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Biomedical subjects

D F Hanley

Publications and source records attributed to D F Hanley.

At least 109 records · Page 6Linked to original sources
PubMed1990

Cerebral cytochrome-C-oxidase copper band quantification in perfluorocarbon exchange transfused cats.

Rapid scanning near infrared spectroscopy (730-960 nm) was utilized to determine cat brain cytochrome-c-oxidase after blood-perfluorocarbon (FC-43) exchange. Spectra were carried out before, during, and after the exchange transfusion on cats with preserved somatosensory evoked potentials and microsphere determined cerebral blood flow (CBF). Carbon dioxide (8%) did not produce an increase in CBF. Difference spectra between the hypercapnic state (8% CO2-92% O2) and post mortem, demonstrated the presence of a broad absorption band centered around 820-845 nm which could be attributed to the oxidized low potential copper ion of cytochrome-c-oxidase. We were unable to further oxidize this band by adding carbon dioxide to the inspired gas mixture. This may be due to the near maximal CBF levels present in this preparation. The spectral data support the hypothesis that near infrared spectroscopy can quantify changes in the redox state of cytochrome-c-oxidase.

Animals↗
PubMed1990

Redox changes in cat brain cytochrome-c oxidase after blood-fluorocarbon exchange.

Rapid scanning near-infrared spectroscopy (730-960 nm) was utilized to determine cat brain cytochrome-c oxidase copper band by blood-perfluorochemical emulsion (Oxypherol) exchange. Spectra were carried out before, during, and after the exchange transfusion on animals with preserved somatosensory-evoked potentials and microsphere-determined cerebral blood flow. Remaining hemoglobin (less than 4% of control) was converted to carboxyhemoglobin that does not absorb in this spectral region. Difference spectra, between an hypercapnic status (8% CO2-92% O2) and postmortem, demonstrated the presence of a broad absorption band centered around 820-845 nm that could be attributed to the oxidized low potential copper ion (CuA) of cytochrome-c oxidase. However, we were unable to further oxidize this band by adding CO2 to the inspired gas mixture, but this inconsistency may be due to the near-maximal cerebral blood flow levels present in this preparation. Cytochrome oxidation by CO2 is normally attributed to increased O2 delivery to the tissue, secondary to an increased cerebral perfusion. We were unable to induce further increases in cerebral blood flow. In contrast, the cytochrome band could be reduced both by lowering fractional O2 concentration and by inducing circulatory arrest. The spectral data support the hypothesis that it is possible to quantify the cytochrome-c oxidase copper band in the near-infrared spectral region.

Animals↗
PubMed1990

Cerebrospinal fluid atrial natriuretic factor in intracranial disease.

We tested the hypothesis that the concentration of atrial natriuretic factor in the cerebrospinal fluid is an indicator of brain injury in patients with intracranial disease. Atrial natriuretic factor concentration was measured in 72 samples of cerebrospinal fluid from 28 patients with intraventricular drains and in nine samples from outpatient controls undergoing diagnostic lumbar puncture. Levels were correlated with diagnosis; systemic fluid administration; concentration of atrial natriuretic factor in the plasma; intracranial pressure; sodium, glucose, and protein concentrations, osmolality, and cell count in the cerebrospinal fluid; sodium concentration in the serum; and hemodynamics. Atrial natriuretic factor concentration was highest in cerebrospinal fluid from patients with intracerebral hematoma, followed by those with obstructive hydrocephalus and subarachnoid hemorrhage (19 +/- 2, 13 +/- 3, and 8 +/- 2 pg/ml, respectively); atrial natriuretic factor concentration was less than 4 pg/ml in the controls. Patients treated with fluid restriction had significantly higher atrial natriuretic factor levels than those receiving maintenance or high-volume fluids (16 +/- 3, 8 +/- 2, 10 +/- 1 pg/ml, respectively). The concentration of atrial natriuretic factor in the plasma was significantly elevated in patients with intracerebral hematoma and subarachnoid hemorrhage (155 +/- 38 and 92 +/- 20 pg/ml, respectively) and did not correlate with fluid administration or the concentration of atrial natriuretic factor in the cerebrospinal fluid. Neither cerebrospinal fluid nor plasma concentrations of atrial natriuretic factor correlated with intracranial pressure; cerebrospinal fluid sodium, glucose, or protein concentrations, osmolality, or cell count; serum sodium concentration; or hemodynamics. We conclude that the concentration of atrial natriuretic factor in the cerebrospinal fluid is a nonspecific indicator of brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1990

Dealing with geographic variations in the use of hospitals. The experience of the Maine Medical Assessment Foundation Orthopaedic Study Group.

Orthopaedists and other physicians in Maine organized the Maine Medical Assessment Foundation to deal with the problem of variations in the rates of hospitalization for orthopaedic conditions. Five musculoskeletal injuries and five orthopaedic procedures were selected for study. The variation in decision-making by orthopaedists was least for fractures of the ankle and fractures of the hip and was greatest for fractures of the forearm, derangement of the knee, and lumbosacral sprain. The rates in an area tended to be consistently high or low for the same treatments. The major reasons for the variations appeared to be related to lack of agreement about optimum treatment. Feedback of data to physicians on variations in patterns of practice reduced the variations.

Ankle Injuries↗
PubMed1989

Diseases that mimic herpes simplex encephalitis. Diagnosis, presentation, and outcome. NIAD Collaborative Antiviral Study Group.

A total of 432 patients underwent brain biopsy for presumptive herpes simplex encephalitis. Three patient groups were identified. The first group, 195 patients (45%), had herpes simplex encephalitis confirmed by the isolation of herpes simplex virus from brain tissue at biopsy (193 patients) or autopsy (2 patients). The second group, 95 patients (22%), had diseases that were identified but that were not caused by herpes simplex virus. Three subgroups were recognized: (1) 38 patients (9%) with treatable disease, (2) 40 patients (9%) with nontreatable but diagnosed viral infection, and (3) 17 patients (4%) with identified diseases neither of viral etiology nor treatable. The third group, 142 patients (33%), remained without a diagnosis. Clinical presentation of patients in the second group was similar to that of those with herpes simplex encephalitis and those without a diagnosis. Patients in the subgroup with nontreatable but diagnosed viral infections had the greatest likelihood of returning to normal.

Adolescent↗
PubMed1989

Sodium and water regulation in a patient with cerebral salt wasting.

Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, less than 45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.

Adult↗
PubMed1989

Localization and regulation of vasopressin mRNA in human neurons.

Vasopressin (prepropressophysin) mRNA is detected in neurons of the supraoptic, suprachiasmatic, and paraventricular nuclei of human postmortem hypothalamic specimens by quantitated in situ hybridization using 35S-labeled single-stranded cDNA probes directed against exon C of the human vasopressin gene. This hybridization displays the anticipated anatomic distribution, as well as several biochemical features supporting its specificity. Hybridization densities in supraoptic neurons, a measure of vasopressin gene expression, display substantial variability from brain-to-brain. We can attribute much of this brain-to-brain variability to differences in antemortem extracellular volume status. This conclusion is based on a) animal models of the human postmortem process, b) animal models of common agonal events, c) good correlations between antemortem volume status and neuronal vasopressin mRNA hybridization densities in human postmortem specimens matched for age and postmortem interval, and d) our inability to correlate human neuronal vasopressin mRNA hybridization densities with other clinical and postmortem features. These results provide an example of antemortem regulation of a human neuroendocrine gene using postmortem tissue.

Aged↗
PubMed1989

Determination of cerebral venous hemoglobin saturation by derivative near infrared spectroscopy.

An "in vivo" method for non-invasive determination of cerebral venous hemoglobin O2 saturation (SvO2) was developed. A specially designed spectrophotometer recorded the Td near IR spectra of transilluminated brain tissue surrounding the SS. The accuracy of the method, based on the principle of DNIRS was tested on eight pentobarbital anesthetized dogs during hypoxic hypoxia (inspired O2 6-21%). Spectral data were transformed into first derivative for correlation with SvO2 data measured from the SS. Linear regression analyses were applied using data from 5 dogs, with SvO2 ranging from 1.5%-70%, to build a 3 wavelength algorithm for predicting brain SvO2. In three dogs, this regression equation was employed to predict SvO2 in 31 separate spectra of varying HH intensity. The standard deviation of differences between SvO2 and predicted values was 3.2%. The predicted values, when regressed against the sampled SvO2, yielded an r value of 0.97. The results demonstrate that it is possible to noninvasively quantify SvO2 utilizing IR spectroscopy.

Animals↗
PubMed1989

Near infrared determined cerebral transit time and oxy- and deoxyhemoglobin relationships during hemorrhagic hypotension in the dog.

The goal of the present study was to investigate the relationships among CBF, CMRO2, MTT and tissue/superior sagittal sinus hemoglobin saturations over a wide range of CPP using a canine model of hypotension. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40-130 mmHg CPP range, but it decreased 50% around 30 mmHg. MTT, calculated by an indicator-dilution technique, progressively and proportionately increased over the 40-130 mmHg CPP range. The HbO2 content, measured in the same area by an optical method, parallely decreased. Around 30 mmHg CPP, MTT disproportionately lengthened (700% of control). CMRO2 maintenance was accompanied by a progressive decrease of tissue HbO2 and sagittal sinus hemoglobin saturation. In this framework, MTT measurement and tissue HbO2 monitoring by NIRS might give a sensitive evaluation of the hemodynamic reserve than CBF measurement in anesthesia and intensive care.

Animals↗
PubMed1989

Noninvasive determination of hemoglobin saturation in dogs by derivative near-infrared spectroscopy.

An in vivo method utilizing derivative near-infrared spectroscopy was developed to noninvasively determine cerebral venous hemoglobin O2 saturation (SVO2). The method was tested on eight pentobarbital-anesthetized dogs ventilated with differing inspired O2 mixtures to force changes in SVO2 over a wide range. Spectral data obtained by transilluminating the tissues surrounding the superior sagittal sinus (SS) were transformed into first derivative units for correlation with SVO2 data measured from the SS. Linear regression analysis was applied to data obtained from five dogs and used to build a three-wavelength algorithm for predicting brain SVO2. In three dogs, SVO2 was varied to test this equation ability to predict SVO2. The standard deviation of differences between measured SVO2 and SVO2 predicted from 31 separate spectra was 3.2%. These predicted values, when regressed against the sampled SVO2, yielded an r value of 0.97. The results demonstrate that during hypoxic hypoxia (HH) it is possible to noninvasively quantify SVO2 with the use of infrared spectroscopy.

Animals↗
PubMed1989

Peripheral baroreceptor control of neurohypophysial blood flow during hemorrhage.

We measured neurohypophysial blood flow (NHBF) in dogs made hypotensive to study the time course of neurohypophysial autoregulation. We found that the neurohypophysis has a unique autoregulatory response in which blood flow increases transiently before establishing a stable perfusion level. During the "hyperemic" phase, the time course of the flow transient correlates with an increased plasma arginine vasopressin (pAVP) neurosecretory transient. However, unlike pAVP, blood flow does not remain elevated. The transitory nature of the flow response led us to evaluate the hypothesis that peripheral baroreceptor activity may be responsible for the hyperemic phase. Bilateral vagotomy and carotid sinus nerve denervation attenuated the increase in neural lobe blood flow (NLBF) to a standardized step to 80 mmHg mean arterial pressure. The pAVP response was enhanced both by vagotomy and carotid sinus denervation. Combined denervation abolished both the pAVP and the NLBF responses. We conclude that NHBF is autoregulated; however, control may be exerted at multiple levels, i.e., via nerves as well as local metabolic mechanisms. The peripheral baroreceptors influence NHBF primarily during periods of changing blood pressure. When blood pressure is stable, local mechanisms appear to be dominant.

Animals↗
PubMed1989

Brain resuscitation. Medical management and innovations.

In this article, we have reviewed the pathophysiology and several therapeutic strategies for cerebral ischemia. It seems likely that there will never be simple therapeutic answers to the complex pathophysiology of cerebral ischemia as we now understand it. Ultimate therapies will probably involve combinations of interventions designed to block several ongoing pathophysiologic processes in neuronal death. Progress in this field will likely be slow and difficult.

Amino Acids↗
PubMed1988

Cardiovascular autonomic dysfunction in Guillain-Barré syndrome. Therapeutic implications of Swan-Ganz monitoring.

Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy that may lead to quadriparesis, ventilatory failure, and autonomic dysfunction. While significant mortality due to ventilatory failure has been associated with this syndrome, this complication can now be readily managed. However, an estimated mortality of 5% to 20% remains attributable to medical complications (pulmonary embolus, sepsis) and to acute cardiovascular collapse due to autonomic failure. In this report, detailed sequential changes in hemodynamic parameters, as measured by Swan-Ganz catheter, associated with severe autonomic cardiovascular instability in a patient with GBS are described. Knowledge of changes in these hemodynamic parameters led to optimal therapy. Long-term Swan-Ganz monitoring in an intensive care setting may dramatically benefit the critically ill patient with GBS and cardiovascular autonomic dysfunction, and may help to eliminate the residual morbidity and mortality associated with this disease.

Aged↗
PubMed1988

Effect of centrally administered encephalinamides on regional cerebral blood flow in the dog.

(D-ala2)-met5-encephalinamide (AM encephalinamide) and (D-ala2)-leu5-encephalinamide (AL encephalinamide) were administered into the cisterna magna in anesthetized dogs to determine whether these opiates effected the neurohypophyseal circulation differently than the circulation of other brain areas. At the beginning of the experimental protocol, animals were given either mock cerebral spinal fluid (CSF) or 5 or 25 mg of AM encephalinamide or 5 mg of AL encephalinamide in equal volumes of mock CSF into the cisterna magna. By 60 min after intracisternal injection, radiolabeled AM encephalinamide distributed throughout the brain with the highest concentration being in the area of the brainstem. Sixty minutes after intracisternal injection, heart rate was decreased 29.0 +/- 5.1%, 41.3 +/- 4.4%, and 36.0 +/- 3.6%, and MABP was decreased 25.2 +/- 8.0%, 26.4 +/- 2.4%, and 32.3 +/- 2.6% in animals treated with AL encephalinamide (5 mg), AM encephalinamide (5 mg), and AM encephalinamide (25 mg), respectively. Neither AL encephalinamide or AM encephalinamide altered CBF or CMRO2 when compared with animals treated with mock CSF, whereas both AL encephalinamide and AM encephalinamide reduced neurohypophyseal blood flow by 30 min (43 +/- 11%, AL encephalinamide; 35 +/- 7%, AM encephalinamide, 5 mg; 46 +/- 8%, AM encephalinamide, 25 mg); the reduction was sustained throughout the 60-min protocol (34 +/- 10%, AL encephalinamide; 37 +/- 3%, AM encephalinamide, 5 mg; 38 +/- 4% AM encephalinamide, 25 mg). Plasma arginine vasopressin was transiently elevated 15 (326 +/- 75%, AL encephalinamide; 323 +/- 109%, AM encephalinamide, 25 mg) and 30 min (271 +/- 68%, AL encephalinamide; 368 +/- 136%, AM encephalinamide, 25 mg) in animals treated with AL encephalinamide or AM encephalinamide (25 mg). Intravenous naloxone administered at the end of the 60-min encephalinamide protocol was associated with a rise toward control values in heart rate and MABP in the AL encephalinamide group and in heart rate, MABP, and neurohypophyseal blood flow in both the AM encephalinamide 5 mg and 25 mg groups. These data suggest that encephalinamides may play a role in the regulation of neurohypophyseal blood flow through their actions on opiate receptors.

Animals↗
PubMed1988

Peripheral chemoreceptor control of neurohypophysial blood flow.

Neurohypophysial blood flow responses to hypoxic hypoxia were studied under conditions of vagotomy, carotid sinus denervation, and combined vagotomy and carotid sinus denervation. Arterial O2 tension was lowered from 128 +/- 3 to 31 +/- 1 Torr, whereas pH and arterial CO2 tension remained constant. Denervation of either carotid sinus or aortic arch chemoreceptors alone does not attenuate the dilation of neurohypophysial vessels that accompanies hypoxic hypoxia. Combined denervation, however, completely blocks this response for the neurohypophysis but not for any other brain region studied. Hypoxic hypoxia resulted in an increase in plasma vasopressin (AVP) from approximately 8 to approximately 40 pg/ml. This increase occurred in the intact, vagotomy, and carotid sinus-denervation conditions. This neurosecretory response was also completely inhibited by combined denervation. For most brain regions peripheral chemoreceptors are not involved in the blood flow response; however, the response of the neurohypophysis appears to be mediated via these chemoreceptors, presumably by altering the neuroeffector activity to this region. In addition our data suggest a temporal relationship between neurohypophysial vasodilation and neurosecretion of AVP.

Animals↗
PubMed1988

Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension.

Two cases of complete sagittal sinus occlusion with multiple brain hemorrhages, elevated intracranial pressure, and disseminated intravascular coagulation are described. These patients were successfully managed using pentobarbital-induced coma to ameliorate intracranial pressure elevation. This therapy was combined with monitoring of intracranial pressure and intermittent drainage of cerebrospinal fluid to further control intracranial pressure elevations. Thrombus and coagulopathy resolved with pentobarbital alone in one patient and after pentobarbital plus heparin therapy in the second patient. It is suggested that cases of severe distal sagittal sinus thrombosis with brain hemorrhage and intracranial hypertension may benefit from combined pentobarbital coma and intraventricular drainage. This allows for stabilization of bleeding tendencies before instituting heparin therapy when necessary. Management of sagittal sinus thrombosis with barbiturates or ventricular drainage is best performed in an intensive care unit environment with continuous monitoring of intracranial pressure and substantial electrophysiologic and neuroradiologic support.

Adult↗