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Biomedical subjects

J J Olin

Publications and source records attributed to J J Olin.

9 recordsLinked to original sources
PubMed2001

Cognitive function after systemic therapy for breast cancer.

An underinvestigated area of breast cancer survivorship involves the possible impairment of cognitive function following adjuvant chemohormonal therapy. Numerous reports of disturbing and disruptive changes in short- and long-term memory, attention span, concentration, and language skills have been made by breast cancer patients who have received chemotherapy. This article reviews the four published studies that have documented cognitive dysfunction following adjuvant chemohormonal therapies commonly used in breast cancer. The studies describe a subset of approximately one-third of participants who experienced long-term cognitive impairment. Patient- and treatment-related factors that may influence cognitive function are outlined. The impact of these cognitive impairments on the individual breast cancer survivor's quality of life is discussed, as is the potential overall impact of this research on future adjuvant therapy. The need for a prospective longitudinal study documenting the neuropsychological sequelae of adjuvant chemohormonal therapy is emphasized.

Adult↗
PubMed2000

New strategies for managing metastatic breast cancer.

In 1999, metastatic breast cancer claimed the lives of almost 45,000 women. For the vast majority of patients, metastatic breast cancer is an incurable disease with a median survival of only 2 to 3 years after diagnosis. The major goal of therapy is palliation. New endocrine agents developed during the last several years provide a greater opportunity for response in receptor-positive patients. New chemotherapeutic options have led to the reemergence of single-agent therapy as an effective palliative approach. Clinical trials remain the mainstay of cutting-edge therapy for metastatic breast cancer and should always be considered, if available. This review will focus on major issues in the treatment of metastatic breast cancer, including new endocrine and chemotherapeutic agents and a suggested strategy for patient management.

Antibiotics, Antineoplastic↗
PubMed1985

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension.

Profound arterial hypotension is a commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Adenosine↗
PubMed1984

Adenosine triphosphate-induced arterial hypotension in the dog.

This study was designed to investigate the potential use of adenosine triphosphate (ATP), a naturally occurring vasodilator, for producing profound intraoperative hypotension. Six mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, paralyzed with pancuronium, and ventilated to a PaCO2 of 40. The mean arterial pressure was lowered to 40 mm Hg with an intravenous infusion of ATP (10.6 +/- 3.5 (SE) mg/kg/minute). Blood flow was determined using the radioactive microsphere technique. Measurements were made before and 20, 40, and 60 minutes after the induction of hypotension and after a 40-minute recovery. Infusion of ATP to lower the mean arterial pressure to 40 mm Hg resulted in a reduction of mean arterial pressure of 64% and an increase in heart rate of 11% accompanied by frequent cardiac arrhythmias. However, cardiac output decreased only 8%. Myocardial flow increased 137%, kidney flow decreased 71%, and masseter muscle flow increased 333%. A severe metabolic acidosis developed with a reduction in pH from control values of 7.39 +/- 0.03 to 7.16 +/- 0.03 after 60 minutes of hypotension. The cerebral metabolic rate of oxygen, determined using the oxygen content of the sagittal sinus, was not affected. Cerebral hemisphere blood flow decreased 21%, caudate nucleus flow decreased 31%, and corpus callosum flow decreased 43%. Blood flow to the brain stem and cerebellum was unchanged. Hypotension was readily induced, maintained, and reversed using ATP, without apparent tachyphylaxis. However, the profound metabolic acidosis and cardiac arrhythmias that occurred may be serious contraindications to the use of this agent clinically.

Acid-Base Equilibrium↗
PubMed1984

Systemic and cerebral effects of prostacyclin-induced arterial hypotension in the dog.

Prostacyclin has strong vasodilating and antiplatelet properties. This study was performed to investigate its potential for producing profound intraoperative hypotension. Five dogs were anesthetized with morphine, nitrous oxide, and oxygen, paralyzed with pancuronium, and ventilated to a PaCO2 of 40 torr. Mean arterial blood pressure (MABP) was lowered to 40 mm Hg with an intravenous infusion of prostacyclin in 0.05 M Tris buffer (average rate of infusion 3 +/- 1 micrograms/kg/min). Blood flow was determined using the radioactive microsphere technique. Measurements were made before and after 20, 40, and 60 minutes of hypotension; and after a 40-minute recovery period. Infusion of prostacyclin reduced MABP 63% while increasing heart rate 51%. Tachyarrhythmias occurred in all dogs, and cardiac index decreased 18%. Myocardial blood flow decreased an average of 29%, cerebral blood flow decreased 30%, cerebellar blood flow decreased 18%, and blood flow in the brain stem and spinal cord was unchanged. Cerebral metabolic rate of oxygen, determined by measuring the oxygen content of the sagittal sinus, was unchanged. Hypotension was easily induced and maintained using prostacyclin, without apparent tachyphylaxis. However, the cardiac changes caused by this drug are more severe than those accompanying hypotension induced by most other agents, and may represent a serious contraindication to its clinical use.

Animals↗
PubMed1983

Effect of dimethyl sulfoxide on the cerebral and systemic circulations of the dog.

Dimethyl sulfoxide (DMSO) has a variety of properties suggesting that it may be a useful agent in the management of central nervous system trauma and stroke. The purpose of this investigation was to determine the systemic and cerebrovascular effects of varying doses of DMSO in a normal animal. Five mongrel dogs were subjected to a constant infusion of 100% DMSO at a rate of 4 g/kg/hour. Using the radioactive microsphere technique, we measured blood flow before giving DMSO and after 2, 4, 6, and 8 g of DMSO per kg had been infused. After 2 g/kg had been given, hemolysis was evident and the intravascular volume increased, resulting in a lowered hematocrit. The cerebral metabolic rate of oxygen remained stable throughout the study. The total cerebral blood flow increased over 20% after a cumulative dose of 6 g/kg. Blood flow to the cerebellum and brain stem was unchanged, while flow to the caudate nuclei and cerebral hemispheres increased. There was a reduction in flow to the corpus callosum and spinal cord. DMSO caused an increase in the cardiac index accompanied by a large increase in the right and left ventricular blood flows, but a reduction in kidney flow. The relationship of this redistribution of blood flow, especially within the cerebrospinal axis, to the therapeutic effects of DMSO bears further investigation.

Animals↗
PubMed1983

Cerebral and systemic circulatory effects of arterial hypotension induced by adenosine.

In six dogs anesthetized with halothane and nitrous oxide, mean arterial pressure (MAP) was lowered to 40 mm Hg for an average of 90 minutes by intravenous infusion of adenosine. The hypotensive effect of the adenosine was potentiated by administering dipyridamole to block its intravascular inactivation. Blood flow to the brain, spinal cord, heart, kidneys, and skeletal muscle was measured six times in each animal using the radioactive microsphere technique. Determinations were made before, during, and 30 minutes after the hypotensive period. During the hypotensive period, MAP was decreased 61% and was related to a proportional decrease in peripheral vascular resistance. Cardiac index decreased 14%. Total cerebral blood flow (CBF) decreased an average of 28% and cerebral vascular resistance decreased 53%. The reduction in CBF was heterogeneous; the cerebral cortex and corpus callosum were most affected and the brain stem least affected. No change occurred in the cerebral metabolic rate of oxygen usage (CMRO2). Left ventricle flow increased 147% and right ventricle flow increased 271%. Blood flow to the kidneys decreased 70%, and to the liver decreased to 6% of control. Jejunum blood flow increased 138% during recovery, while stomach flow varied but showed no statistical change. There was no tachyphylaxis, rebound hypertension, or toxicity associated with the adenosine-induced hypotension. These properties suggest that adenosine may be a useful agent for inducing arterial hypotension in neurosurgical patients.

Adenosine↗
PubMedDate not supplied

The effect of intravenous dipyridamole on the cerebral and systemic circulations of the dog.

In 7 dogs anesthetized with halothane and nitrous oxide, dipyridamole was administered in a loading dose of 1 mg/kg supplemented with 0.5 mg/kg every 30 minutes. Cardiovascular parameters and organ blood flows (using the radioactive microsphere technique) were measured before and at 30 minute intervals after each administration of dipyridamole, for a total of 105 minutes. The administration of dipyridamole was associated with a 20% reduction in systemic arterial pressure, a 31% reduction in peripheral vascular resistance, and a 13% increase in cardiac index. Cerebrovascular resistance decreased 21%, but regional cerebral blood flow and metabolism were unchanged. Blood flow to the heart increased 355% in the right ventricle and 213% in the left ventricle. Blood flow to the jejunum decreased 52% while blood flow to the kidney and liver decreased slightly. The circulatory effects of dipyridamole are probably related to its interference with the inactivation of endogenous adenosine. The differential effects of dipyridamole on organ flow are similar to those seen following the IV infusion of adenosine.

Animals↗