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

A case of 25-year-old woman with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) was reported. She had short stature, episodic vomiting with headache, several episodes with homonymous hemianopsia, progressive intellectual decline, generalized convulsion, muscular atrophy, sensory disturbance on the left side of the body, and primary amenorrhea. Lactate, pyruvate and the lactate to pyruvate ratio were elevated in the serum and cerebrospinal fluid. Muscle biopsy revealed ragged-red fibers. On electron microscopy there were subsarcolemmal aggregations of abnormal mitochondria with proliferation of crista and inclusions. Activities of the respiratory chain enzymes of the muscle mitochondria were normal. She showed a failure of GH response to arginine and levodopa and delayed response of serum GH to growth hormone releasing factor (GRF). She also showed decreased gonadotropin levels and delayed response of the hormone to LH-RH. In this case, a dysfunction of the hypothalamo-pituitary axis may be related to the short stature and primary amenorrhea. It is suggested that the hypothalamo-pituitary hypofunction may be one of the characteristic features in MELAS.
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PMID:[Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) associated with hypothalamo-pituitary hypofunction--a case report]. 206 Feb 43

1. Regional haemodynamic responses to i.v. bolus doses (0.1-10.0 mg kg-1) of NG-nitro-L-arginine methyl ester (L-NAME) were measured in conscious, Long Evans rats (n = 8) chronically instrumented with renal, mesenteric and hindquarters pulsed Doppler flow probes and intravascular catheters. 2. L-NAME caused dose-dependent pressor effects associated with renal, mesenteric and hindquarters vasoconstrictions. The mesenteric vascular bed showed earlier onset with more rapid, and greater, maximum vasoconstrictions than the renal or hindquarters vascular beds; however, the hindquarters vasoconstriction was more persistent. D-NAME was without significant effects (n = 2). 3. Primed infusion of L-arginine (100 mg kg-1 bolus followed by 100 mg kg-1 h-1 infusion), starting 10 min after an i.v. bolus injection of L-NAME (10 mg kg-1), caused significant reversal of the pressor responses, and renal and mesenteric vasoconstrictions, but not of the hindquarters vasoconstriction. Primed infusions of L-arginine (100 mg kg-1, 100 mg kg-1 h-1) starting 5 min after L-NAME (1 mg kg-1) additionally caused some reversal of the hindquarters vasoconstriction, but this effect was transient. 4. Primed infusion of L-arginine (100 mg kg-1, 100 mg kg-1 h-1) starting 30 min before i.v. bolus injection of L-NAME (10 mg kg-1) caused significant attenuation of the pressor effects and the renal and mesenteric vasoconstrictions but not of the hindquarters vasoconstriction. 5. In a separate group of rats (n = 8) chronically instrumented with thoracic aortic electromagnetic flow probes for the measurement of cardiac haemodynamics, i.v. bolus injection of L-NAME (10mgkg-1) produced significant reductions in total peripheral conductance, cardiac output, stroke volume, peak thoracic aortic flow and the maximum rate of rise of aortic flow; these were coincident with the maximum pressor and vasoconstrictor effects. 6. These results, collectively, are consistent with L-NAME interfering with L-arginine-nitric oxide pathways that have important influences on regional vascular conductances in vivo. The pressor effect resulting from L-NAME-induced vasoconstrictions is offset by a substantial reduction in cardiac function that may depend on direct and/or indirect effects of L-NAME on the heart.
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PMID:Regional and cardiac haemodynamic effects of NG-nitro-L-arginine methyl ester in conscious, Long Evans rats. 207 81

Pressor effects of NG-monomethyl-L-arginine (L-NMMA), a selective inhibitor of nitric oxide production from L-arginine, on mean blood pressure (MBP) were investigated in conscious Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). L-NMMA (0.1-10 mg/kg, i.v.) elicited a dose-dependent increase in the MBP of WKY and SHRSP. The pressor response to L-NMMA was more marked in SHRSP than in WKY. These results suggest that nitric oxide may play an important role in the blood pressure regulation in the conscious SHRSP.
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PMID:Pressor effect of NG-monomethyl-L-arginine in SHRSP. 208 8

The purpose of this study was to investigate the formation and action of a nitric oxide-related endothelium-derived relaxing factor in cerebral arteries of cattle. Pial artery segments (0.6-1 mm o.d.) were incubated in oxygenated (20%) Krebs-Henseleit buffer containing indomethacin. Addition of acetylcholine (0.1 microM) to rings precontracted by serotonin (0.1 microM) resulted in a significant (p less than 0.05) relaxation. This response disappeared after removal of the endothelium and addition of hemoglobin, a nitric oxide scavenger, and NG-monomethyl-L-arginine, an inhibitor of L-arginine-derived nitric oxide biosynthesis. L-Arginine (10 microM) considerably attenuated the inhibitory action of NG-monomethyl-L-arginine. Relaxations induced by 3-morpholinosydnonimine and nitroglycerin (0.1 microM), two exogenous sources of nitric oxide, were unaffected by NG-monomethyl-L-arginine (10 microM) but abolished by hemoglobin. These data strongly suggest nitric oxide as the mediator of endothelium-derived relaxation in pial arteries of the cattle.
Stroke 1990 Dec
PMID:Nitric oxide is the endothelium-derived relaxing factor in bovine pial arterioles. 212 88

Regional central nervous system and peripheral hemodynamic effects of the intrathecal (i.t.) administration of a substance P (SP) receptor antagonist, [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-substance P ([D-Arg]-SP), were studied in anesthetized rats. It was found that [D-Arg]-SP (3.3 nmol i.t.) reduced mean arterial pressure and cardiac output due to a reduction in stroke volume. Total peripheral resistance was not altered. Whereas most vascular beds showed no alterations in vascular resistance, a renal vasoconstriction was noted. The hypotensive effect of [D-Arg]-SP was blocked by phentolamine (10 mg/kg i.v.) but not by propranolol (1 mg/kg i.v.). In the absence of changes in vascular arterial resistance due to [D-Arg]-SP, it appears that a change in venous return may contribute to the [D-Arg]-SP-induced reduction in stroke volume. These data provide evidence that a spinal cord SP system may tonically affect sympathetic neurons controlling venous, but not arterial, vasomotor tone. [D-Arg]-SP (i.t.) did not alter brain blood flow but significantly decreased blood flow in the thoracolumbar spinal cord 15 to 20 min after administration. The reduction in spinal cord flow did not appear to be responsible for the [D-Arg]-SP-induced hypotension because kainic acid (i.t.), an agent that interacts with glutamate receptors, produced similar pressor responses in the presence and absence of [D-Arg]-SP. In addition, whereas the pressor effect of low doses of a SP agonist [pGlu5, MePhe8, MeGly9]-substance P (5-11) were blocked by [D-Arg]-SP, a higher dose produced the typical pressor effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intrathecal administration of a substance P receptor antagonist: studies on peripheral and central nervous system hemodynamics and on specificity of action. 244 Oct 24

The peptide, 7B2, originally isolated from pituitary, has been shown to be present in endocrine tumors of high concentrations in pancreatic islet tumors. Plasma from most of these patients showed very high 7B2 immunoreactivity (IR-7B2) though there is a lack of knowledge concerning physiological and pathological changes in plasma IR-7B2 levels in other conditions. To assess whether or not there is any alteration in circulating IR-7B2 levels due to age, sex or any specific condition, plasma levels of IR-7B2 were measured in the fasting state in 106 healthy subjects aged 3 months to 91 years, 101 diabetics, 28 patients with hyperthyroidism. 7 patients with primary hypothyroidism, 13 patients with liver cirrhosis, 43 patients with chronic renal failure, 35 patients with cerebral vascular accident, and 26 pregnant subjects. Twenty-four cord bloods were also included. The responses of circulating IR-7B2 to oral glucose, intravenous arginine infusion, volus thyrotropin (TRH) or volus luteinizing hormone-releasing hormone (LH-RH) injection were also evaluated. Particularly high IR-7B2 levels were found to exist in cord blood. Postnatally the concentrations decreased gradually with age to adult values (15.6 +/- 2.9pmol/liter (mean +/- SE) in 20's-60's), though plasma IR-7B2 levels again increased significantly in over 70's (37.1 +/- 3.2pmol/liter; P less than 0.01). There was no significant difference in plasma 7B2 levels in either sex. Among the pathological conditions studied, significantly high IR-7B2 levels were observed in patients with chronic renal failure (175.1 +/- 35.9pmol/liter). Some of the pregnant patients in their third trimester also showed high plasma IR-7B2 levels. A small but significant rise in plasma IR-7B2 was observed after a glucose load in control subjects and diabetics. Intravenous LH-RH exerted a rise in plasma 7B2 concentrations though arginine and TRH showed no significant effect on plasma IR-7B2 concentrations. Compared with the plasma concentrations, ten to fifty-fold high levels of IR-7B2 were observed in cerebrospinal fluid (CSF) from patients with cerebrovascular accidents or multiple sclerosis. These results suggested that the kidney plays a major role in 7B2 degradation and that LH-RH simulates IR-7B2 release from the pituitary gland. Whether reduced clearance or increased production was responsible for the IR-7B2 elevation in subjects under 10 years or over 70 years requires investigation. Furthermore, high levels of IR-7B2 in CSF might indicate its specific role for the central nervous system.
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PMID:[Immunoreactive 7B2 concentrations in plasma and cerebrospinal fluid in pathophysiological conditions and the responses to oral glucose load, intravenous LH-RH, TRH and arginine infusion]. 251 84

To determine the hemodynamic effects of a hypotensive dose of atrial natriuretic factor (ANF), a synthetic peptide containing 26 amino acids of endogenous rat ANF (Arg-Arg-Ser-Ser-Cys-Phe-Gly-Gly-Arg-Ile-Asp-Arg-Ile-Gly-Ala-Gln-Ser-Gly -Leu-Gly-Cys-Asn-Ser-Phe-Arg-Tyr-COOH) was studied in two groups of barbiturate anesthetized rats. In the first experiment, a 20-minute infusion of a hypotensive dose, 95 pmole/min i.v., of the synthetic ANF decreased mean arterial pressure (MAP) by 40 +/- 3 mm Hg from a baseline of 128 +/- 5 mm Hg, and cardiac output (CO) (microsphere method) by 7.8 +/- 1.8 ml/min/100 gm from a baseline of 23.5 +/- 1.3 ml/min/100 gm. Synthetic ANF did not significantly affect the total peripheral resistance (TPR) measured at the end of the 20-minute infusion. Sodium nitroprusside (SNP), infused at an equihypotensive dose of 20 micrograms/kg/min i.v., produced the same hemodynamic profile in seven other animals; in contrast, 0.3 mg/kg i.v. of hydralazine (n = 7) lowered MAP by 56 +/- 6 mm Hg and reduced TPR index by 3.0 +/- 0.6 mm Hg/ml/min/100 gm, but did not change CO. Other than an increase in coronary blood during SNF infusion, there were no significant changes in the distribution of cardiac output. Infusion of the saline vehicle had no significant effects on any of these parameters. The results of the second experiment in anesthetized rats confirmed that hypotensive doses of 40 and 100 pmole/kg/min i.v. lowered CO (dye dilution method) from a baseline of 33 +/- 6 to a minimum of 24 +/- 2 ml/min/100 gm (p less than 0.05) without affecting TPR. In addition, synthetic ANF did not significantly affect heart rate (HR) but it slightly reduced cardiac contractility (dp/dt50). These results suggest that the hypotensive dose of synthetic ANF reduced cardiac output, partially by diminishing stroke volume, and perhaps contractility.
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PMID:Cardiac and hemodynamic responses to synthetic atrial natriuretic factor in rats. 294 28

Arginine-vasopressin (AVP) content was measured by radioimmunoassay in the plasma and brain of stroke-prone spontaneously hypertensive rats (SHRsp) and normotensive Wistar Kyoto (WKY) control rats. AVP was reduced in plasma, hypothalamus, amygdala, septum and brain stem of the hypertensive animals. In view of the possible sensitizing effect of vasopressin on the baroreceptor reflex, the reduction of this peptide in the brain stem could contribute to hypertension in SHRsp.
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PMID:Reduced content of vasopressin in the brain of spontaneously hypertensive as compared to normotensive rats. 725 7

The role of nitric oxide (NO) in the cardiovascular actions of diaspirin cross-linked hemoglobin (DCLHb) was studied in anesthetized rats. The regional circulatory and systemic hemodynamic effects of DCLHb (400 mg/kg iv) were studied using a radioactive microsphere technique in control (untreated) and L-arginine (a NO precursor) pretreated rats. DCLHb produced a significant increase in blood pressure (75%), cardiac output (42%), stroke volume (36%), and total peripheral resistance (45%), without affecting heart rate, when administered to control rats. L-Arginine pretreatment significantly attenuated DCLHb-induced systemic hemodynamic effects. DCLHb-induced increase in blood flow to the skin and spleen was completely blocked, and that to the heart was partially blocked, by L-arginine pretreatment, suggesting that cardiovascular actions induced by DCLHb could be antagonized by the NO precursor L-arginine. The NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) produced significant increases in regional vascular resistance, leading to a decrease in blood flow to all the organs except the heart, where an increase in blood flow and a decrease in vascular resistance was observed. DCLHb, when administered in L-NAME-pretreated rats, accentuated the decrease in blood flow to the gastrointestinal system, spleen, mesentery and pancreas, skin, and musculoskeletal system. These studies provide evidence that the NO precursor L-arginine can attenuate the effects of DCLHb and that DCLHb can potentiate the effect of the NOS inhibitor L-NAME. The role of NO in the mechanism of action of DCLHb was further studied by estimating plasma guanosine 3',5'-cyclic monophosphate (cGMP) in control, DCLHb-treated, L-NAME-treated, and L-NAME followed by DCLHb-treated rats. DCLHb and L-NAME significantly decreased the concentration of circulating cGMP in blood plasma. L-NAME pretreatment potentiated DCLHb-induced decrease in cGMP levels. Because the formation of cGMP is stimulated by NO, these studies provide additional evidence for the involvement of NO in the mechanism of action of DCLHb. It is concluded that NO plays an important role in the cardiovascular effects of DCLHb.
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PMID:Role of NO mechanism in cardiovascular effects of diaspirin cross-linked hemoglobin in anesthetized rats. 748 71

In order to clarify insulinotropic effects of the myelin basic protein (MBP) we studied mode of association and distribution of MBP in the pancreatic islets and tested the insulin-releasing activity of various MBP peptides. Rat pancreatic islets were first stimulated in a static incubation with 10 microM bovine MBP (bMBP) at a substimulatory (3.5 mM) glucose concentration. The islets exposed to MBP released significantly more insulin and glucagon in a second incubation in the absence of added stimulant and in the presence of 11.5 mM arginine than the incubated, non-stimulated islets and islets initially stimulated with 15 mM glucose. Response to stimulation with 15 mM glucose in the second incubation by islets exposed first to MBP was impaired compared to incubated, non-stimulated islets. Immunoelectron microscopy showed that MBP had entered into the islet cells and associated with membranes of intracellular vacuoles, most of which represented enlarged, often fused insulin granules. MBP was also present at the islet edge and in the intercellular spaces. Of the purified MBP peptides of sizes of 4.8-13.6 kDa, produced from the digestion with brain acid proteinase and with pepsin and covering the entire bMBP sequence, only the large peptides (1-88, 9.8 kDa and 43-169, 13.6 kDa) stimulated insulin secretion significantly. Heterogeneous peptide mixtures, obtained from a time-course digestion of bMBP by myelin calcium-activated neutral protease, consisting of peptides of approximate molecular weights of 8-11 kDa and larger, also stimulated insulin release. The glucagon-releasing activity of MBP peptides was low and followed the same pattern as the insulin-releasing activity. The present results suggest that MBP-induced fusion of the membranes of hormone granules is involved in MBP-induced insulin release. The hormone-releasing activity of the large peptides in addition to that of the intact molecule is explained as being due to the ability of these peptides to associate with membranes. MBP-induced hormone release and related effects could be associated with neuropathological conditions such as stroke and multiple sclerosis.
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PMID:Evidence supporting membrane fusion as the mechanism of myelin basic protein-induced insulin release from rat pancreatic islets. 749 48


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