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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of phosphorus depletion on cardiac muscle function in six awake dogs were evaluated with surgically implanted transducers to serially measure ascending aortic root blood flow and high fidelity left ventricular pressure. After the animals recovered from surgery, phosphorus depletion was induced by feeding them a synthetic phosphorus-deficient diet plus aluminum carbonate gel for 35 days, followed by the same diet with phosphorus supplementation for 21 days. In addition to the cardiac studies, sequential measurements of phosphorus content in skeletal muscle and phosphorus in serum were obtained to ascertain the level of phosphorus depletion. Serum inorganic phosphorus concentration (mg/100 ml) decreased from 5.1 +/- 0.1 on day 0 to 0.9 +/- 0.1 on day 35 (P less than 0.01), and total muscle phosphorus (content mmul/100 g fat-free dry weight) decreased from 28.0 +/- on day 0 to 22.6 +/- 0.5 on day 35 (P less than 0.01). During the period of phosphorus depletion, there was no significant change in heart rate; however, stroke volume (milliliter) and peak blood flow velocity (centimeter per second) declined from 24 +/- 2 to 17 +/- 2 (P less than 0.01) and 121 +/- 12 to 98 +/- 7 (P less than 0.01), respectively. Maximum ascending aortic blood flow acceleration (centimeter per second square) and maximum left ventricular time rate of change of pressure (mm Hg per second) also decreased from 4,630 +/- 313 to 3,817 +/0 346 (P less than 0.01) and 2,582 +/- 347 to 2,120 +/- 297 (P less than 0.01) during phosphorus depletion. After repletion all values returned to control values. These results indicate that moderate diet-induced phosphorus depletion can depress myocardial performance. With repletion of phosphorus, myocardial performance improves.
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PMID:Reversible depression in myocardial performance in dogs with experimental phosphorus deficiency. 74 74

A total of 35 cases of periarticular new bone formation (PNBF) was observed among 160 patients with coma following severe craniocerebral trauma. All cases were associated with blunt trauma and none with penetrating wounds. Only 6 of 500 cases of acute non-traumatic hemiplegia developed PNBR, and all 6 of them followed craniotomy, brain surgery and coma. New bone formation first appeared mainly between 50 and 120 days after craniocerebral injury with prolonged coma. Three-quarters of the patients with PNBF showed involvement of the shoulder joint, but this was not associated with previous subluxation. Metabolic studies were done in some patients; no disturbances were found in the metabolism of calcium, phosphorus or alkaline phosphatase. The pathologic process of PNBF seemed to stabilize some 6 to 8 months following trauma, and surgery after this period produced functional improvement in the 3 patients in whom it was tried. No satisfactory pathophysiological explanation has been found for the phenomenon of PNBR. Prolonged coma is common to all patients who suffered from PNBF and is probably an etiologic factor. The absence of PNBF in cases of cerebrovascular accident with subluxations of the gleno-humeral joint and intensive physiotherapy seems to contradict the suggestion of microtrauma as an etiological factor.
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PMID:Periarticular new bone formation in patients suffering from severe head injuries. 81 2

In order to evaluate chemically the macroscopic scoring methods for severity of arteriosclerosis in the cerebral arteries, concentrations of total lipids, esterified and free cholesterol and lipid phosphorus were compared to the macroscopic severity of lesions in the cerebral arteries obtained from 376 Japanese persons after unexpected death. An increase of cholesterol content was correlated significantly with an increase of Baker's score and/or Gore's atherosclerotic index. The correlation coefficient between Baker's score and total or esterified cholesterol was the highest among the tested correlations (r = 0.82, n = 376).
Stroke
PMID:Cerebral atherosclerosis in Japanese. Part 4: relationship between lipid content and macroscopic severity of atherosclerosis. 100 34

Though major differences exist in subcategory mortality levels, cardiovascular disease remains a leading cause of death among both Asian Chinese and Westerners. This paper examines the possible relationship between cardiovascular mortality and biochemical, diet and lifestyle factors based on two surveys in China. Statistically significant associations indicate five variables negatively correlated: molybdenum, oleic acid, liquor consumption (males), legumes, and age at first pregnancy with ischemic heart disease; molybdenum, oleic acid (females) and age at first pregnancy with hypertensive heart disease; and legumes and age at first pregnancy with stroke. Five variables were positively correlated: triglycerides and herpes antibodies with ischemic heart disease; salt and phosphorus (females) with hypertensive heart disease; and only albumin (males) with stroke. Some findings confirm those observed in the West (salt, triglycerides, herpes, legumes, oleic acid, and liquor), but molybdenum and age at first pregnancy have not been emphasized previously. Still others significant in the West have not been observed here, such as cholesterol and smoking.
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PMID:Diet and blood nutrient correlations with ischemic heart, hypertensive heart, and stroke mortality in China. 134 47

The authors investigated early human focal ischemia with phosphorus-31 nuclear magnetic resonance spectroscopy at 1.89 T to characterize the temporal evolution and relationship of brain pH and phosphate energy metabolism. Data from 65 symptomatic patients were prospectively studied; none of the patients had had ischemic stroke in the internal carotid artery territory before. Twenty-eight neurologically normal individuals served as control subjects. Serial ischemic brain pH levels indicated a progression from early acidosis to subacute alkalosis. When acidosis was present there was a significant elevation in the relative signal intensity of inorganic phosphate (Pi) and significant reductions in signal intensities of alpha-adenosine triphosphate (ATP) and gamma-ATP compared with those of control subjects. Ischemic brain pH values directly correlated with the relative signal intensity of phosphocreatine (PCr) and the PCr index and inversely correlated with the signal intensity of Pi. There was a general lack of correlation between either ischemic brain pH or phosphate energy metabolism and the initial clinical stroke severity. The data suggest a link between high-energy phosphate metabolism and brain pH, especially during the period of ischemic brain acidosis, and the authors propose that effective acute stroke therapy should be instituted during this period.
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PMID:Human focal cerebral ischemia: evaluation of brain pH and energy metabolism with P-31 NMR spectroscopy. 141 Mar 69

31-Phosphorus magnetic resonance spectroscopy was used in a rat model of 10 min severe incomplete forebrain ischaemia (2-vessel occlusion with hypotension) to assess the effect of mild brain hypo- and hyperthermia (+/- 2 degrees C) on intracellular pH and high energy phosphates. In three experimental groups intracerebral temperature was maintained at levels of 34, 36 and 38 degrees C during ischaemia and early reperfusion. The steady level of intracellular pH during ischaemia was 6.63, 6.58 and 6.53 in the 34, 36, and 38 degrees C groups, respectively. The rate of initial recovery of intracellular pH in reperfusion was 0.046 +/- 0.012 pH units per min (+/- s.d.) in the 36 degrees C group compared to 0.056 +/- 0.010 (+/- s.d., P less than 0.05) in the 34 degrees C group and 0.032 +/- 0.009 (+/- s.d., P less than 0.01) in the 38 degrees C group. The recovery in early reperfusion of phosphocreatine and ATP was slower in the 38 degrees C group compared to the other groups. The findings were consistent with recent studies, suggesting that even mild hypothermia may afford protection to the ischaemic brain, and furthermore indicate that mild hyperthermia as fever or even subfebricity may be deleterious for the outcome in stroke patients.
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PMID:The effects of brain temperature on temporary global ischaemia in rat brain. A 31-phosphorous NMR spectroscopy study. 163 61

A study was performed to determine quantitatively the alterations in phosphorus metabolite concentrations and pH in regions of the human brain damaged by chronic stroke. Image-guided phosphorus-31 magnetic resonance spectroscopy was performed on the brains of eight healthy subjects and six patients with cerebral infarction of more than 3 months duration. Phosphorus metabolite concentrations in infarcted regions were reduced 8%-67%. Significant decreases occurred in phosphomonoester (PME), phosphodiester (PDE), and adenosine triphosphate (ATP) concentrations, while inorganic phosphate (Pi) and phosphocreatine (PCr) concentrations showed smaller, nonsignificant decreases. The PCr/ATP ratio was significantly increased, while the ATP/Pi ratio was somewhat lower. The phospholipid ratio PDE/PME was also significantly increased, while the ratios of phospholipid (PME, PDE) to phosphate (PCR, Pi) metabolites were significantly decreased. The pH of the infarcted region indicated significantly more alkalinity than in the normal brain. The results suggest that chronic stroke is associated with significant changes in brain metabolite concentrations and pH that are different from those reported for other brain diseases.
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PMID:Decreased phosphorus metabolite concentrations and alkalosis in chronic cerebral infarction. 172 5

The influence of piracetam on the level of inorganic and phospholipid phosphorus in blood of ischemic stroke patients was evaluated. In healthy patients piracetam (2G, i.v.) diminished the concentration of inorganic phosphorus and essentially lowered the content of ion connected with phospholipids. In stroke patients inorganic phosphorus was primarily enhanced and organic lowered. Treatment with piracetam lowered the concentration of both inorganic and phospholipid phosphorus in blood.
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PMID:[Effect of piracetam on inorganic phosphates and phospholipids in the blood of patients with cerebral infarction in the earliest period of the disease]. 181 Nov 78

Hyperglycemia is often associated with an increased frequency of cerebrovascular disease and exacerbation of neuronal injury in focal ischemic cerebral infarction. We used a combination of high-field proton MR imaging and 1H and 31P MR spectroscopy to investigate whether hyperglycemia would adversely influence cerebral metabolism and eventual infarct size following unilateral occlusion of the middle cerebral artery (MCA) of cats pretreated with the calcium channel blocker nicardipine. Normoglycemic animals injected with 10 micrograms/kg of nicardipine (8 micrograms.kg-1.hr-1 maintenance dose) manifested only mild disturbances in phosphorus metabolism and cerebral pH regulation compared with untreated controls, and showed a significant reduction in infarct size 7 hr after MCA occlusion. By comparison, hyperglycemic cats (plasma glucose, 200-300 mg/dl) had significantly reduced cerebral high-energy phosphates, elevated lactic acid, and larger ischemic lesions in the occluded MCA territory, irrespective of whether they were treated with nicardipine. These results indicate that moderate hyperglycemia can exaggerate ischemic brain damage by enhancing formation of tissue lactic acid and impairing normal phosphorus metabolism. One implication of this study is that dextrose should not be provided to patients with acute ischemic stroke.
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PMID:Hyperglycemia augments ischemic brain injury: in vivo MR imaging/spectroscopic study with nicardipine in cats with occluded middle cerebral arteries. 188 34

We used phosphorus-31 nuclear magnetic resonance spectroscopy in a rat model of 10 minutes' severe incomplete forebrain ischemia (two-vessel occlusion with hypotension) to study the effects of preischemic and postischemic treatment with 3 mg/kg i.v. U74006F on the recovery of high-energy phosphates and intracellular pH during early reperfusion. The mean +/- SD time to 85% recovery of phosphocreatine was 14.1 +/- 8.4 minutes in the control group (n = 10) compared with 6.6 +/- 3.5 minutes (p less than 0.05) in the preischemic (n = 8) and 4.2 +/- 1.0 minutes (p less than 0.001) in the postischemic (n = 11) treatment groups. The mean +/- SD time to 80% recovery of adenosine triphosphate was 15.4 +/- 8.5 minutes in the control group compared with 6.3 +/- 1.8 (p less than 0.005) and 5.4 +/- 2.8 (p less than 0.001) minutes in the preischemic and postischemic treatment groups, respectively. There were no differences in intracellular pH between the control and either of the treatment groups. We conclude that U74006F led to quicker recovery of high-energy phosphates during early reperfusion, and this beneficial effect was also seen with postischemic treatment.
Stroke 1991 Sep
PMID:Quicker metabolic recovery after forebrain ischemia in rats treated with the antioxidant U74006F. 192 63


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