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At least 199 records · Page 11Linked to original sources
PubMed2005

Model for complex heart rate dynamics in health and diseases.

A physiologically motivated, dynamical model of cardiovascular autonomic regulation is shown to be capable of generating long-range correlated and multifractal heart rate. Virtual disease simulations are carried out systematically to account for the disease-induced relative dysfunction of the parasympathetic and the sympathetic branches of the autonomic control. Statistical agreement of the simulation results with those of real life data is reached, suggesting the possible use of the model as a state-of-the-art basis for further understanding of the physiological correlates of complex heart rate dynamics.

Animals↗
PubMed1960

Central vasomotor effects of a new ganglion-blocking agent--1: 2: 2: 6: 6-pentamethyl piperidine (pempidine).

The central vasomotor effects of pempidine were studied in dogs and cats anaesthetized with pentobarbitone sodium, and in spinal cats. Pempidine lowered the threshold of electrical stimulation of the medulla oblongata to evoke a pressor response when given intravenously to cats in a dose insufficient to block autonomic ganglia. Injection of a small dose into the cerebral ventricles of dogs produced an increase in the pressor responses to occlusion of the carotid artery and to electrical stimulation of the central end of the cut vagus. In the spinal cat small doses of pempidine, given either intravenously or intrathecally, augmented the rise in blood pressure resulting from compression of the spinal cord. Since all these effects were produced by pempidine in doses insufficient to cause ganglionic block, the observed effects are attributed to central facilitation of the vasomotor responses. Thus pempidine has a stimulant action on the spinal and supraspinal centres.

Animals↗
PubMed1995

Effects of chronic vitamin E deficiency on vascular function--a study of sympathetic nerves, smooth muscle and endothelium of the mesenteric arterial bed of the rat.

1. Male rats were deprived as weanlings of dietary vitamin E for 2, 4, 6, 10 and 12 months. Mesenteric arterial beds from these rats and from age-matched controls were isolated and perfused with Krebs solution at a constant flow rate (5 ml min-1). The function of perivascular sympathetic nerves, smooth muscle and endothelium was assessed. 2. At 12 months vitamin E deficient rats exhibited the characteristic symptoms of vitamin E deficiency, namely poor coat condition, muscle wasting, kyphoscoliosis and impaired gait. In the isolated mesenteric arterial bed electrical field stimulation (EFS) of perivascular nerves (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent vasoconstrictor responses which were unaffected by vitamin E deficiency except at 12 months, at which age responses were significantly greater than those of the controls at 24 and 32 Hz (P < 0.01). 3. Exogenous noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent vasoconstriction which was similar in vitamin E-deficient and control preparations at all ages. Potassium chloride (0.15 mmol) also produced similar vasoconstrictor responses in vitamin E-deficient and control preparations at each age. 4. Tone of the preparations was raised by continuous perfusion with methoxamine (4-70 microM), producing similar increases in perfusion pressure in vitamin E-deficient and control preparations at each age. Endothelium-dependent dose-dependent vasodilatation to adenosine 5'-triphosphate was significantly impaired in mesenteric arterial beds from 12 month-old vitamin E-deficient rats compared with the controls (P < 0.05). Relaxation to acetylcholine was not significantly different at any age. 5. Endothelium-independent vasodilatation to sodium nitroprusside was similar in vitamin E-deficient rats and age-matched controls. 6. These results suggest that long term (12 months) deprivation of dietary vitamin E may impair endothelial function in mesenteric arteries of the rat. Sympathetic perivascular nerve constrictor function was increased at 12 months. There were no functionally expressed changes in the vascular smooth muscle, which appears to be more resilient to the effects of oxidative stress in vitamin E deficiency.

Animals↗
PubMed1995

Effects of chronic vitamin E deficiency and a high polyunsaturated fatty acid diet on rat mesenteric arterial function.

1. Male rats were deprived as weanlings of dietary vitamin E and fed on a high polyunsaturated fatty acid (PUFA) diet for 6 months. Rats fed on a high PUFA or on an untreated diet served as controls. Mesenteric arterial beds were isolated and perfused at a constant flow rate (5 ml min-1) and the function of sympathetic nerves, smooth muscle and endothelium was assessed. 2. Electrical field stimulation (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent vasoconstriction of the mesenteric arterial preparations. Response curves were similar between untreated control and PUFA-fed control groups. Maximum vasoconstrictor responses (at 24 and 32 Hz) were significantly attenuated in rats deprived of vitamin E and on a high PUFA diet compared to the PUFA-fed controls (P < 0.05). 3. Exogenous noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent constriction of the mesenteric arterial beds. Preparations from rats fed on a high PUFA diet elicited significantly smaller responses compared to the control group. There was no significant difference in constrictor responses of PUFA rats deprived of vitamin E compared to the PUFA controls. Vasoconstrictor responses to doses of adenosine 5'-triphosphate (ATP) (5-5000 nmol) were significantly impaired in vitamin E-deficiency with a high PUFA diet compared to a high PUFA diet alone (P < < 0.001). Constrictor responses to potassium chloride (0.15 mmol) were significantly impaired in vitamin E-deficient PUFA rats compared to the PUFA-fed control group (P < 0.05). 4. Vasodilator responses were assessed in preparations in which tone was raised by continuous perfusion with methoxamine (4-25 microM). Mesenteric arterial beds from PUFA-fed rats deprived of vitamin E acquired significantly less tone, 59.8 +/- 4.6 mmHg (n = 7), than PUFA-fed controls 116.9 +/- 7.6 mmHg (n = 7) (P < 0.001) and were refractory to further increases in tone with further additions of methoxamine. Methoxamine-induced tone of PUFA-fed controls was greater than in P that in the untreated controls (83.9 +/- 7.4 mmHg; n = 5) (P < 0.05). Responses to the endothelium-dependent vasodilators acetylcholine (ACh) and ATP were significantly reduced in preparations from rats fed on the vitamin E-deficient high-PUFA diet compared to PUFA controls. Vasodilator responses to ACh were greater in PUFA controls than in untreated controls and this reached statistical significance at 5 nmol ACh. 5. Vasodilator responses to sodium nitroprusside, which acts directly on the vascular smooth muscle, were similar in untreated control and PUFA control groups. Responses were significantly attenuated in vitamin E-deficient PUFA rats compared to the PUFA control group (P < < 0.001). 6. These results indicate that a combination of a high PUFA diet and vitamin E deficiency impairs mesenteric arterial function at the level of the vascular smooth muscle. A high PUFA diet alone attenuates responses to NA and augments endothelium-dependent vasodilation. The detrimental effects of loss of antioxidant activity due to vitamin E-deficiency on vascular function may be exacerbated by a high PUFA diet.

Animals↗
PubMed2006

Nitric oxide in hypertension.

Hypertension is a major risk factor for cardiovascular disease, and reduction of elevated blood pressure significantly reduces the risk of cardiovascular events. Endothelial dysfunction, which is characterized by impairment of nitric oxide (NO) bioavailability, is an important risk factor for both hypertension and cardiovascular disease and may represent a major link between the conditions. Evidence suggests that NO plays a major role in regulating blood pressure and that impaired NO bioactivity is an important component of hypertension. Mice with disruption of the gene for endothelial NO synthase have elevated blood pressure levels compared with control animals, suggesting a genetic component to the link between impaired NO bioactivity and hypertension. Clinical studies have shown that patients with hypertension have a blunted arterial vasodilatory response to infusion of endothelium-dependent vasodilators and that inhibition of NO raises blood pressure. Impaired NO bioactivity is also implicated in arterial stiffness, a major mechanism of systolic hypertension. Clarification of the mechanisms of impaired NO bioactivity in hypertension could have important implications for the treatment of hypertension.

Adrenergic beta-Antagonists↗
PubMed1976

Blood flow changes in the submaxillary gland of the rat on parasympathetic and sympathetic nerve stimulation.

Blood flow and secretion from the submaxillary gland of the rat was recorded. Stimulation of the chordalingual nerve evoked vasodilatation which was little, it at all, decreased after administration of atropine. The secretion evoked on parasympathetic nerve stimulation was greatly reduced but not totally abolished by parasympatholytic agents. Stimulation of the cervical sympathetic trunk evoked secretion, which was mediated both via alpha and beta-adrenoceptors and vasoconstriction which was abolished by dihydroergotamine, and thus seemed to be mediated via alpha-adrenergic receptors. After alpha-adrenoceptor blockade vasodilatation was seen on sympathetic nerve stimulation. This was abolished by the beta-adrenoceptor blocking agent propranolol.

Acetamides↗
PubMed1977

Electrical activity in sympathetic fibres to hind limb muscles of the cat produced by hypothalamic stimulation.

Electrical stimulation of the "Defence Area" of the hypothalamus in anaesthetized cats was accomplished by stereotaxic placement of bipolar stainless steel electrodes; the spinal cord was sectioned at L4. The muscle blood flow in one hind limb was recorded with an electromagnetic flowmeter. Increases of between 100% and 300% were observed during hypothalamic stimulation. Electroneurographic recordings from small nerve filaments supplying tibialis anterior muscle revealed two populations of neurones whose activity was abolished by lumbar sympathectomy. It appears that the increased blood flow in skeletal muscle during stimulation of the hypothalamic "Defence Area" is brought about by a simultaneous inhibition of vasoconstrictor activity and increase in cholinergic vasodilator discharge.

Animals↗
PubMed1966

Electrical and mechanical response of arteries to stimulation of sympathetic nerves.

1. When common carotid arteries of sheep were studied in vitro by the sucrose-gap method, application of acetylcholine or nicotine caused small irregular spikes of depolarization. The discharge was prevented by hexamethonium, Hydergine, phentolamine, or chronic denervation, indicating that it represented electrical activity of groups of smooth muscle cells induced by the stimulation of sympathetic nerve fibres.2. The size of spikes produced by acetylcholine or nicotine, together with counts of the total number of smooth muscle cells in cross-sections of the arterial strips, indicated that the larger groups of smooth muscle cells activated by one sympathetic nerve fibre contained approximately 1300 cells.3. Sections of arteries treated with hot formaldehyde vapour contained numerous fluorescent fibres which were intensified by previous injection of noradrenaline into the animal and were scanty or absent after chronic sympathetic denervation. They are therefore believed to be post-ganglionic sympathetic nerve fibres.4. Most of these fibres ran circularly in the outer (1/2)-(3/4) of the media. A few ran longitudinally in the adventitia. There were none in the inner (1/4)-(1/2) of the media.5. Electrical stimulation of the cervical sympathetic nerve of anaesthetized sheep caused large contractions of the common carotid artery of the same side, reducing its external diameter by 30-39%.

Acetylcholine↗
PubMed1967

The effect of oxytocin and adrenaline on blood flow in the hind limb of the dog following chronic lumbar sympathectomy.

1. In a number of dogs the last two lumbar ganglia were removed unilaterally. At various dates up to the 56th day after operation the dogs were anaesthetized and the effect of oxytocin and adrenaline on hind-leg blood flow studied. Oxytocin alone reduced leg flow in all dogs after operation.2. Until approximately day 11 after operation oxytocin given during an infusion of adrenaline increased leg blood flow, as it does in normal dogs not given adrenaline infusion. After that date it reduced the flow even during adrenaline infusion. The timing of this change suggests that the normal response to adrenaline depends on the presence of undegenerated nerve fibres.3. In one animal the sympathetic nerves were crushed between the last two lumbar ganglia and beyond the last, and hind-leg blood flow frequently measured by means of venous occlusion plethysmography until day 204, when the animal was anaesthetized and acute observations made. Electrical stimulation of the sympathetic chain above the site of crushing caused a reduction in leg flow, indicating that at least some of the nerve supply had regenerated. However, oxytocin reduced leg flow when used alone and exerted no apparent effect in the presence of adrenaline.4. It is suggested that sympathetic nerves to vascular smooth muscle have a function or functions other than transmitter release and that when crushed nerves regenerate the functions do not recover at the same rate.

Animals↗
PubMed1967

The effects of alteration of CO2 and pH on intestinal blood flow in the cat.

1. The effect of alteration of arterial blood pH on intestinal blood flow in the cat has been determined under conditions of constant perfusion pressure.2. Arterial blood pH was altered over the range 7.12-7.70 by infusion of acid and alkali. When end-tidal CO(2) was held constant, there was no change in intestinal blood flow.3. When arterial blood pH was altered over the range 7.19-7.55 by the administration of CO(2) at constant respiratory volume and rate, flow increased with increasing CO(2).4. The intestinal vascular bed was less responsive to noradrenaline at pH 7.2 than at pH 7.6. The change in sensitivity was evident when end-tidal CO(2) was controlled and depended therefore on a change in hydrogenion concentration.5. The dilator effect of CO(2) did not depend upon alteration of sensitivity to noradrenaline since it was seen after adrenergic blockade.

Animals↗
PubMed1972

Adrenergic and cholinergic innervation of the hamster Harderian gland.

Examination of Harderian glands of adult male and female golden hamsters by appropriate histochemical techniques reveals that adrenergic nerves are associated only with the blood vessels. Acetylcholinesterase-positive fibers are present in the connective tissue surrounding the gland, along the ducts, and among the acini.

Acetylcholinesterase↗