PubMed Health⌕ Search

Biomedical subjects

J R Harp

Publications and source records attributed to J R Harp.

8 recordsLinked to original sources
PubMed1979

Cerebral energy levels during trimethaphan-induced hypotension in the rat: effects of light versus deep halothane anesthesia.

Hypotension may be expected to produce less perturbation of metabolism in the brain when cerebral metabolic rate is lowered by deep anesthesia. Male Wistar rats having unilateral carotidartery ligation were exposed to mean arterial pressure (MAP) of 40 torr for 22 min by an intravenous infusion of trimethaphan during anesthesia with halothane, 0.6 or 2 per cent, in oxygen. Cortical tissue metabolite levels on the side of the ligated carotid artery were more abnormal in rats receiving halothane, 0.6 per cent, than in those receiving halothane, 2 per cent. Values at halothane, 0.6 per cent, were adenosine triphosphate (ATP), 1.71 +/- 0.05 (+/-SEM) mumol/g, phosphocreatine (PCr) 1.97 +/- 0.07 mumol/g. and lactate 16.5 +/- 5.1 mumol/g; corresponding values at halothane, 2 per cent, were ATP 2.27 +/- 0.02, PCr 4.02 +/- 0.23, and lactate 4.75 +/- 0.9 mumol/g. ATP and PCr values were significiantly lower (P less than 0.05) and the lactate value was significantly higher with halothane, 0.6 per cent, than with halothane 2 per cent. Cerebral oxygen consumption decreased 47 per cent in rats anesthetized with halothane, 2 per cent. Preservation of cortical metabolite levels in deeply anesthetized animals suggests a protective effect of cerebral metabolic depression.

Adenosine Triphosphate↗
PubMed1979

Additive effects of hypothermia and phenobarbitol upon cerebral oxygen consumption in the rat.

The quantitative effects of a combination of hypothermia and phenobarbital on cerebral oxygen uptake (CMRo2) was studied in rats, curarized and artificially ventilated with 70% nitrous oxide in oxygen. Cerebral blood flow (CBF) was measured with a modification of the KETY & SCHMIDT (1948) technique, using 133xenon as a tracer. Arteriovenous difference in oxygen content over the brain was measured and CMRo2 was calculated. Four groups were studied. Group 1 was a control group. The three experimental groups were injected with phenobarbital intraperitoneally: Group 2 with 50 mg/kg body weight; Group 3 with 150 mg/kg; and Group 4 with 50 mg/kg of phenobarbital, and, in addition, body temperature was lowered to 32 degrees C in this group. CMRo2 in groups 2, 3 and 4 was reduced by 22, 37 and 43%, respectively, compared to Group 1. The changes in CBF were of the same magnitude. In a previous study we have found that CMRo2 decreases by 5% per 1 degree C decrease in body temperature. The value for CMRo2 in Group 4 is close to the value obtained if the effect of 50 mg/kg body weight of phenobarbital on CMRo2 is added to the effect of a temperature reduction of 5 degrees C. It is concluded that the effects of barbiturates and hypothermia on CMRo2 are additive.

Animals↗
PubMed1976

The effect of halothane anaesthesia upon cerebral oxygen consumption in the rat.

The influence of halothane (0.6 and 2%) upon cerebral (cortical) blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) was studied in artificially ventilated rats, using a modified technique of Kety & Schmidt (1948). The values obtained in halothane anaesthesia were compared to those recorded in nitrous oxide anaesthesia, or to those measured in unanesthetized animals given an analgesic drug (fentanyl citrate). Although it could be confirmed that halothane induces vasodilatation in the brain, there were relatively small differences in CBF between the groups. The results demonstrate that, in the rat, halothane depresses CMRo2 in a dose-dependent way. With 0.6% halothane, CMRo2 was reduced by 20-30% and, with 2% halothane, CMRo2 was reduced by about 50%. Thus, in the rat the effect of 2% halothane upon metabolic rate is comparable to that observed in barbiturate anaesthesia.

Anesthesia, Inhalation↗
PubMed1975

Influence of changes in arterial PCO2 on cerebral blood flow and cerebral energy state during hypothermia in the rat.

In order to study the relationship between arterial PCO2 and cerebral blood flow (CBF) in hypothermia, the body temperature of artifically ventilated rats was decreased to 22 degreesC, and changes in CBF were evaluated from arteriovenous differences in oxygen content (AVDO2) at PaCO2 values of 15, 30, 40 and 60 mm Hg. The results were compared to those obtained at normal body temperature (37 degrees C) over the PaCO2 range 15-60 mm Hg. Separate experiments were performed to evaluate CBF and CMRO2 at 22 degrees C and a PaCO2 of 15 mm Hg, using an inert gas technique for CBF. The tissue contents of phosphocreatine, ATP, ADP, AMP and lactate were measured in hypothermic animals at PaCO2 values of 15, 30 and 60 mm Hg. The results showed that changes in CBF were of the same relative magnitude in hypothermia and normothermia when PaCO2 was increased from about 35 to about 60 mm Hg. However, with a decrease in PaCO2 the reduction in CBF was much more pronounced in hypothermia, and at PaCO2 15 Mm Hg CBF was less then 20% of the value measured in normothermic and normocapnic animals. The results of the metabolite measurements gave no evidence of tissue hypoxia in spite of the pronounced reduction in CBF. Although the results demonstrate that the brain of a hypothermic animal is protected against the harmful effects of a lowered CBF, it may not warrant recommending hyperventilation in clinical cases of hypothermia, especially not in patients with arteriosclerosis or cerebrovascular diseases.

Adenosine Diphosphate↗
PubMed1975

Metabolic changes in the cerebral cortex of the rat induced by intravenous pentothalsodium.

The effects of thiopental on cerebral metabolism were evaluated by means of measurements of cerebral metabolic rate for oxygen (CMRO2) and of tissue levels of organic phosphates, glycolytic substrates, citric acid cycle intermediated and selected amino acids. Shortly after the beginning of thiopental administration, CMRO2 was reduced to half the normal value, and there were signs of retardation of glycolytic flux at the phosphofructokinase step. Inhibition at this regulatory enzymatic step could be related to an increase in phosphocreatine and a fall in inorganic phosphate concentration. The rise in phosphocreatine, and the unchanged levels of ATP, ADP and AMP demonstrate that induction of anaesthesia with thiopental is unrelated to energy failure. Changes in citric acid intermediated included a fall in malate, and probably also in citrate, alpha-ketoglutarate and fumarate, with a tendency towards reduction in the pool of citric acid cycle intermediates; and the amino acid changes were dominated by a progressive rise in aspartate. It is suggested that these changes are secondary to a reduced rate of pyruvate delivery, and to a decrease in malate/oxaloacetate ratio.

Adenosine Diphosphate↗
PubMedDate not supplied

Cerebral energy metabolite levels and survival following exposure to low inspired oxygen concentration.

To determine the relationship between brain energy metabolites and neurologic status after ischemia-hypoxia, we measured cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine, and lactate. Rats with permanent unilateral carotid occlusion were exposed to 5, 10, and 15 min of hypoxic atmosphere (FIO2 0.048) and, to examine metabolic restitution, 60 min after recovery in rats exposed to the same hypoxic mixture for 15 min. At 5 and 10 min of hypoxia, there were significant reductions in phosphocreatinine and elevations in tissue lactate, but only after 15 min of hypoxia, did ATP levels significantly decrease. By 60 min after recovery, phosphocreatinine values returned to the normal range, ATP values to 15% less than normal, and tissue lactate toward normal. In parallel survival studies, neurological status was examined following hypoxic exposure (PaO2 18 to 19 torr) for 5 an 10 min. Evidence for neurological injury in the form of posthypoxic seizures occurred at a point in time preceding significant changes in brain tissue ATP level. Since injury occurs prior to ATP reduction, changes in brain tissue ATP level may not be an appropirate endpoint for determining brain tissue injury in hypoxia.

Adenosine Triphosphate↗