Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GIK (glucose-insulin-potassium) solution has been administered to myocardial infarction patients as a polarizing therapy, but the effects of GIK administration on vasospasm after subarachnoid hemorrhage have never been reported. We used GIK solution to treat 7 cases of symptomatic vasospasm with congestive heart failure due to hypervolemia-hypertensive treatment. The GIK solution, composed of 200cc of 50% glucose solution, 250cc of water, 40 mEq of KCl, and 20 units of actrapid insulin, was administered continuously through a central venous catheter. The GIK therapy improved congestive heart failure following elevation of cardiac output in 7 cases, and simultaneously stabilized the serum glucose level within the range of 88-175 mg/dl. After GIK administration, remarkable improvement in the consciousness level was achieved in all cases, and cerebral infarction due to vasospasm appeared in only one case in spite of severe subarachnoid hemorrhage. It is thought that GIK therapy will be effective in the treatment of symptomatic vasospasm with congestive heart failure through the normalization of hemodynamics, the improvement of hyperglycemia and protection against cerebral ischemia.
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PMID:[Treatment of symptomatic vasospasm with GIK (glucose-insulin-potassium) infusion]. 220 88

Hypertensive crisis is an acute emergency requiring aggressive management. Its incidence has decreased in recent years but still is prevalent in the medical community. From review of past and present treatment regimens, the following recommendations can be considered. (1) In the treatment of malignant hypertension with associated CHF, sodium nitroprusside is still an excellent agent. It has a rapid onset of action and blood pressure can be easily titrated. Nitroglycerin is also another agent that can be used in this situation. (2) In the treatment of malignant hypertension with associated aortic dissection, trimethophan camsylate is the preferred agent. An alternative choice is the combination of nitroprusside and labetalol. (3) In the treatment of malignant hypertension with associated myocardial ischemia, an excellent choice is nitroglycerin. Labetalol also should be considered in this situation. (4) In the treatment of hypertension during pregnancy, hydralazine is still a good choice. Labetalol has also been shown to be efficacious. (5) In the treatment of malignant hypertension with associated cerebral ischemia, the following drugs should be considered: nitroprusside, nitroglycerin, and labetalol. The most important attribute of these agents is that they are nonsedating and rapid in onset. (6) In the treatment of postoperative hypertension the choices best suited are labetalol, enalapril, nitroprusside, and nitroglycerin. These agents are rapid in onset and all can be administered intravenously.
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PMID:Hypertensive crisis. 267 90

In a prospective multicenter study, 244 men with highly or moderately differentiated prostatic cancer in stage I, II or III (VACURG) were consecutively randomized to three groups of treatment: Group A (77 patients) received polyestradiol phosphate (Estradurin, Leo) 80 mg i.m. every fourth week + ethinyl estradiol (Etivex, Leo) 150 micrograms daily, group B (72 patients) estramustine phosphate (Estracyt, Leo) 280 mg twice daily, and group C (76 patients) no therapy. Only men without current or previous other malignancy and without cardiovascular disease were admitted to the study. After 4 1/2 years 125 of the 244 patients had left the study, 9 because of cancer progression (stage IV, VACURG). The most serious complications were cardiovascular, including ischemic heart disease, cardiac decompensation, cerebral ischemia and venous thromboembolism, which occurred in 24 patients from group A and 9 from group B as compared to only one patient in group C. The subgroup superficial or deep venous thrombosis comprised 11 group A and 2 group B patients. Estrogens (E + e) offered as palliative treatment to patients with non-generalized prostatic carcinoma is burdened with a high incidence of serious cardiovascular complications.
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PMID:Cardiovascular complications of estrogen therapy for nondisseminated prostatic carcinoma. A preliminary report from a randomized multicenter study. 352 68

In order to study the influence of repetitive episodes of ventricular fibrillation (VF) during defibrillator implantation on the electrical activity of the brain, we performed an electroencephalographic (EEG) monitoring during implantation procedure in 18 patients. For defibrillation threshold testing 62 episodes of VF (1-6 episodes per patient) were induced. The mean duration of VF was 20 +/- 12 s; the mean duration of hypotension during an episode (defined as a mean arterial pressure of 50 mm Hg or less) was 33 +/- 16 s. EEG monitoring was performed using the International 10-20 System. The duration of cardiac arrest-related EEG alteration was assessed by an experienced neurologist and could be determined in 41 test-episodes; in 21 episodes analysis was not possible due to poor recordings. Ischemia-related EEG changes started 7.8 +/- 4.6 s after VF induction and lasted 64 +/- 49 s (range, 12-240). The duration of EEG alteration was significantly (p < .001) correlated with the duration of VF episodes (r = .71) and the associated hypotension (r = .82). With regard to patients the duration of ischemia related EEG changes also correlated significantly (p = .001) with the individual cumulative duration of VF (r = .85) and the associated hypotension (r = .88). In females EEG changes lasted longer than in males (p = .03); this finding, however, was only based on 2 women. Other clinical parameters, such as patient age, degree of congestive heart failure, left ventricular ejection fraction, stroke volume and cardiac index, the order of episodes within the testing sequence, and the time interval between episodes did not correlate with the duration of EEG alteration after VF induction. The duration of ischemia-related EEG alteration during VF episodes depends on the duration of cardiac arrest. In females EEG changes tended to last longer than in males, however, this finding has to be confirmed. An association with other clinical parameters has not been observed. Limitation of VF duration appears to be the most important factor to avoid prolonged cerebral ischemia.
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PMID:[Cerebral ischemia during implantation of automatic defibrillators]. 750 66

Ischemic brain edema promotes focal cerebral ischemia by increasing intracranial pressure and thereby reducing perfusion pressure, obstructing capillaries and prolonging transport routes within ischemic tissue. There is clinical and experimental evidence that osmotic agents counteract these mechanisms. Moreover, glycerol may act as a free radical scavenger, antioxidant, and activator of plasma prostaglandin (PGI2), resulting in vasodilation. Improvements in ischemic brain energy metabolism after glycerol administration has also been postulated. Results of clinical trials on glycerol treatment of acute ischemic stroke were not conclusive: some demonstrated improved survival in the acute stage, in others survivors benefited in terms of neurological status and/or daily living activities. Other trials did not reveal any superiority of glycerol treatment over placebo. Glycerol is given intravenously as a 10% solution or orally. By the oral route higher intravascular glycerol concentration can be achieved with smaller quantities of fluid. Possible side effects include elevation of blood glucose level with subsequent lactate acidosis in the ischemic brain, serum hyperosmolarity after long-term glycerol administration and--when given intravenously--volume overload in patients with congestive heart failure and hemolysis that may cause renal failure.
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PMID:[Treatment of ischemic cerebral infarct with glycerine]. 756 70

The purpose of this report is to determine the role of various imaging modalities, and the outcome of early intervention in neonates with high flow pial arteriovenous malformations (AVM). This report describes 4 neonates with pial AVM associated with congestive cardiac failure, and reviews previous reports. Among the 4 infants in our series, 3 underwent early surgical resection of the AVM, complete in 2 and partial in 1. One infant suffered hemorrhagic infarction postoperatively and has a mild deficit on clinical follow-up; the other 2 patients had no worsening of mild neurologic deficits after surgery, and subsequent development has been normal. The fourth infant had absent deep venous drainage and died from intracranial hemorrhage following transvenous embolization. A single vessel arteriogram in 1 infant led to underestimation of the lesion and unexpected findings at surgery. Complete angiographic study is important in planning treatment, as the vascular anatomy of the lesions may be complex. Cranial ultrasound is useful in early diagnosis, but may miss the superficial lesions. Untreated infants with pial AVM have a poor prognosis due to cardiac failure or progressive cerebral ischemia and neurologic regression. This series illustrates the benefits of complete angiographic investigation and early treatment.
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PMID:Neonatal superficial cerebral arteriovenous malformations. 790 36

The pathogenesis, clinical manifestations, and management of orthostatic hypotension (OH) are reviewed. OH is a decline in blood pressure that occurs when one moves from a lying to a standing position that results in symptoms of cerebral hypoperfusion, most commonly lightheadedness and syncope. The disorder may result from primary autonomic disorders, such as Shy-Drager syndrome; reversible nonautonomic causes, such as reduced blood volume; underlying diseases, such as diabetes mellitus; and drugs. Elderly people are predisposed to OH. The diagnosis of OH is based on the documentation of postural hypotension accompanied by symptoms of cerebral ischemia. The goal of therapy is to relieve symptoms. Nonpharmacologic approaches are preferred and include increasing sodium intake, avoiding rapid postural changes, and wearing elastic garments. OH is difficult to treat pharmacologically because of varying responses and adverse effects. The drug of choice for all types of OH is fludrocortisone acetate, although caution must be used in patients with congestive heart failure. Prostaglandin synthetase inhibitors can also be used for all types of OH but have had more limited success. Sympathomimetics with or without monoamine oxidase inhibitors, beta-adrenergic antagonists, and ergot alkaloids should be administered only to patients with certain types of OH, and patients must be monitored closely. Clonidine, midodrine, yohimbine, octreotide, dopamine antagonists, desmopressin, and epoetin alfa have not been well studied and should be limited to patients with severe, refractory disease. Although no uniformly effective treatment regimen exists, OH can often be adequately managed with a combination of nondrug and drug therapies.
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PMID:Management of orthostatic hypotension. 820 84

In the general population, peripheral atherosclerosis is a strong predictor of cardiovascular disease and death. In patients with known coronary artery disease, it is unclear whether the presence of additional noncoronary atherosclerosis is of further prognostic value. In the Bypass Angioplasty Revascularization Investigation, 5-year outcome was compared between patients with and without clinically evident noncoronary atherosclerosis. Within the subgroup with noncoronary atherosclerosis, surgery, and angioplasty treatment strategies were compared. Noncoronary atherosclerosis was defined as claudication, peripheral vascular surgery, abdominal aortic aneurysm, history of cerebral ischemia, or carotid disease. Among 1,816 patients, 303 (17%) had noncoronary atherosclerosis. These patients were more likely to have a history of congestive heart failure, diabetes, and hypertension, and were more likely to smoke. Coronary angiographic variables were similar between the 2 groups. Five-year survival was 75.8% for patients with noncoronary atherosclerosis and 90.2% for those without (p < 0.001). The adjusted relative risk of death was 1.7 for any noncoronary atherosclerosis, 1.5 for lower extremity disease alone, 1.7 for cerebral disease alone, and 2.3 for both conditions. Among the 303 patients with noncoronary atherosclerosis, the adjusted relative risk of death for surgery versus angioplasty was 0.87 (p = 0.40). However, the study has limited power to detect a treatment effect in this small subgroup. Thus, patients with combined coronary and clinically evident noncoronary atherosclerosis are a high-risk group with significantly worse long-term outcome compared patients with isolated coronary disease.
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PMID:Long-term prognostic value of clinically evident noncoronary vascular disease in patients undergoing coronary revascularization in the Bypass Angioplasty Revascularization Investigation (BARI). 948 22

In utero, the ductus arteriosus shunts deoxygenated blood away from the pulmonary artery and towards the placental circulation where foetal gas exchange occurs. As a result of an intricately intertwined network of both physiological and biochemical changes, this vessel constricts rapidly after birth. Deoxygenated blood is diverted away from the placenta and through the lungs now vital for gas exchange. Premature closure of the ductus in utero can cause pulmonary hypertension and even death. Conversely, failure to close after birth can exacerbate respiratory distress, precipitate congestive heart failure and increase the risk of subsequent intestinal ischaemia leading to necrotising enterocolitis, bronchopulmonary dysplasia, renal hypoperfusion and/or cerebral ischaemia. In this review we summarise current knowledge of the delicately orchestrated control of the ductus arteriosus, focusing on the role of cyclo-oxygenase isoforms on prostaglandin production, on the interaction between prostaglandins and oxygen, and on the effects of these on ductal patency. We also seek to describe some of the standard and nonstandard therapeutic approaches available to the clinician when natural closure fails, reviewing alternative protocols for indomethacin administration and comparing indomethacin treatment with newer approaches such as ibuprofen. In summary, we will follow the course of this unique blood vessel as it is transformed over several hours from an organ absolutely vital to survival into programmed obsolescence.
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PMID:Patent ductus arteriousus in the premature neonate: current concepts in pharmacological management. 1093 44

Animal studies evaluating gender difference, the effects of gonadectomy and estrogen replacement and clinical studies in post-menopausal women with and without estrogen replacement therapy (ERT) proved that estrogen exerts significant benefits on the cardiovascular system. Since effects on the plasma lipoprotein profile is responsible for only approximately 25-40% of the cardiovascular protection exerted by estrogens, it is postulated that direct effects of estrogen on the vascular wall must play an important role. Indeed, experimental and clinical evidence accumulated over the past decade, and reviewed briefly here, indicate that at least a part of cardiovascular benefits of 17 beta-estradiol can be attributed to the direct effect of the ovarian sex steroid hormone on vascular endothelial cells. Maintenance and upregulation of endothelial nitric oxide production and suppression of EDCF generation by 17 beta-estradiol may play an important role in preventing or reversing endothelial dysfunction, associated with atherosclerosis, hypertension and other cardiovascular diseases. Stimulation of angiogenesis (especially collateral vessel formation in ischemic tissues) by the ovarian steroid hormone could be beneficial in coronary artery disease, peripheral vascular disease, cerebral ischemia (stroke) and congestive heart failure. Despite these indisputable beneficial effects, several key questions remain to be answered in the future, including the better understanding of the apparently opposite effects of estrogen on prevention of cardiovascular disease vs. treatment of existing disease.
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PMID:Effect of estrogen on endothelial function and angiogenesis. 1237 55


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