Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the hemodynamic effects of dibutyryl cyclic AMP (DBcAMP) in congestive heart failure (CHF), right-sided cardiac catheterization was performed in 11 patients with CHF, and hemodynamic variables were investigated before and after infusion of various doses of DBcAMP at a rate of 0.025 to 0.2 mg/kg/min (mean 0.14 +/- 0.077 [standard deviation]). DBcAMP reduced total systemic vascular resistance index from 3,171 +/- 1,158 to 1,880 +/- 554 dynes s cm-5 X m2 (mean +/- standard deviation) and pulmonary arterial end-diastolic pressure from 23 +/- 13 to 20 +/- 11 mm Hg, and increased cardiac index from 2.24 +/- 0.60 to 3.41 +/- 1.02 liters/min/m2. Mean arterial blood pressure decreased from 91 +/- 14 to 84 +/- 13 mm Hg, and heart rate increased from 91 +/- 16 to 99 +/- 13 beats/min. The increase in cardiac index was accompanied by a proportional decrease in total systemic vascular resistance index in all patients except 1. In 8 patients the decrease in pulmonary arterial end-diastolic pressure was accompanied by an increase or no change in the left ventricular stroke work index. In 6 patients, DBcAMP was given in incremental doses of 0.05, 0.1, and 0.2 mg/kg/min every 20 minutes, and 5 of 6 patients tolerated the full dose and showed dose-related hemodynamic changes for the incremental doses of DBcAMP. These data suggest that DBcAMP has powerful vasodilating effects on resistance vessels in patients with CHF; hence, it can be a useful vasodilating agent for treatment of CHF.
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PMID:Hemodynamic effects of dibutyryl cyclic AMP in congestive heart failure. 630 1

Agents that increase cellular cyclic adenosine monophosphate (cyclic AMP) levels exert several effects on cardiac function. These include increases in heart rate and both the force of contraction and rate of relaxation. The latter effects, which might appear to be contradictory, actually represent essential components of the response needed to allow the heart to increase its stroke volume when heart rate is accelerated. This article reviews the mechanisms by which cyclic AMP exerts both contraction-promoting and relaxation-promoting effects in the integrated response of the heart to sympathetic stimulation.
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PMID:Cyclic adenosine monophosphate effects on the myocardium: a man who blows hot and cold with one breath. 630 77

Concentrations of cyclic AMP and cyclic GMP in arterial and internal jugular venous (IJV) blood were determined at the resting wakeful state in thirty surgical patients without neurological deficits. The levels of cyclic AMP in artery and IJV were 32.1 +/- 3.0 and 40.0 +/- 4.1 pmol/ml (means +/- standard errors), respectively, while those of cyclic GMP in artery and IJV were 12.2 +/- 2.7 and 14.4 +/- 3.0 pmol/ml, respectively. Concentrations of both cyclic nucleotides in IJV were significantly higher (P less than 0.001) than those in artery. IJV-arterial differences for cAMP and cGMP were 7.9 +/- 1.7 and 2.1 +/- 0.5 pmol/ml, respectively. The results indicate that both cyclic nucleotides are constantly produced and released from the normal human brain.
Stroke
PMID:Production of cyclic nucleotides from normal human brain. 631 3

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension]. 632 58

The effect of three modes of anesthesia was evaluated with regard to regional damage to central cyclic nucleotide systems in the gerbil brain as a consequence of bilateral ischemia (clamping the common carotids) followed by various periods of recirculation. The injection of thiopental as much as 90 min before stroke prevented damage to chemical activation [catecholamines, guanosine triphosphate (GTP), or forskolin] of adenylate cyclase. However, the basal enzyme activity was lower in all brain regions whether thiopental was administered to stroke or sham-operated animals. Injection of ketamine drastically shortened the survival times of gerbils undergoing stroke followed by recirculation. About 90% of the animals could tolerate a maximum of only 15 min stroke with 15 min recirculation. At this time frame the patterns of activation of adenylate cyclase in only the olfactory tubercle and hippocampus were altered. When procaine was used as a local anesthetic agent during surgery, damage to catecholamine-, GTP-, or forskolin-activated adenylate cyclase was evident to varying degrees in the frontal cortex, hippocampus or olfactory tubercle, but not in the nucleus accumbens and olfactory bulb of gerbils subjected to 60-min stroke followed by 15 or 150 min of recirculation. The degree of enzyme damage was neither correlated with the fed vs. fasted state of the animal nor with the whole blood concentration of glucose. A depression in the amplitude of visually evoked potentials correlated to neurological signs and to enzyme damage. During anesthesia, ketamine increased steady-state concentrations of cyclic AMP in the frontal cortex and hippocampus from gerbil brains that had been rapidly inactivated by microwave irradiation. Thiopental increased steady-state cyclic AMP in only the olfactory tubercle. Cyclic GMP concentrations were unchanged by any anesthetic agent. In animals completely recovering from anesthesia and occluded for a brief period followed by 10 min of reflow, steady-state concentrations of only cyclic AMP were augmented.
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PMID:Regional cyclic AMP systems during secondary ischemia in gerbils: influence of anesthetic agents. 632 54

The potential efficacy of the calcium channel blocker verapamil in modifying ischemic brain injury was evaluated in anesthetized rats subjected to 60 or 90 min of diffuse forebrain ischemia produced by bilateral occlusion of the carotid and vertebral arteries. Treated animals received verapamil, 2 mg/kg intravenously, prior to ischemia. Four hours of postischemic recirculation was permitted by reversing the carotid occlusions. Intermittent high-voltage slow-wave activity was noted on electroencephalograms shortly after verapamil infusion, prior to ischemia. The ischemic insult induced an isoelectric EEG, which tended to persist during recirculation in both treated and untreated animals. Similarly, verapamil pretreatment failed to influence brain water content or cerebral energy metabolites (phosphocreatine, ATP, ADP, AMP) or cerebral energy charge when assayed after four hours of recirculation. Thus, verapamil failed to confer a protective effect on brain electrical activity, water content, or energy metabolites following ischemia in this model.
Stroke
PMID:Verapamil: failure of metabolic amelioration following global forebrain ischemia in the rat. 643 33

Adenylate cyclase activity was investigated in either homogenate or particulate fractions from the frontal cerebral cortex of the gerbil following five experimental conditions of bilateral ischemia. After periods of 15 min ischemia, 15 min ischemia plus 15 min of recirculation or 60 min ischemia the enzyme generally displayed enhanced responses to GTP, norepinephrine (NE), dopamine (DA), NE + GTP and DA + GTP. Pretreatment of the gerbils with methylprednisolone, allopurinol or indomethacin did not significantly influence the outcome of these findings. When the animals were subjected to 60 min ischemia plus 15 min of reflow, enzyme responses to the stimulatory agents including forskolin and NaF were all reduced. Pretreatment with methylprednisolone, allopurinol or indomethacin prevented the damage to adenylate cyclase in the 60 min ischemia plus 15 min reflow animals. When animals were made ischemic for 15 min followed by one week of recovery, enzyme sensitivity to GTP, calmodulin-Ca++, NE, combinations thereof and forskolin were reduced in only the particulate fractions. Enzyme damage was reversed following methylprednisolone. Enzyme damage may result from generation of free radicals during reflow and drugs that either inhibit synthesis pathways generating free radicals, stabilize cell membranes or act as free radical scavengers may be therapeutically beneficial under specific conditions of stroke.
Stroke
PMID:Protective action by methylprednisolone, allopurinol and indomethacin against stroke-induced damage to adenylate cyclase in gerbil cerebral cortex. 670 40

It is shown that the amount of ATP in rats under hypothermia up to heat stroke lowers and that of ADP and AMP somewhat rises. Ionol administration normalizes the ATP level and increases the ADP and AMP contents. Inhalation of CO2 and especially administration of ionol contribute to a higher resistance of the animals to hyperthermia.
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PMID:[Influence of hyperthermia and protective effect of ionol and carbon dioxide gas on ATP, ADP and AMP content of the rat brain]. 678 22

The metabolic effects of intraperitoneal administration of promethazine on normoxic, hypoxemic and hypoxemic-oligemic rat brain were assessed by measurement of the cerebral contents of energy phosphates, and selected glycolytic-citric acid cycle intermediates. In normoxic brain promethazine (25-100 mg/kg-1) was associated with unaltered adenylates, increased glucose and aspartate and decreased pyruvate, lactate and malate; a pattern which was compatible with cerebral metabolic depression. Hypoxemic animals receiving either saline or promethazine (25 mg/kg-1) showed equivalent decreases in ATP and increases in lactate which indicated that promethazine had no significant effect on the metabolism of the acutely hypoxic brain. In animals exposed to hypoxemia plus right carotid artery occlusion (oligemia) the promethazine treated group (25 mg/kg-1) showed significantly lower ATP and higher AMP contents which suggested an adverse effect on the metabolism of the acutely hypoxic-oligemic brain. It is concluded that promethazine does not beneficially alter the energy metabolism of the acutely hypoxic or hypoxic-oligemic brain.
Stroke
PMID:Effects of promethazine on the energy metabolism of normoxic and hypoxic rat brain. 710 46

Thirteen patients with stroke and one with TIA had repeated examinations with computed tomography (CT) of the head, examination of the cerebrospinal fluid (CSF) for adenylate kinase, glutathione, lactate, and albumin and clinical evaluations during the first fortnight after onset. In 9 patients with cerebral infarction edema shown on the CT scans was maximal on days 2--5, after which it diminished. In 2 patients with intracerebral hemorrhage the edema appeared early as a zone of low-attenuation around the high-attenuation area. Most patients with large lesions deteriorated clinically during development of the edema. In 3 patients the CT scans were inconclusive, probably because the lesion was too small. Adenylate kinase activity was present in all CSF samples during the period 6 hours-5 days, while glutathione was occasionally present in the CSF in 12 of the 14 patients. These findings are believed to indicate cell swelling and a leak in the plasma membrane. Based on these observations, it is suggested that initial ischemic edema is intracellular in patients with cerebral infarction, and that adenylate kinase in CSF is a sensitive marker for this type of edema.
Stroke
PMID:Ischemic edema in stroke. A parallel study with computed tomography and cerebrospinal fluid markers of disturbed brain cell metabolism. 722 57


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