Hypertensive patients cerebral blood

Napoli et al. [286] found that the nifedipine treatment of stroke-prone spontaneously hypertensive rats (SPSHR) suppressed the plasma and LDL oxidation and the formation of oxidation-specific epitopes and increased the survival of rats independently of blood pressure modification. Their results suggest that the protective effects of calcium blockers of dihydro-pyridine-type on cerebral ischemia and stroke may, at least in part, depend on their antioxidant activity. In vivo antioxidant effect of nilvadipine on LDL oxidation has been studied in hypertensive patients with high risk of atherosclerosis [287], It was found that there was a significant decrease in the level of LDL cholesterol oxidation in patients after nilvadipine treatment. 

Moriwaki H, Uno H, Nagakane Y et al. (2004). Losartan, an angiotensin n (ATI) receptor antagonist, preserves cerebral blood flow in hypertensive patients with a history of stroke. Journal of Human Hypertension 18 693-699... 

Traon AP, Costes-Salon MC, Galinier M et al. (2002). Dynamics of cerebral blood flow autoregulation in hypertensive patients. Journal of Neurology Science 195 139-144 van der Grond J, Eikelboom BC, Mali WPThM (1996). Flow-related anaerobic metabolic changes in patients with severe stenosis of the internal carotid artery. Stroke 27 2026-2032... 

Ciclosporin-induced vasculopathy, with endothelial injury and derangement of the blood-brain barrier, is the postulated mechanism of neurological damage. Transient cerebral perfusion abnormalities, demonstrable in SPECT scans of the brain, have been suggested as a reliable indicator of ciclosporin neurotoxicity (SEDA-20, 344). Clinical symptoms as well as CT and/or MRI scans were very similar to those observed in hypertensive encephalopathy, with predominant and reversible white-matter occipital lesions (23). There was complete neurological recovery in most patients after blood pressure was normalized, and deaths due to intracranial hemorrhage are reported only exceptionally. 

Indometacin is used for non-invasive closure of symptomatic ductus arteriosus in the preterm infant. Intravenous administration causes an instant reduction in cerebral blood flow, increasing cerebral vascular resistance. The clinical significance for the nervous system of these hemodynamic changes is unknown (11,12), but they seem to be linked to the effects seen in the central nervous system. Advantage has been taken of this effect for reducing intracranial hypertension in patients with severe head injury (SEDA-15, 99). 

Nervous System Halothane dilates the cerebral vasculature, increasing cerebral blood flow under most conditions. This increase in blood flow can increase intracranial pressure in patients with space-occupying intracranial masses, brain edema, or preexisting intracranial hypertension. Thus, halothane is relatively contraindicated in patients at risk for elevated intracranial pressure. Halothane also attenuates autoregulation of cerebral blood flow. 

The lack of response in the other patients suggests that pulmonary vasoconstriction is not the cause of the desaturation and that perhaps other factors, such as cerebral blood flow requirements, have a significant effect on pulmonary blood flow (superior vena cava flow) in these patients. We have delivered nitric oxide to two patients following the total cavopulmonary anastomosis (Fontan), with an elevated transpulmonary gradient in the presence of left atrial hypertension due to a restrictive atrial septal defect in one patient and pulmonary venous obstruction by the Fontan baffle in another. Inhaled nitric oxide produced a reliable decrease in transpulmonary gradient in both, with an increase in saturation in one (with a fenestrated... 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

A significant reduction of the ICP was seen, which was similar to the results of Marion and Shiozaki, who used hypothermic therapy in traumatic brain injuries (37,38). With an unaffected mean arterial blood pressure (MABP) and increased cerebral perfusion pressure (CPP), hypothermic therapy appeared to benefit stroke patients, as uncontrolled intracranial hypertension is the main cause of death in the first week after stroke. However, rewarming the patients consistently led to a secondary rise of ICP, which required additional ICP therapy with mannitol. In some cases it even exaggerated the initial ICP levels (Fig. 3). 

The consequences of the hypertensive interaction are variable. Many individuals remain unaware of relatively minor increases in blood pressure. However, if the rise is large and rapid (an increase of 30 mmHg or more in systolic pressure within 20 minutes), the patient experiences a sudden severe occipital headache and palpitation, which may be associated in rare instances with subarachnoid hemorrhage or cardiac failure, if the cerebral vasculature or cardiac musculature are already weakened. 

Intravenous administration of indometacin increases blood pressure, coronary vascular resistance, and myocardial oxygen demands, decreasing coronary flow. A controlled short-term study showed that indometacin increased blood pressure in patients with mild untreated essential hypertension (SEDA-17, 108). In view of the increasing use of parenteral administration, the acute hemodynamic effects of indometacin may now occur more often, especially in the elderly (5). The mechanism is poorly understood, but apparently a direct action is exerted on the resistance vessels in various regions. This is probably independent of indometacin s action on prostaglandin formation. The chnical relevance is largely unknown, but other NSAIDs should probably be prescribed for patients with occlusive vascular diseases affecting the cerebral and/or coronary vessels. 

Transient cerebral ischemia, with aphasia and hemipar-esis in one patient and cerebellar dysfunction and loss of consciousness in another, has been observed with nifedipine (12). In addition, rapidly progressive hemiparesis, aphasia, and confusion, accompanied by a substantial fall in blood pressure, occurred in a patient whose hypertension (230/136 mmHg) was treated with sublingual nifedipine (13). Transient retinal ischemia, which may be recurrent, has also been attributed to nifedipine (14,15). Hypotension or cerebral steal are the likely mechanisms. 

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