Carotid artery pressure

Baroreceptor. Specialized pressure-sensitive tissue located in carotid arteries. Nerve impulses proportional to arterial blood pressure are conducted from this tissue to the brain which in turn exerts control over the blood pressure. 

The baroreceptor reflex is a central reflex mechanism, which reduces heart rate following an increase in blood pressure. Each change in blood pressure is sensed by baroreceptors in the carotid arteries, which activate the autonomic nervous system to alter heart rate and thereby readjust blood pressure. 

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

SNVP is a lipophilic N-substituted valeryl analog of SNAP. It caused prolonged nitric oxide mediated vasodilatation in rats [70, 71]. In vivo, SNVP prevented the hyper-aggregability of circulating platelets caused by angioplasty of rabbit carotid arteries. Here, only minor effects on blood pressure were observed, whereas platelet adhesion was strongly inhibited [71]. 

Dogs given norepinephrine by infusion at 0.185-2.04 Ug/kg per minute for long periods (9-35 h) until their blood pressures became approximately the same as they had been before the Infusions began were then given intravenous Injections of I at 20 or 40 mg/kg, tyra-mlne at 0.1 or 0.5 mg/kg, or nicotine at 0.5 mg/kg.The concentration of norepinephrine In carotid arterial blood was estimated before and at intervals after the Injection of one of the test compounds. Except after the lower dose of tyramlne, when the maximal Increase In the concentration of norepinephrine in the blood appeared at 5 min after the injection, the peak concentration of norepinephrine in carotid arterial blood occurred at 3 min after Injection. 

Aviram, M. et al., Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation, Clin. Nutr., 23,423, 2004. 

The clinical manifestations of PAD are associated with reduction in functional capacity and quality of life, but because of the systemic nature of the atherosclerotic process there is a strong association with coronary and carotid artery disease. Consequently, patients with PAD have an increased risk of cardiovascular and cerebrovascular ischemic events [myocardial infarction (Ml), ischemic stroke, and death] compared to the general population (4,5). In addition, these cardiovascular ischemic events are more frequent than ischemic limb events in any lower extremity PAD cohort, whether individuals present without symptoms or with atypical leg pain, classic claudication, or critical limb ischemia (6). Therefore, aggressive treatment of known risk factors for progression of atherosclerosis is warranted. In addition to tobacco cessation, encouragement of daily exercise and use of a low cholesterol, low salt diet, PAD patients should be offered therapies to reduce lipid levels, control blood pressure, control blood glucose in patients with diabetes mellitus, and offer other effective antiatherosclerotic strategies. A recent position paper... 

Trimethylgermyl-2-furyl) substituted 1,4-dihydropyridine administered i.v. in a 0.05 mgkg-1 dose increased the blood flow in the common carotid of cats by 31%, and in a 0.1 mgkg-1 dose it dilates the coronary vessels by 11% and decreased the arterial pressure by 12%5. 

Schwab et al. used mild hypothermia (33-34°C) in 20 patients with acute severe middle cerebral artery (MCA) infarction for 48-72 h and found mild hypothermia to be safe and feasible (38). Schwab subsequently reported a series of 25 patients with severe MCA infarction treated with the same protocol (39). Intracranial pressure (ICP) was monitored for 3-7 d, and was found to decrease with initiation of hypothermia. ICP increased during re warming in several patients, but not to the levels seen prior to induction of hypothermia. Pneumonia was seen in 40% of patients treated with hypothermia in this trial, which is within the expected range of occurrence in patients with prolonged ventilation (40). Shimizu et al. used mild hypothermia (33°C) in five patients with embolic infarctions involving the internal carotid artery and MCA territories. The hypothermia was maintained for 3-7 d (41). It was found to be safe, but the number of patients was too small to report any efficacy. Another acute stroke trial using convection air to induce mild hypothermia without anesthesia was found to be feasible (42). Temperatures in this trial were reduced only to 35.5°C, and shivering... 

For determination of LVP, a Millar micro tip catheter (type PC 350) is inserted via the left common carotid artery into the left ventricle. LVEDP is measured on a high-sensitivity scale. From the pressure curve, dP/dtmax is differentiated and heart rate is counted. The LVP-signal also triggers a cardiotachometer. 

Left ventricular pressure (LVP) (mm Hg) is determined by inserting a microtip-catheter via the carotid artery retrogradely. 

Anaesthetized rats are fixed in supine position on a temperature-controlled (37 °C) heating-table. Following catheterization of a carotid artery (for measurement of blood pressure) and a jugular vein, the test compound is administered. After a defined latency period, the tail of the rat is transected with a razor-blade mounted on a self-constructed device at a distance of 4 mm from the tip of the tail. Immediately after transection, the tail is immersed into a bath filled with isotonic saline solution (37 °C). 

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