Hemorrhage, brain, effect

The presence of blood in the brain parenchyma causes damage to surrounding tissue through a mass effect and the neurotoxicity of blood components and their degradation products. Compression of tissue surrounding hematomas may lead to secondary ischemia. Much of the early mortality of hemorrhagic stroke is due to an abrupt increase in intracranial pressure that can lead to herniation and death. 

Stroke A stroke occurs when there is an interruption of blood supply to the brain. An ischemic stroke occurs when a clot prevents blood flow in the brain. A hemorrhagic stroke is when there is a rupture of a blood vessel in the brain. In either case, the brain cells in the affected area die. This area is called an infarct. Medical treatment is required to arrest the damage. More effective treatment can be administered within 6 hours of the onset of stroke. A stroke may result in weakness, paralysis, impairment of speech and memory, or even death. Medical treatment includes the use of anticoagulants to treat stroke victims. 

Miyake M, Grinberg OY, Hou H, et al. The effect of RSRl3, a synthetic allosteric modifier of hemoglobin, on brain tissue p02 (measured by EPR oximetry) following severe hemorrhagic shock in rats. Adv Exp Med Biol 2003 530 319. 

Inhalation exposure to high chloroform concentrations induced narcosis (Lehmann and Flury 1943 Sax 1979) and reversible impairment of memory retrieval in animals. High, single, oral doses of chloroform caused ataxia, incoordination, anesthesia, and brain hemorrhage in mice (Balster and Borzelleca 1982 Bowman et al. 1978). Behavioral effects were observed at lower oral doses. 

Predictable effects that derive from the known pharmacological drug properties. Examples are masculin-ization of the female fetus by androgenic hormones brain hemorrhage due to oral anticoagulants bradycardia due to p-blockers. 

Antithrombin HI (ATHI). There are only a few references concerning the evaluation of antithrombin III (AT III) in cerebrospinal fluid. Extension of evaluated groups of patients is not sufficient a comparison with other CSF protein fractions and with CSF cytological findings was not done. Some experimental works describe the vasorelaxant effect of AT III on brain arteries, and the inhibitory influence of AT III in subarachnoid hemorrhage on onset of vasospasms is expected (W2). AT III also plays a possible role in etiopathogenesis of ischemic stroke (A19, W2). 

Serotonin-specific inhibitors (SSRI) include fluoxetine, paroxetine, sertraline, citalopram and others. They are not more effective than the tricyclic antidepressants but may suit some patients better and are generally safer in overdose (see Geddes et al., 1999). While the SSRIs are devoid of the cardiac effects (membrane stabilisation, inhibition of conduction) of the tricyclics in overdose, they increase the risk of hemorrhage into the gut or brain. 

B. Perfusion of the brain is preserved when hemorrhage occurs. Thus, a greater proportion of the initial dose of anesthetic should appear in the brain, and a dose smaller than what is needed for a normovolemic patient is all that is required. Also, since flow to tissues associated with redistribution of the drug and termination of anesthesia is compromised, anesthesia should be deep and extended. Titrate this patient to a safe level of effect. While poor perfusion of the liver may reduce the exposure of drugs to metabolic enzymes, most intravenous anesthetics rely very little on hepatic clearance to terminate the anesthetic effect when a single bolus is administered. Furthermore, the question implies a direct influence of blood pressure on the efficiency of hepatic enzymes, and there is no evidence to support such a contention. Option C is not true. The opposite of option D is true. No evidence exists that binding of anesthetics is altered by these conditions. 

Severe side-effects (hemorrhages in rats and dogs brain) have been reported after systemic application of several selected adenosine kinase inhibitors (Erion, 2000). Nevertheless, ABT-702 in particular is still reported to be in preclinical development. 

In the previous sections we have, by part, already reviewed delayed effects after cerebral ischemia, such as the risk of hemorrhagic complications that may occur as petechial bleedings or parenchymal hematoma. We have seen that the blood-brain barrier opens to various degrees with a substantial time... 

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