to nerve stimulation. Prejunctional supersensitivity to l-NE was observed in the portal vein after 6-OHDA but hot in helically cut strips of caudal artery. Prejunctional supersensitivity of the caudal artery to NE was seen, however, if the vessel geometry was kept intact, suggesting that the uptake mechanism for catecholamines only plays a major role in the termination of action of exgenous NE when norepinephrine is applied through the nerve plexus. We conclude that in vitro treatment with 6-OHDA rapidly produces functional adrenergic denervation of both portal vein and caudal artery of the rat and provides an accurate assessment of the importance of the neuronal uptake mechanism to NE sensitivity.
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The relative effects of bretylium, guanethidine and bethanidine on smooth muscle responses to different rates of sympathetic nerve stimulation have been compared. The responses studied were vasoconstriction in the femoral vascular bed and contraction of the spleen in anaesthetized cats, vasoconstriction in perfused ears of rabbits and inhibition of pendular movements in rabbit isolated ileum preparations. Except in the isolated ileum, the action of bretylium on curves relating the frequency of nerve stimulation and the effect on response was different from that of guanethidine. Whereas bretylium caused relatively greater inhibition of responses to high stimulus frequencies and depressed the slopes of the curves, guanethidine preferentially suppressed responses to low stimulus frequencies and caused roughly parallel shifts of the curves. In each situation tested bethanidine was the most potent of the three blocking agents and in general its effect on frequency/response curves was intermediate between those of bretylium and guanethidine.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.