Temporal profile and significance of metabolic failure and trophic changes in the canine cerebral arteries during chronic vasospasm after subarachnoid hemorrhage

1993 ◽  
Vol 78 (5) ◽  
pp. 807-812 ◽  
Author(s):  
Yuhei Yoshimoto ◽  
Phyo Kim ◽  
Tomio Sasaki ◽  
Kintomo Takakura
Keyword(s):  
Subarachnoid Hemorrhage ◽  
High Performance ◽  
Close Association ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Content Type ◽  
Temporal Profile

✓ To investigate the pathogenetic significance of metabolic failure observed in spastic cerebral arteries after subarachnoid hemorrhage (SAH), the temporal profile of alterations in the arterial content of high-energy phosphates was studied. A canine model of double hemorrhage was used. Constriction of the basilar artery was measured angiographically on Days 3, 5, 7, and 14 after SAH in separate groups of animals. Adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), guanosine triphosphate (GTP), guanosine diphosphate, creatine phosphate (CrP), and creatine (Cr) levels in the arteries were assayed using high-performance liquid chromatography. A time-dependent development of angiographic spasm was confirmed. A mild vasospasm was seen in the group studied 3 days after SAH, progressed in the Day 5 group, remained comparably severe in the Day 7 group, and resolved partially in the Day 14 group. The content of high-energy phosphates (ATP, GTP, and CrP) declined rapidly over the course of the study, and a significant reduction in ATP, GTP, and CrP was observed in the Day 3 group. Levels of ATP and CrP decreased further in the Day 5 and 7 groups. The decrement in GTP was completed in the early phase; a significant reduction took place in the Day 3 group, with no progression thereafter and no recovery though Day 14. Total adenylate (ATP + ADP + AMP) and total creatine (Cr + CrP) content diminished markedly over the course of the study. These results indicate that metabolic failure and trophic disturbance in the cerebral artery occurs with a rapid onset following SAH and progresses in close association with the development of vasospasm, suggesting a significant causal relationship with the pathogenesis.

High-energy phosphate levels in the cerebral artery during chronic vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (6) ◽  
pp. 991-996 ◽  
Author(s):  
Phyo Kim ◽  
James D. Jones ◽  
Thoralf M. Sundt
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
High Performance ◽  
Venous Blood ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Content Type ◽  
Chronic Vasospasm

✓ High-energy phosphate levels were measured in the canine cerebral artery during chronic vasospasm. Subarachnoid hemorrhage and vasospasm were induced by percutaneous injections of autologous venous blood into the cisterna magna. Narrowing of the artery was confirmed by angiography 7 days later. Levels of adenosine phosphates (adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP)), guanosine phosphates (guanosine triphosphate (GTP) and guanosine diphosphate (GDP)), and creatine phosphate (CrP) in the basilar artery were quantified using high-performance liquid chromatography. The total creatine (Crtotal) content was measured by a spectrophotometric method after acid hydrolysis of CrP. Levels of ATP, GTP, and CrP were markedly reduced in the spastic arteries, and ratios of ATP:ADP, GTP:GDP, and CrP:Crtotal were significantly decreased. The results indicate a serious disturbance in the energy metabolism that takes place in the cerebral artery during chronic vasospasm.

Regional cortical metabolism in focal ischemia

1980 ◽  
Vol 52 (6) ◽  
pp. 755-763 ◽  
Author(s):  
Robert A. Ratcheson ◽  
James A. Ferrendelli
Keyword(s):  
Interindividual Variability ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Focal Ischemia ◽  
Metabolic Changes ◽  
High Energy Phosphates ◽  
Cerebral Vessel ◽  
Content Type ◽  
Glucose Levels

✓ Regional cortical levels of organic phosphates and carbohydrates were measured in cat brains, enzymatically inactivated by the technique of “funnel freezing” 1 hour after occlusion of a middle cerebral artery (MCA). Significant metabolic alterations occurred in all hemispheres ipsilateral to the site of occlusion. However, there was marked interindividual variability, with changes ranging from only slight increases in lactate, pyruvate, and adenosine monophosphate (AMP) in small regions of cortex at one extreme, to profound depletion of high-energy phosphates, depression of glucose and pyruvate levels, and increased lactate, adenosine diphosphate (ADP) and AMP levels in much of the hemisphere of the most severely involved animals. In contrast, metabolic changes in the hemisphere contralateral to the site of occlusion were very few or nonexistent. In addition, in all ipsilateral hemispheres there were regions peripheral to the areas of greatest metabolic alteration where there was excessive elevation of glucose levels. The results demonstrate that occlusion of a major cerebral vessel does not produce metabolic changes that are consistent in their distribution or severity. However, the findings of this study probably depict some of the complicated metabolic events that occur clinically during thrombotic or embolic infarction of brain.

Selective hemoglobin inhibition of endothelium-dependent vasodilation of rabbit basilar artery

1986 ◽  
Vol 64 (3) ◽  
pp. 445-452 ◽  
Author(s):  
Shigeru Fujiwara ◽  
Neal F. Kassell ◽  
Tomio Sasaki ◽  
Tadayoshi Nakagomi ◽  
Richard M. Lehman
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Degradation Products ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Isometric Tension ◽  
Content Type ◽  
Adenosine Antagonist ◽  
Dose Dependent ◽  
Fine Print

✓ The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10−7−10−4 M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10−6 M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10−7-10−5 M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10−7-10−4 M) also relaxed isolated rabbit basilar artery already contracted by 10−6 M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.

Ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage

1986 ◽  
Vol 64 (2) ◽  
pp. 292-297 ◽  
Author(s):  
Thomas A. Duff ◽  
Grayson Scott ◽  
John A. Feilbach
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Prolonged Exposure ◽  
Cerebral Arteries ◽  
Content Type ◽  
Ultrastructural Evidence ◽  
Experimental Subarachnoid Hemorrhage ◽  
Catecholamine Histofluorescence ◽  
Increased Sensitivity ◽  
The Media ◽  
Adult Cats

✓ Loss of catecholamine histofluorescence, increased sensitivity to norepinephrine, and changes in alpha1 receptor binding have led to the proposal that denervation hypersensitivity may play a role in cerebrovascular spasm. Because the significance of these alterations has remained unclear, the present study was undertaken to determine whether there was direct ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. Under general anesthesia, adult cats were subjected to pre-pontine injection of blood or serum (5 to 7 ml) via a transclival approach. The animals were sacrificed 4, 7, or 10 days later and basilar artery segments were prepared for electron microscopy. Control vessels appeared normal, whereas those bathed in blood revealed unequivocal changes in neural and supporting elements, including: 1) disintegration of both clear- and dense-core vesicles; 2) fragmentation of varicosities; 3) loss of Schwann cell cytoplasm; and 4) axonal degeneration. These changes were most pronounced 7 days after instillation of blood, and correlated in time with maximal injury of the media and endothelium. Although the development of smooth-muscle hypersensitivity remains unsettled, this study indicates that prolonged exposure to blood can cause extensive denervation of cerebral arteries.

Content Variations of ATP-Related Compounds and Quality Assessment of Tilapia Fillets during Iced Storage

2014 ◽  
Vol 1073-1076 ◽  
pp. 1767-1775
Author(s):  
Lei Lei Sun ◽  
Hui Huang ◽  
Lai Hao Li ◽  
Xian Qing Yang ◽  
Shu Xian Hao ◽  
...  
Keyword(s):  
Quality Assessment ◽  
High Performance ◽  
Storage Time ◽  
Degradation Products ◽  
Thiobarbituric Acid ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Significant Linear Correlation ◽  
Tilapia Fillets ◽  
Iced Storage

To explore the biochemical changes of tilapia fillets during iced storage, contents of adenosine triphosphate (ATP) and its degradation products were monitored by high performance liquid chromatography (HPLC), along with ATPase and the freshness indicators such as the values ofK,Ki,H,Fr, total volatile base nitrogen (TVB-N) and thiobarbituric acid (TBA) were determined to evaluate the quality of iced tilapia fillets. The results showed that ATP, adenosine diphosphate (ADP) and adenosine monophosphate (AMP) in iced tilapia fillets degraded sharply into inosine monophosphate (IMP) at the first day of storage, then almost kept stable in a low level over the rest of iced storage time. Meanwhile, IMP degraded into hypoxantjine (Hx) and inosine (HxR) with the extending storage time, and Hx as well as HxR accumulated. The changes of values ofK,Ki,H,Frwith iced storage time presented a significant linear correlation (P<0.01, r=0.945, 0.943, 0.924, -0.943, respectively). ATPase activities were associated with the degradation of ATP. The contents of IMP, Hx, HxR, values ofK,Ki,H,Frand ATPase activities can be used as practical and effective indicators for quality assessment of tilapia fillets during iced storage instead of TVB-N and TBA.

PHOSPHORYLATION COUPLED TO THE OXIDATION OF SULFITE AND 2-MERCAPTOETHANOL IN EXTRACTS OF THIOBACILLUS THIOPARUS

1967 ◽  
Vol 13 (7) ◽  
pp. 873-884 ◽  
Author(s):  
E. A. Davis ◽  
E. J. Johnson
Keyword(s):  
Electron Donor ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Thiobacillus Thioparus ◽  
Ph Values ◽  
Cell Extracts ◽  
Endogenous Level ◽  
Sulfite Oxidation

The effect of 10−4 M 2, 4-dinitrophenol (DNP) on the production of high energy phosphate bonds during sulfite and 2-mercaptoethanol (2-ME) oxidation by cell extracts of Thiobacillus thioparus was determined. Phosphorylation was measured indirectly by14CO2fixation and directly by32PO4esterification. DNP-sensitive phosphorylation was demonstrated by coupling sulfite oxidation with the concomitant phosphorylation of adenosine monophosphate (AMP) to14CO2fixation beginning with ribose-5-phosphate. Esterification of32PO4was measured at pH values of 6.4, 7.2, and 8.0 with AMP and adenosine diphosphate (ADP) as the phosphate acceptor and sulfite as the electron donor. The optimal pH for the greatest DNP-sensitive phosphorylation was 7.2 with AMP. DNP at 10−4 M significantly reduced32PO4esterification at all pH values tested and with the three ADP concentrations employed. Maximum DNP-sensitive phosphorylation of ADP was demonstrated with 5 μmoles of ADP at pH 7.2. The maximum P:O ratio was 0.13. With 2-ME as the nonphysiological electron donor and AMP as the phosphate acceptor, no phosphorylation above the endogenous level was measured at the three pH values tested. With ADP as the phosphate acceptor and 2-ME as the electron donor,32PO4esterification significantly above the endogenous level was demonstrated at pH 6.4 with 5 μmoles of ADP; this phosphorylation was sensitive to 10−4 M DNP.

Altered reactivity of human cerebral arteries after subarachnoid hemorrhage

1995 ◽  
Vol 83 (3) ◽  
pp. 510-515 ◽  
Author(s):  
Hisashi Onoue ◽  
Nobuyoshi Kaito ◽  
Masahiko Akiyama ◽  
Masato Tomii ◽  
Shogo Tokudome ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Vasoactive Agents ◽  
Content Type ◽  
Vasoactive Substances ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F ◽  
Human Cadavers ◽  
Endothelium Dependent Relaxation

✓ To investigate the effects of subarachnoid hemorrhage (SAH) on the responsiveness of human cerebral arteries to vasoactive substances, the authors measured the isometric tension generated in helical strips of basilar and middle cerebral arteries isolated from human cadavers Contractions caused by KCl, prostaglandin F2α, noradrenaline, and serotonin were reduced in arteries obtained from cadavers with aneurysmal SAH damage and compared to those obtained from cadavers with no indication of intracranial diseases. Endothelium-dependent relaxation elicited by substance P and bradykinin, and endothelium-independent relaxation induced by prostaglandin I2 and nitroglycerin were also markedly decreased in arteries affected by SAH. However, the reduction in relaxation response to prostaglandin I2 was significantly less than that to the other vasodilator agents. These results indicate that human cerebral artery functions are severely impaired after SAH and that poor responses to vasoactive agents may result primarily from dysfunction of smooth-muscle cells.

Subarachnoid hemorrhage—induced upregulation of the 5-HT1B receptor in cerebral arteries in rats

2003 ◽  
Vol 99 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Jacob Hansen-Schwartz ◽  
Natalie Løvland Hoel ◽  
Cang-Bao Xu ◽  
Niels-Aage Svendgaard ◽  
Lars Edvinsson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Real Time ◽  
Cerebral Vasospasm ◽  
Cerebral Arteries ◽  
Specific Treatment ◽  
Content Type ◽  
Sequence Of Events ◽  
Arterial Blood ◽  
Receptor Phenotype ◽  
Fine Print

Object. Cerebral vasospasm following subarachnoid hemorrhage (SAH) leads to reduced blood flow in the brain. Inspired by organ culture—induced changes in the receptor phenotype of cerebral arteries, the authors investigated possible changes in the 5-hydroxytryptamine (HT) receptor phenotype after experimental SAH. Methods. Experimental SAH was induced in rats by using an autologous prechiasmatic injection of arterial blood. Two days later, the middle cerebral artery (MCA), posterior communicating artery (PCoA), and basilar artery (BA) were harvested and examined functionally with the aid of a sensitive in vitro pharmacological method and molecularly by performing quantitative real-time reverse transcription—polymerase chain reaction (PCR). In the MCA and BA the 5-HT1B receptor was upregulated, as determined through both functional and molecular analysis. In response to selective 5-HT1 receptor agonists both the negative logarithm of the 50% effective concentration was increased (one log unit in the MCA and one half unit in the BA), as was the agonist's potency (increased by 50% in the MCA and doubled in the BA). In addition, the authors found an approximately fourfold increase in the number of copies of messenger RNA coding for the 5-HT1B receptor as determined by quantitative real-time PCR. In the PCoA no upregulation of the 5-HT1B receptor was observed. Conclusions. Changes in the receptor phenotype in favor of contractile receptors may well represent the end stage in a sequence of events leading from SAH to the actual development of cerebral vasospasm. Insight into the mechanism of upregulation may provide new targets for developing specific treatment against cerebral vasospasm.

Alterations in endothelium-dependent responsiveness of the canine basilar artery after subarachnoid hemorrhage

1988 ◽  
Vol 69 (2) ◽  
pp. 239-246 ◽  
Author(s):  
Phyo Kim ◽  
Thoralf M. Sundt ◽  
Paul M. Vanhoutte
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basilar Artery ◽  
Calcium Ionophore ◽  
Adenosine Diphosphate ◽  
Canine Model ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Content Type ◽  
Endothelium Dependent Relaxation

✓ To investigate the alteration of endothelium-dependent responses in chronic vasospasm after subarachnoid hemorrhage (SAH), experiments were carried out in the double-hemorrhage canine model. After the presence of vasospasm was confirmed by cerebral angiography on Days 0 and 7, pharmacological studies on the basilar artery were conducted in vitro on Day 8. In the SAH group, endothelium-dependent relaxation was abolished in response to arginine vasopressin and was significantly reduced in response to thrombin. Endothelium-independent relaxation in the SAH group was preserved in response to papaverine and was minimally reduced in response to sodium nitroprusside. Endothelium-dependent contraction in response to arachidonic acid, acetylcholine, the calcium ionophore A23187, adenosine diphosphate, mechanical stretching, and hypoxia persisted in the SAH group. The maximal contraction to KCl and uridine triphosphate, which is endothelium-independent, was diminished in the SAH group, but no changes in sensitivity were noted in the concentration-response relationships. A significant correlation was observed between the degree of vasospasm determined angiographically and the loss of endothelium-dependent relaxation. The loss of endothelium-dependent relaxation and the persistence of endothelium-dependent contraction suggest that the deterioration in the endothelium-dependent responses may be an important component in the pathogenesis of cerebral vasospasm.

THE INFLUENCE OF SYMPATHOMIMETIC AMINES, MONOAMINE OXIDASE INHIBITORS, AND ANTIHYPERTENSIVES UPON THE ENERGY METABOLISM IN THE RAT HEART

1966 ◽  
Vol 44 (4) ◽  
pp. 605-613 ◽  
Author(s):  
W. G. Hilliard ◽  
W. T. Oliver ◽  
G. R. Van Petten
Keyword(s):  
Energy Metabolism ◽  
Monoamine Oxidase ◽  
Rat Heart ◽  
Antihypertensive Drugs ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Monoamine Oxidase Inhibitors ◽  
Sympathomimetic Amines ◽  
Cardiac Energy Metabolism

This investigation was undertaken to determine the effects of three classes of catecholamine-releasing drugs on cardiac energy metabolism. The levels of adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), inorganic phosphate (IP), and phosphocreatine (CP) of the rat heart were measured. The sympathomimetic amines tyramine, ephedrine, methylamphetamine, and (+)- and (−)-amphetamine caused significant decreases in CP. Tyramine and (+)- and (−)-amphetamine also significantly depressed ATP. Of the antihypertensive drugs investigated, bretylium and guanethidine decreased the amount of CP present, and the latter compound also significantly decreased ATP. The administration of reserpine was without significant effect on cardiac high-energy phosphate levels. Among the monoamine oxidase inhibitors, tranylcypromine significantly lowered ATP and CP, whereas pheniprazine produced no significant changes. This study showed that those drugs which have been reported to release cardiac catecholamines also reduced cardiac levels of CP and ATP. The hypothesis is advanced that this effect is due to increased utilization of energy by two mechanisms: (a) stimulation of the active recapture mechanism for adrenergic neurotransmitters, and (b) the positive inotropic and chronotropic responses of the heart to the drug-released catecholamines. In either case, the observed decreases in the levels of ATP and CP in the heart are effects of sympathomimetic amines which have been heretofore unreported.

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