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Biomedical subjects

R F Albrecht

Publications and source records attributed to R F Albrecht.

At least 109 records · Page 6Linked to original sources
PubMed1982

Cerebral blood flow and metabolism following ketamine administration.

The effects of ketamine on cerebral blood flow (CBF), cerebral metabolic rate (CMRO2) and intracranial pressure (ICP) were evaluated in ventilated or spontaneously breathing goats after peripheral administration of 5 mg . kg-1 and central administration of 0.1-2.0 mg. In mechanically ventilated normocarbic goats intravenous ketamine 5 mg . kg-1 had no effect on CBF, but did produce a significant reduction in CMRO2 (4.3 +/- 0.4 vs 3.7 +/- 0.3 ml O2 . min-1/100 g) five minutes after injection. However, in spontaneously breathing goats, ketamine caused a significant increase in CBF (77 +/- 7 vs 109 +/- 12 ml . min-1/100 g), a significant reduction in CMRO2 (4.3 +/- 0.3 vs 3.8 +/- 0.4) and an increase of PCO2 from 4.5 +/- 0.5 to 5.4 +/- 0.9 kPa (34 +/- 4 to 41 +/- 7 torr). Small doses of ketamine (0.1-2.0 mg) injected directly into the cerebral circulation failed to cause any significant change in CBF. Intracranial pressure showed a significant increase from 13 +/- 3 to 19 +/- 3 mm Hg in spontaneously breathing goats and no change in ventilated goats. These data suggest that ketamine is a mild depressant of cerebral metabolic rate and has no other cerebral vascular effects.

Anesthesia↗
PubMed1982

Effects of prostaglandins on the cerebral circulation in the coat.

The role of prostaglandins in producing cerebrovasodilation during hypercapnia was tested in goats. Cerebral blood flow (CBF) changes with increasing arterial PCO2 were measured before and after prostaglandin synthesis inhibition with indomethacin or ibuprofen. Both drugs produced significant decreases in CBF under control anesthetized conditions but had no significant effect on the cerebrovascular response to increased arterial PCO2. The effects of direct intracerebrovascular infusion of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha) and prostacyclin were also measured. In the dose range tested (0.1-1) microgram/min) PGF2 alpha had no significantly greater than that produced by PGE2. The effectiveness of each compound in producing cerebrovascular changes is consistent with the endogenous distribution of prostaglandins within the brain. These results suggest that prostaglandins, particularly PGI2, may be important in modulating cerebrovascular tone but have no role in increasing CBF during hypercapnia.

Animals↗
PubMed1982

Maintenance of cerebral blood flow and metabolism during pharmacological hypotension in aged hypertensive rats.

Cerebral blood flow (CBF) and cerebral oxygen metabolism (CMRO2) were measured in aged (24 month) spontaneously hypertensive rats (SHR) during sodium nitroprusside (SNP) and nitroglycerin induced hypotension. Both CBF and CMRO2 were decreased in SHR during hypotension induced with SNP. Significant decrements in CMRO2 were observed in aged SHR during even moderate hypotension (80-90 torr). Cerebral autoregulatory responses during nitroglycerin infusion in aged SHR were similar to SNP treated WKY and CMRO2 was maintained at control levels under all hypotensive test conditions. These results indicate that aged SHR are susceptible to cerebral ischemia during SNP induced hypotension, probably due to the combined effects of aging and hypertension on the cerebral vasculature. NTG moderated the decreases in CBF and CMRO2 seen during hypotensive challenges and may decrease the risk of stroke during hypotensive anesthesia.

Animals↗
PubMed1982

Cerebrovascular and cerebral metabolic responses of aged rats to changes in arterial PCO2.

Cerebrovascular and cerebral metabolic responses to changes in arterial PCO2 were tested in young (4 month) and aged (24 month) Sprague-Dawley rats. Rats were anesthetized with 70% nitrous oxide and 30% oxygen, paralyzed with tubocurare and artificially ventilated. Cerebral blood flow (CBF) was measured with radioactive microspheres and cerebral oxygen metabolism (CMRO2) was analyzed from arterial and sagittal sinus oxygen content differences. CBF increased in both young and aged rats with increasing arterial PCO2. Aged rats had significantly depressed cerebrovascular reactivity to changes in CO2 compared to young rats (p less than 0.05). CMRO2 was not significantly different between young and aged rats and did not significantly change with changes in arterial PCO2.

Aging↗
PubMed1982

Blood flow to oral tissues: and experimental study with enflurane, sodium nitroprusside, and nitroglycerin.

Hypotensive anesthesia is currently being used in oral and maxillofacial surgery to reduce blood loss and provide a relatively bloodless surgical field. Radioactively labeled microspheres were used to determine and compare the hemodynamic effects of sodium nitroprusside (SNP), nitroglycerin (NTG), and deep enflurane anesthesia on oral tissues during controlled hypotension when compared with controls. Sodium nitroprusside and NTG produced significant reductions in blood flow to the maxilla, mandible, and tongue, while deep enflurane anesthesia did not. In the masseter and suprahyoid muscles, increases in tissue blood flow were found with SNP and enflurane. Nitroglycerin produced no significant change in blood flow in the masseter and the suprahyoid. These results demonstrate that in spite of a similar cardiac index with all agents tested, local oral blood flow varied significantly with the different agents tested. These differences in tissue blood flow suggest that SNP and NTG may be preferable to deep enflurane anesthesia for maxillary osteotomies to achieve greater flow reduction and diminish blood loss.

Anesthesia, Inhalation↗
PubMed1982

Cerebrovascular and metabolic effects of SNP-induced hypotension in young and aged hypertensive rats.

Cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) were measured in young (4 months) and aged (24-26 month) spontaneously hypertensive (SHR) rats and Wistar Kyoto (WKY) controls under control anesthetized conditions (70 per cent N2O, 30 per cent O2) and during hypotension induced with intravenous sodium nitroprusside (SNP) infusions. CBF was measured with radioactive microspheres and cerebral arterial-venous blood O2 measurements were determined from arterial and sagittal sinus blood samples. Arterial blood PCO2 was maintained at approximately 35 mmHg and body temperature at 37 degrees C. Under control conditions blood pressure was increased in SHR but there was no significant difference in CBF or CMRO2 between SHR and WKY or young and aged rats. CBF and CMRO2 were maintained in WKY when mean blood pressure was decreased to 65 mmHG with SNP infusion. CBF was significantly decreased in young and aged hypertensive rats during SNP-induced hypotension. CMRO2 was also decreased in both young and aged hypertensive animals. These results support previous reports that SNP-induced hypotension will maintain CBF and CMRO2 in normotensive subjects, but suggest that the direct cerebrovasodilating effects of SNP are moderate and will not reverse the cerebrovascular changes induced by chronic hypertension.

Aging↗
PubMed1982

Cardiovascular and regional blood flow changes during halothane anesthesia in the aged rat.

The authors investigated the cardiovascular and regional hemodynamic changes that occur in the aged rat under unanesthetized control conditions and during the induction of halothane anesthesia. Regional blood flow changes were measured in young (4-month-old) and aged (27-29-month-old) F-344 rats using radioactive microspheres under unanesthetized conditions and during three levels of halothane anesthesia. Blood halothane levels were measured at each anesthetic level. The inspired concentrations of halothane were adjusted in young vs. aged rats so that each group was tested at the same depth of anesthesia. Results indicate that aged rats had significantly lower blood pressures than young rats in an unanesthetized state and at all levels of halothane anesthesia. Tissue blood flow was similar between young and aged rats in skeletal muscle and skin, while blood flow to renal and small intestinal tissues was consistently higher in young rats. Heart blood flow was initially 100 per cent higher in young rats but decreased to similar levels as aged at the highest levels of halothane anesthesia used. Cerebral blood flow was similar initially in young vs. aged, but increased in young rats with deeper levels of halothane anesthesia while decreasing in aged rats. These results indicate significant regional hemodynamic differences in young compared to aged rats under unanesthetized conditions as well as in response to halothane anesthesia.

Aging↗
PubMed1981

The influence of aging and hypertension on cerebral autoregulation.

Cerebral autoregulation was tested here in 3- and 18-month-old spontaneously hypertensive rats (SHR) and Wistar Kyoto controls (WKY). Cerebral blood flow (CBF) was measured in each rat using radioactive micropheres under unanesthetized control conditions and after hypotension induced by ganglionic blockade. Under control conditions there was no significant difference in CBF between SHR and WKY. During drug induced hypotension CBF decreased significantly in all except 3 month WKY. CBF was decreased significantly more in 18 month SHR after ganglionic blockade compared to other test groups. These results indicate an influence of both age and hypertension in altering the ability of the cerebrovasculature to autoregulate.

Aging↗
PubMed1981

Central cardiovascular activity of prostaglandin E2, prostaglandin F2 alpha and prostacyclin.

Prostacyclin (PGI2), prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) were tested here in unanesthetized male Sprague-Dawley rats for their effects on the cardiovascular system as mediated by the central nervous system. Cannulae were chronically implanted into the third cerebral ventricle, femoral arteries and femoral veins of rats. Both PGE2 and PGF2 alpha induced increased arterial blood pressure and tachycardia by an action on the central nervous system. The changes seen with PGE2 were larger than those observed with PGF2 alpha. Only transient depressor effects were seen with PGI2 and these changes appeared to be due to the leakage of the substance into the peripheral vascular system.

Animals↗
PubMed1979

Clinical biochemistry of epilepsy. I. Nature of the disease and a review of the chemical findings in epilepsy.

In idiopathic or generalized epilepsy, serum glucose and cholesterol concentrations tend to be low, especially just before the seizure. Glucose tolerance curves are abnormal and variable. The electrolyte balance is disturbed, and epileptics tend to go readily into alkalosis. Serum [Na+] is usually unaffected, but [K+] is normal to low between attacks and increases during and after the seizure. Serum [Cl-] is usually high just before the seizure. Epileptics are generally mildly hypocalcemic, especially in the period before the seizure. Serum urea and nonprotein nitrogen values are low between paroxysms but increase after the seizure. Serum protein concentration is usually normal. Stress, which releases epinephrine and corticotropin, results in high serum citrate concentration, which probably contributes to decreased serum [Ca2+] just before a seizure. In the healthy individual, any increase in serum citrate is accompanied by increasing [Ca2+]. In the rabbit, convulsions can be induced with corticotropin, a result of increased serum citrate concentration coupled with a decrease in [Ca2+]. The net result is severe hypo-ionic-calcemia. A similar phenomenon has been reported in a few humans. Administration of insulin causes serum citrate concentrations to decrease. Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic.

Adrenocorticotropic Hormone↗
PubMed1979

Clinical biochemistry of epilepsy. II. Observations on two types of epileptiform convulsions induced in rabbits with corticotropin.

We propose than an alarm mechanism is operative in animals, designed to regulate neuromuscular irritability by regulating [Ca2+]. Epinephrine or corticotropin (ACTH), injected intramuscularly into animals, causes a hypercitricemia, resulting in decreased [Ca2+]. This increases muscular excitability to facilitate escape. To avoid over reaction, [Cl-] is shifted into the plasma without a concomitant shift of Na+, thus generating an acidosis and an increase in ionization of Ca. Plasma pH, pCO2, total CO2, and [K+] decrease, and [Mg2+] increases. The acidosis, decrease in K+, and increase in [Mg2+] serve to counteract the effect of the decrease in [Ca2+], to protect against tetany. In the rabbit the hypercitricemia observed upon ACTH administration is accompained by a severe hypocalcemia and drop in blood pressure, resluting in tetanic convulsions. This seems to indicate calcitonin release, independent of the hypercitricemia. Thyroidectomized rabbits show only mild hypocalcemia when given ACTH, but develop a severe acidosis and typical grand mal epileptiform seizures. Administration of ACTH and then calcitonin to the goat, an animal resistant to the effects of ACTH alone, simulates the effect observed in the rabbit with respect to changes in blood components and blood pressure. Changes in the blood in the goat and rabbit resemble those in humans before an epileptic seizure. alpha-Melanotropin, containing a portion of the ACTH sequence, reacts in a manner similar to ACTH but more rapidly.

Adrenocorticotropic Hormone↗
PubMed1978

Responses to fasting and lipid infusion of epinephrine-induced arrhythmias during halothane anesthesia.

Sensitivities to epinephrine in fasted and non-fasted rats anesthetized with halothane or pentobarbital were determined. The arrhythmic threshold for epinephrine, i.e., the dose which upon injection produced four or more premature ventricular contractions, was significantly lower for 12-hour (5.5 +/- 3.2 microgram/kg), 24-hour (2.2 +/- 1.3 microgram/kg) and 48-hour (2.25 +/- 0.6 microgram/kg) fasted rats than for non-fasted rats (10.9 +/- 3.4 microgram/kg) at the same dose of halothane (2.0 per cent). Fasting had no effect on the arrhythmic threshold for epinephrine in rats anesthetized with pentobarbital (35 mg/kg). Infusion of a 10 per cent fatty acid emulsion caused a significant lowering of the arrhythmic threshold for epinephrine of fed rats, while infusion of acetoacetic acid had no effect on the arrhythmic threshold. It is concluded that the combination of fasting and halothane anesthesia renders the heart more sensitive to epinephrine than halothane anesthesia alone.

Anesthesia, General↗