Diabetes mellitus by itself, is a frequent and increasing public health problem. The prevalence in most Western countries varies between 2 to 5% and it is rapidly increasing in Asiatic countries due to changes in dietary habits during the last years. The association between diabetes mellitus and hypertension has been described in 60 to 65% of diabetics. In hypertension we find insulin resistance mainly in skeletal muscle involving the conversion of glucose to glycogen independently of blood flow. The degree of resistance is related to the severity of hypertension and varies between races. States of
Summary:Purpose: Amygdala kindling is an epilepsy model involving long-term network plasticity in the nervous system. In this model, repeated weak stimulation of the amygdala eventually leads to severe motor seizures. The mechanisms for worsening behavioral seizures, and the possible role of enhanced connectivity between the amygdala and other structures have not been thoroughly investigated.Methods: We performed simultaneous field potential recordings from the amygdala, frontal cortex, and medial thalamus during kindling in rats. Seizures were analyzed for signal power compared with baseline and for correlation between recording sites. Interictal signals were analyzed for changes in coherence between electrode contacts in kindled animals compared with sham kindled controls.Results: We found that increased behavioral severity of seizures was related to increased seizure duration and to increased signal power in the frontal cortex and medial thalamus. Kindling was associated with increased connectivity between the amygdala and frontal cortex, based on increased amygdalafrontal signal correlation during seizures. In addition, during the interictal period, increased coherence was noted between amygdala and frontal contacts in kindled animals compared with controls.Conclusions: We found evidence for increased connectivity between the amygdala and frontal cortex both during seizures and in the interictal period, as a result of kindling. Enhanced connections between limbic and neocortical circuits may be important for the development of epilepsy, as well as for normal long-range network plasticity in the nervous system.
The application of cobalt chloride to the peripheral cut end of the greater superficial petrosal nerve (g.s.p.n.) in rats revealed that only a few fibers in the plexus of nerves on the adventitial surface of the internal carotid artery were in axonal continuity with the g.s.p.n. A similarly small contribution of cholinergic fibers to cerebral blood vessels from this nerve was suggested by the observation that section of the g.s.p.n. resulted in an insignificant reduction in the density of the AChE-staining plexus in the internal carotid and cerebral arteries and in the incidence of at most 2% degenerate terminals of those observed on the middle cerebral artery. Alternative explanations of the results are discussed: that the AChE-staining fibers are postganglionic, that the time course for degeneration is unusually slow and that non-cholinergic fibers stain non-specifically for AChE. It is concluded that a cholinergic dilator pathway is most probably carried by the g.s.p.n. but that it is not unique.
Systemic arterial pressure is a dynamic and reactive physiological parameter depending on a great many factors. The endothelial cells of the vascular system are responsible for many biochemical reactions maintaining vascular homeostasis and therefore arterial pressure. Arterial hypertension, atherosclerosis and endothelial dysfunction constitute risk factors increasing morbidity
Endotoxaemia is a syndrome linked to the development of equine laminitis; however, the relationship between them is uncertain. The aim of this experiment was to evaluate the effect of an experimental acute sublethal endotoxaemia model on in vitro equine palmar digital vascular reactivity. Rings of arteries and veins of each forelimb were obtained from 11 clinically healthy horses submitted to two surgical procedures, 3 weeks apart. Before the second surgery, 0.25 microg/kg of lipopolysaccharide from Escherichia coli O55:B5 in saline, was administered i.v. in 30 min. After 3 h, the vessels were harvested and submitted to in vitro vascular reactivity experiments and histopathology. The response to depolarizing Krebs solution (DKS, 40 mm), phenylephrine (PHE), acetylcholine (ACh) and sodium nitroprusside (SNP) were evaluated. All horses showed colic pain and watery diarrhoea, tachycardia, tachypnea, hyperthermia and leucopenia. Concentration-response curve (CRC) to PHE was shifted to the left in arteries rings from endotoxemic horses without any effect on vein rings. The CRC to ACh was shifted to the right with a reduction in the maximal response. The response to SNP and DKS was similar between groups. There was no evidence of histopathological effects. The increased response to PHE in digital arteries together with a reduction of the endothelium-dependent response to ACh in arteries and veins, confirm the existing reports where endotoxaemia was found to modify the digital vascular reactivity during the acute phase. As the digital endothelial function is impaired, there may be an increased potential to develop a digital prothrombotic state with a reduced vasodilatory capacity.
The effect of stimulating the greater superficial petrosal nerve (g.s.p.n.) upon retroglenoid venous blood flow has been tested in anaesthetized, paralysed and artificially ventilated rats. In 11 out of 15 tests, blood flow increased by an average of 25% with a time to peak response of 28 s. This response was abolished with the injection of atropine 0.1 mg kg-1 injected intra-arterially. With both petrosal nerves intact, the administration of 6-7% CO2 in air or 15% O2 in N2 caused average increases in blood flow of 105% and 45% respectively. These responses were not affected by bilateral section of the g.s.p.n. Similar experiments were carried out in 5 anaesthetized, spontaneously breathing rabbits in which, in addition to PaCO2 and PaO2, PO2, PCO2 and blood flow in the caudate nucleus were measured continuously using chronically implanted mass spectrometer catheters and heated thermistors. Caudate nucleus blood flow increased in response to hypoxia and hypercapnia and this response was not significantly affected by section of one or both g.s.p.n., sinus or vagus nerves. With section of sinus and vagus nerves, blood flow changed passively with arterial pressure.
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