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Biomedical subjects

R Busto

Publications and source records attributed to R Busto.

At least 199 records · Page 11Linked to original sources
PubMed1980

The dissociation of cerebral blood flow, metabolism, and function in the early stages of developing cerebral infarction.

Temporal and site correlation of local cerebral blood flow (1-CBF), tissue redox state, energy metabolism, tissue pH, and cerebral electrophysiological activity in induced cerebral ischemia was performed in rats in an effort to obtain helpful clues for the management of occlusive cerebrovascular disease. CBF decreased acutely in both the embolized and nonembolized hemispheres but returned toward normal in 5 minutes. However, total cerebral oxidative metabolism remained depressed throughout the 30-minute observation period despite improved perfusion. The change in CBF correlated with the development and resolution of tissue acidosis, which was maximal 3 minutes after embolization but became alkaline after 30 minutes, possibly due to accumulation of sodium lactate. Oxidized form of nicotinamide-adenine dinucleotide and cytochrome a,a3 quickly became reduced in the ischemic core, but a tardyspontaneous postischemic tissue perfusion resulted in their hyperoxidation. The CBF-metabolism uncoupling as well as postischemic hyperoxidation of the electron transport system, which is associated with accumulation of pyruvate and lactate, probably resulted from stagnation of electron flow at the entrance to the mitochondrial respiratory processes. Seizures could not account for these results, as paroxysmal changes in the EEG usually appeared only in the nonembolized hemisphere and were not dependent upon lack of energy. These studies confirm that metabolic failure may persist in ischemic tissue despite adequate reperfusion, which may, in fact, contribute to tissue damage through hyperoxidation.

Adenosine Triphosphate↗
PubMed1978

The sequential uptake of (14C) deoxyglucose in brain after embolic stroke.

An i.v. bolus of (14C) deoxyglucose was injected into 4 groups of rats which simultaneously were embolized through the internal carotid artery. 15 and 30 min post embolization there was a massive decrease in (14C) deoxyglucose uptake in both deep and cortical structures. At 4 h a small zone of increased (14C) deoxyglucose uptake persisted around each embolized microsphere.

Animals↗
PubMed1977

Sequential cerebral biochemical and physiological events in controlled hypoxemia.

Effects of controlled hypoxemia on cerebral functional activity were studied in rats using cyclic adenosine monophosphate (cAMP) and aminergic neurotransmitters in the brain tissue as special references. Evidence is presented that: (1) mild hypoxemic stress (PaO2 60 to 40 torr) may activate cerebral glycolysis with no evidence of anaerobic metabolism but that further reduction of PaO2 impairs cellular respiration, as evidenced by accumulation of glycolytic products; (2) glycogenolysis in the brain tissue, leakage of potassium ions from the brain cell, increase in brain water, and suppression of neural functional activity occur concomitant with accumulation of cAMP and prior to the fall of adenosine triphosphate; (3) the diminution of cerebral high-energy phosphates during hypoxia is associated with and may be caused by hypoxemia-induced neuroglycopenia and occurs at PaO2 15 torr; (4) induced hypoxemia per se does not affect the level or aminergic neurotransmitter substances in brain tissue.

Adenosine Diphosphate↗
PubMed1977

Pulsus paradoxus in childhood asthma--its prognostic value.

One hundred asthmatic children were examined for pulsus paradoxus, a palpable diminution or obliteration of the peripheral pulse during inspiration, while in bronchospasm. Pulsus was measured with a sphygmomanometer and the difference in systolic pressure between inspiration and expiration was noted. Seventy-five children with mild asthma had no palpable pulsus and responded with complete subsidence of symptoms with one or two injections of aqueous epinephrine, 1-1000. Twenty-five children had palpable pulsus ranging from 10 mm to 30 mm. Five patients with pulsus between 10 and 15 mm were admitted to the hospital with status asthmaticus and pneumonia; eight other patients responded to parenteral epinephrine. Twelve children had pulsus of 20 mm or greater and all were hospitalized for uncomplicated status asthmaticus. Pulsus paradoxus may be found in acute exacerbation of childhood asthma and its degree correlates with both the severity and response to bronchodilating agents.

Adolescent↗
PubMed1976

Brain energy metabolism during the process of dying and after cardiopulmonary resuscitation.

In order to study the problem of how fast and to what degree severe hypoxic brain tissue changes are reversed after reoxygenation, we challenged the viability of the brain by exposing experimental animals to anoxia of such a duration that cardiopulmonary resuscitation was just possible. The brain tissue concentrations of glucose, lactate, pyruvate and of ATP, ADP, AMP and phosphocreatine were determined. Two series of experiments were carried out. In the first, groups of rats deprived of oxygen for 1, 2, 4 and 6 min were studied in order to show brain tissue changes in the period of impending death as well as the changes coinciding with the onset of clinical death (blood pressure zero). In addition, one group maintained at a rectal temperature of 37 +/- 0.5 degrees C and ventilated for 60 min with an oxygen free gas mixture was included aimed at representing a state of irreversibility. In the second series, restitution after 6 min of no oxygen supply was studied 10 min, 1/2 h, 1 h, and 2 h after cardiopulmonary resuscitation. Attempts were also made to correlate biochemical changes to EEG status and to clinical recovery. The restitution study showed that oxidative phosphorylation of the brain tissue was rapidly resumed with normalization of the adenylate energy charge in all animals in which the pump function of the heart could be restored by our artificial means. However, there was a strikingly poor correlation between recovery of mitochondrial function and restitution of EEG or clinical recovery. Thus, it seems likely that a delayed functional restitution is not due to energy failure but to other biochemical changes or to biophysical alterations not revealed by the present type of study.

Adenosine↗
PubMed1975

Catecholamines in experimental brain ischemia.

Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls. There was an instantaneous increase of cAMP. Norepinephrine was reduced within two minutes after embolization and remained low for four hours. Dopamine increased by five minutes after embolization and returned to normal after four hours. Results were qualitatively similar, but less, in the nonembolized hemisphere. Accumulation of cAMP is thought to be due to a direct effect of ischemic hypoxia and may be the initiating factor in increased glycolysis that occurs in ischemia. Decrease in NE may be secondary to its generalized release from presynaptic terminals throughout the brain and could be a factor in cortical vasocontriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.

Animals↗
PubMed1975

Effects of hypothermia and hyperthermia on brain energy metabolism.

The influence of elevated and reduced body temperatures upon the metabolic state of the brain was evaluated from the tissue concentrations of phosphocreatine (PCr) ATP, ADP and AMP and from the concentrations of glucose, lactate and pyruvate in immobilized and artificially ventilated rats anesthetized with 70% N2O. The results were compared to the results obtained in normothermic animals. It was found that rats with body temperatures of 32 degrees and 22 degrees C had the same brain tissue concentrations of high energy phosphates and the same adenylate energy charge as the controls, but hypothermia led to a progressive decrease of both cerebral and arterial lactate and pyruvate concentrations. A metabolic acidosis but no excess lactate appeared in the blood. At a body temperature of 42 degrees C, the metabolic pattern in the brain agreed with a state of hypoxia at a time when there was no sign of substrate depletion. Arterial blood showed excess lactate which may indicate an inadequacy of the oxygen supply also to other tissues.

Adenosine Diphosphate↗
PubMed1975

Effect of hyperventilation on dynamics of cerebral energy metabolism.

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA. Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.

Adenosine Triphosphate↗
PubMed1975

Effects of high-dose cyanate upon cerebral energy metabolism of the rat.

The effect of sodium cyanate (25, 50, 75, and 100 mg/kg body weight i.p. daily for 10 days) upon cerebral metabolism and the EEG of Wistar rats was studied. This treatment resulted in a dose-related carbamylation of hemoglobin and left shift in the oxygen dissociation curve. Animals receiving the highest dose of cyanate developed a significant systemic metabolic acidosis. In brain there was dose-dependent decrease in phosphocreatine, TCO2 and cytoplasmic NADH/NAD+ ratio, reflecting the calculated drop in intracellular pH. Glucose levels were elevated despite a normal calculated energy charge, which suggests a balanced slowing of the energy-producing and energy-utilizing systems. The higher doses of cyanate produced spontaneous seizure activity on the EEG.

Animals↗