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Biomedical subjects

D F Hanley

Publications and source records attributed to D F Hanley.

At least 91 records · Page 5Linked to original sources
PubMed1993

Extracellular potassium activity and cerebral blood flow during moderate hypoglycemia in anesthetized dogs.

Moderate hypoglycemia (MH) may be associated with blunting of cerebral hypocapnic vasoconstriction. Coincident with this change, electroencephalogram (EEG) flattening occurs. Previous reports show that brain extracellular potassium activity ([K+]o) increases in association with the onset of isoelectricity during severe hypoglycemia and that K+ increases cause pial vessel vasodilation. Using a model of MH, we tested the hypothesis that increases in [K+]o (approximately 15 mM) correlate with blunting of cerebral hypocapnic vasoconstriction. Cerebral blood flow (CBF), [K+]o, and EEG were measured during normocapnia [arterial Pco2 (Paco2) = 35 Torr)] and hypocapnia (PaCO2 = 15 Torr) in MH (< 2 mM) and normoglycemic dogs. During MH, increases in [K+]o occurred in association with EEG flattening (from 4.2 +/- 0.5 to 13.8 +/- 3.8 mM). During normoglycemia and MH without [K+]o elevations, hypocapnic vasoconstriction occurred. [K+]o elevations with MH were associated with increased CBF and decreased vascular resistance (146 +/- 5 and 42 +/- 2% of control, respectively) during normocapnia, and blunting of cerebral hypocapnic vasoconstriction (93 +/- 16% normocapnic control) when [K+]o increased during hypocapnia. This study shows that increases in [K+]o during MH are necessary for both normocapnic increases in CBF and blunting of cerebral hypocapnic vasoconstriction. Increases in [K+]o may represent a mechanism for decreases in cerebral vascular resistance during MH.

Animals↗
PubMed1993

Vasopressin and oxytocin: modulators of neurohypophysial blood flow.

We examined the role of arginine vasopressin (AVP) as a mediator of neurohypophysial (NH) blood flow regulation in anesthetized dogs. First, we evaluated the NH hyperemia that occurs during hemorrhagic hypotension in the presence (n = 7) and absence (n = 7) of the selective AVP-V1 receptor antagonist [d(CH2)5Tyr(Me)]AVP. AVP-V1 blockade did not alter NH transient or steady-state flow responses to a standardized decrease to 80 mmHg mean arterial blood pressure. We then determined whether exogenous AVP alters NH and regional cerebral blood flow (CBF) (n = 8). Sequential intracarotid infusions resulted in sagittal sinus blood AVP concentrations ranging from 6.97 +/- 3.3 x 10(3) to 2.45 +/- 0.47 x 10(6) pg/ml. No change in NH blood flow (control 428 +/- 162 vs. 487 +/- 75 ml.min-1.100 g-1) was observed even at the highest blood level. However, CBF at the highest AVP level increased from a control value of 20 +/- 3 to 40 +/- 4 ml.min-1.100 g-1, while cerebral oxygen consumption remained unchanged. Administration of a selective AVP-V1 receptor antagonist, [d(CH2)5Tyr(Me)]AVP, blocked AVP-induced elevation in CBF in a third set of dogs (n = 5). Oxytocin was also given by intracarotid infusion at a constant rate (1-200 micrograms/ml) in a final group (n = 5). NH blood flow was unchanged at all doses, whereas CBF increased from control (24 +/- 2 to 38 +/- 5 ml.min-1.100 g-1) at the highest dose. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Relapse in Guillain-Barré syndrome after treatment with human immune globulin.

Seven adult patients received human immune globulin intravenously as initial therapy for Guillain-Barré syndrome. Although all patients initially stabilized or improved, five patients deteriorated 1 to 16 days after completion of treatment. In all five patients, clinical worsening included loss of at least one functional grade together with a decreased forced vital capacity. We subsequently treated each patient with a course of plasma exchange, which led to varying degrees of clinical improvement in four. In contrast to previously reported relapse rates for Guillain-Barré syndrome, our experience suggests that clinically significant relapses may occur in patients more often following human immune globulin therapy than after either plasma exchange or no therapy.

Adolescent↗
PubMed1993

Altered cerebrovascular CO2 reactivity following subarachnoid hemorrhage in cats.

The authors tested the hypothesis that cerebral blood flow (CBF) reactivity to CO2 was blunted following subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage was produced in five cats by performing four cisterna magna injections of blood in each (SAH Group). A second group of six cats was treated with an antifibrinolytic agent (AF) in addition to four cisterna magna blood injections (SAH+AF Group). Four cats received AF and four cisterna magna injections of saline (Control Group). The presence or absence of basilar artery vasospasm was determined by comparing baseline and follow-up selective angiograms. Cerebral blood flow reactivity was determined by randomly varying the concentration of inspired CO2 to alter PaCO2 from 20 to 75 mm Hg. Regional CBF was measured with radiolabeled microspheres. Basilar artery vasospasm was seen following subarachnoid injection of blood but not of saline. Normocapnic CBF was similar in all three groups in the brain stem (mean +/- standard error of the mean: SAH Group 46 +/- 6, SAH+AF Group 46 +/- 6, and Control Group 44 +/- 9 ml/min/100 gm) and in the supratentorial compartment (SAH Group 53 +/- 8, SAH+AF Group 61 +/- 9, and Control Group 51 +/- 13 ml/min/100 gm). At intermediate levels of hypercarbia (PaCO2 50 +/- 3 mm Hg), CBF increased similarly in all three groups (SAH Group 161% +/- 32%, SAH+AF Group 118% +/- 33%, and Control Group 174% +/- 19% compared to baseline); at higher levels of PaCO2 (60 +/- 3 mm Hg), CBF values were SAH Group 265% +/- 50%, SAH+AF Group 205% +/- 47%, and Control Group 159% +/- 30% of baseline. At the highest level of PaCO2 (75 +/- 6 mm Hg), supratentorial CBF did not increase as much in the SAH+AF Group as in the Control Group (179% +/- 59% vs. 463% +/- 58% of baseline, respectively). The authors conclude that, in this model of SAH, there is no change in normocapnic CBF; however, blood flow reactivity to hypercarbia is blunted. It is possible that this may result from a combination of narrowing of proximal large vessels and globally impaired reactivity of small vessels.

Angiography↗
PubMed1992

Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage.

Hyponatremia is common following subarachnoid hemorrhage and has alternatively been attributed to either the inappropriate secretion of antidiuretic hormone or natriuresis causing intravascular volume contraction. We prospectively studied body sodium and intravascular volume regulation in 19 patients, beginning within 3 days after acute aneurysmal subarachnoid hemorrhage occurred, in order to determine the impact of hypervolemic therapy on both hyponatremia and volume contraction and to ascertain whether humoral factors account for hyponatremia. Serial measurements of plasma arginine vasopressin, atrial natriuretic factor, renin activity, aldosterone, and catecholamines were correlated with body sodium and fluid balance, change in blood volume, serum sodium concentration, and osmolality. Six patients (32%) developed hyponatremia, but only 2 had a negative sodium balance. In most patients, levels of atrial natriuretic factor were elevated, while plasma renin activity and aldosterone concentrations were generally suppressed. Plasma arginine vasopressin levels were not suppressed during hypo-osmolality and did not correlate with serum osmolality in hyponatremic patients. Only 1 patient had a decrease in blood volume, which was associated with marked rises in aldosterone and plasma renin activity, but normal serum sodium and plasma atrial natriuretic factor levels. We conclude that following subarachnoid hemorrhage: (1) Hypervolemic therapy prevents volume contraction but not hyponatremia, (2) humoral factors may favor both sodium loss and water retention, and (3) arginine vasopressin regulation is disturbed and may contribute to hyponatremia.

Adult↗
PubMed1992

Presyncope caused by central hypovolaemia is not preceded by evoked potential alterations.

The mechanism(s) responsible for the onset of presyncope during a central hypovolaemic challenge have gone undefined for many years. It has been speculated that a decrease in cerebral blood flow initiates presyncopal responses, which in turn lead to greater decreases in cerebral oxygen delivery and unconsciousness. Somatosensory evoked potentials (SEP) were monitored as a measure of cerebral functioning in ten subjects during presyncopal symptom limiting lower body negative pressure (a central hypovolaemic challenge). SEP latency and amplitudes have been correlated with cerebral oxygen uptake, so SEP activity can serve as an indirect indicator of cerebral homeostasis. SEPs were generated by electrically stimulating the median nerve and recoding the resulting potentials over the contralateral cerebral cortex. While heart rate and mean blood pressure both fell at presyncope, there were no changes noted in either SEP latency or amplitude at any point before (latency = 22.9 +/- 9 ms; amplitude = 2.86 +/- 0.24 microV), during (22.6 +/- 0.9 ms; 2.68 +/- 0.2 microV), or after (22.7 +/- 0.9 ms; 2.37 +/- 0.23 microV) the occurrence of presyncope. We conclude that the onset of presyncope is not associated with a decrease in cerebral function.

Adult↗
PubMed1992

Mechanisms regulating neurohypophysial blood flow and function during isotonic volume expansion.

Regional cerebral and neurohypophysial blood flow responses to isotonic extracellular fluid volume expansion were studied in pentobarbital-anesthetized dogs using radiolabeled microspheres. Measurements were made at baseline and after increasing pulmonary capillary wedge pressure by 8 +/- 2 mmHg. Plasma arginine vasopressin (AVP) decreased by 50%, and neural lobe blood flow (NLBF) decreased by 47%. Blood flow through median eminence and other brain regions was unchanged. We investigated potential mechanisms responsible for the NLBF changes. Following control vagotomy, AVP concentration increased during the first hour and then returned to control values for hours 2 and 3, whereas NLBF was unchanged for the first hour and fell after 2 and 3 h. Vagus section abolished the decrease in NLBF but not the AVP response to volume expansion. The contribution of left atrial and pulmonary baroreceptors to this response was tested by inflation of a balloon in the left atria to produce a 13 +/- 1 mmHg rise in atrial pressure. This led to a 20% reduction in NLBF, a 35% reduction in AVP concentration, and a 270% increase in plasma atrial natriuretic factor (ANF). However, ANF release does not account for the NLBF changes, since intravenous ANF infusion had no effect on NLBF or AVP concentration. These data suggest that the NLBF response to volume expansion is mediated by the vagus with input from multiple cardiopulmonary baroreceptors.

Animals↗
PubMed1992

Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in dogs.

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.

Animals↗
PubMed1992

Neural mechanisms regulating neurohypophysial resistance arteries.

We defined the extent of vasoactive intestinal polypeptide (VIP) and noradrenergic influences on isolated 100- to 200-microns-diameter vessels from the resistance arterial circulation of the neurohypophysis. A dual extracranial (inferior hypophysial) and intracranial (superior hypophysial) arterial supply to the neurohypophysis was confirmed. The inferior hypophysial artery demonstrates noradrenergic and VIP-like perivascular nerves, whereas the superior hypophysial artery shows primarily VIP-like innervation. Pharmacological sensitivity of the inferior hypophysial to VIP [mean effective dose (ED50) = 10(-8.2) M] and to norepinephrine (ED50 = 10(-5.7) M) was demonstrated. The superior hypophysial reacted only to VIP (ED50 = 10(-8.6) M). The physiological relevance of these findings was tested with transmural nerve stimulation. Frequency-dependent vasodilation of both inferior and superior hypophysial arteries was demonstrated. This dilation could not be blocked with atropine or propranolol. Frequency-dependent vasoconstriction was identified in extracranial vessels including the inferior hypophysial artery. This constriction is only partially blocked by prazosin, phentolamine, and guanethidine. When neurohypophysial resistance vessels are compared with larger circle of Willis arteries and similar-size pial vessels of other cerebral regions, they appear to have regionally unique neural mechanisms for regulating blood flow. Specifically whether controlled by periarterial nerves or other tissue influences, the inferior hypophysial artery appears to meet anatomic, pharmacological, and physiological definitions of neural control for both dilator and constrictor activities of flow to the neurohypophysis.

Animals↗
PubMed1992

Intracranial pressure measurement/cranial vault mechanics: clinical and experimental observations.

The absolute value of intracranial pressure (ICP) should be considered in conjunction with evaluation of a patient's clinical condition. In addition, other aspects of cranial vault mechanics may be important in multiple disease states. Among the important physiological measures of cranial vault sufficiency are hydrodynamic interaction between brain tissue, blood and cerebrospinal fluid (CSF)--volume-pressure relation, CSF dynamics--CSF outflow resistance, CSF production rate, sagittal sinus pressure, and appearance of ICP waves. Clinical and experimental studies brought together in this review provide an insight into the dynamics of ICP and the cranial vault.

Brain Injuries↗
PubMed1991

Preoperative lumbar epidural morphine improves postoperative analgesia and ventilatory function after transsternal thymectomy in patients with myasthenia gravis.

OBJECTIVE: To test the hypothesis that preoperative lumbar epidural morphine improves postoperative pain control and ventilatory function after transsternal thymectomy in patients with myasthenia gravis. DESIGN: The study design was randomized, placebo-controlled, and double-blind. SETTING: After surgery, all patients were admitted to the Neuroscience Critical Care Unit for evaluation and treatment. PATIENTS: All patients with myasthenia gravis who presented to the hospital for thymectomy were asked to participate in the study. Twenty patients were randomized to either the placebo or epidural morphine groups. INTERVENTIONS: Patients received either epidural morphine (7 mg in 14 mL of sterile saline) or saline (14 mL) before induction of anesthesia. Supplemental iv opioids were administered intraoperatively, with need determined by the anesthesiologist. MAIN OUTCOME MEASURES: The main outcome measures were indicators of postoperative pain (e.g., Visual Analog Pain Score, requirement for supplemental opioid administration, respiratory rate) and ventilatory function (e.g., forced vital capacity, negative inspiratory pressure). RESULTS: Immediately after surgery, the Visual Analog Pain Score in the placebo group was twice as high as the score in the epidural morphine group (placebo 7.0 +/- 1.3; epidural morphine 3.5 +/- 1.2, p less than or equal to .05). During the first eight postoperative hours, the placebo group required more opioids (0.22 +/- 0.03 vs. 0.12 +/- 0.04 mg/kg morphine equivalents, p less than or equal to .06) than the epidural morphine group. Later, both groups received similar amounts of opioids. Patients receiving epidural morphine had better initial recovery of forced vital capacity (at 8 hrs: 55 +/- 6% [epidural morphine] vs. 34 +/- 5% [placebo] of preoperative value, p less than or equal to .05). Respiratory rate was lower for the first 12 postoperative hours in the epidural morphine group, without a difference in PaCO2. There was no difference between groups for the duration of postoperative intubation or ventilation. CONCLUSIONS: Preoperative lumbar epidural morphine facilitates postoperative analgesia and improves initial postoperative ventilatory performance.

Adult↗
PubMed1991

Cerebrovascular CO2 reactivity during delayed vasospasm in a canine model of subarachnoid hemorrhage.

While the in vitro reactivity of cerebral conducting vessels following subarachnoid hemorrhage has been extensively studied, in vivo cerebrovascular CO2 reactivity has not been systematically investigated. We tested the hypothesis that, in the canine model of subarachnoid hemorrhage, the rise in cerebral blood flow normally seen with hypercapnia is blunted during delayed vasospasm. Four groups of animals were studied: one received two 4-ml subarachnoid injections of nonheparinized arterial blood into the cisterna magna (n = 8), one received three subarachnoid injections of 5 ml blood (n = 5), one received two subarachnoid injections of 4 ml saline (n = 5), and a control group (n = 5) had no subarachnoid injections or angiography. Basilar artery diameter was measured from baseline and follow-up angiography. We determined CO2 reactivity by randomly varying the concentration of inspired CO2 and measuring regional cerebral blood flow with radiolabeled microspheres. Basilar artery diameter was not affected by saline injection and was reduced by 26 +/- 2.9% in the two-hemorrhage group and 55 +/- 1.9% in the three-hemorrhage group. Baseline cerebral blood flow and CO2 reactivity were similar in all four groups. We conclude that, in this model of delayed vasospasm, regional cerebral vascular CO2 reactivity is intact and extrapolation of in vitro data regarding basilar artery diameter and reactivity to cerebral blood flow must be done cautiously.

Animals↗
PubMed1991

Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Following subarachnoid hemorrhage, the plasma concentration of atrial natriuretic factor is elevated and appears to be independent of atrial stretch. While the hypothalamus and circumventricular organs contribute to sodium and intravascular volume regulation, their influence on atrial natriuretic factor is not known. We tested the hypothesis that, following subarachnoid hemorrhage, suprasellar cisternal blood, intraventricular blood, or ventricular enlargement would be associated with elevated plasma levels of atrial natriuretic factor. Computed tomograms of 26 patients performed less than or equal to 3 days after hemorrhage were analyzed to determine the presence of suprasellar or intraventricular blood and enlargement of the third or lateral ventricle. These results were correlated with the plasma atrial natriuretic factor and serum sodium concentrations. The initial atrial natriuretic factor concentration was elevated and was higher in patients with suprasellar or intraventricular blood than in those without (suprasellar: 131 +/- 20 and 54 +/- 10 pg/ml, respectively; intraventricular: 137 +/- 25 and 84 +/- 31 pg/ml, respectively). The atrial natriuretic factor concentration remained higher over the week following hemorrhage in patients with suprasellar blood than in those without (127 +/- 16 and 68 +/- 12 pg/ml, respectively). The atrial natriuretic factor concentration was not correlated with hyponatremia (125-134 meq/l) or age-corrected ventricular size. Hyponatremia did not correlate with the presence of intraventricular or suprasellar blood. Our data suggest that suprasellar and intraventricular blood disturb hypothalamic function, resulting in an elevated plasma atrial natriuretic factor concentration. The presence of a direct relation between atrial natriuretic factor and hyponatremia remains unclear.

Adult↗
PubMed1991

Diaphragmatic performance during recovery from acute ventilatory failure in Guillain-Barré syndrome and myasthenia gravis.

Diaphragmatic muscle performance during acute ventilatory failure due to Guillain-Barré syndrome and myasthenia gravis was assessed to evaluate (1) diaphragmatic function during weaning from ventilatory support and (2) diaphragmatic tension-time integral (TTdi) during ventilatory failure. We used a multilumen nasogastric tube and a pneumotachograph to measure transdiaphragmatic pressure per breath (Pdi), maximum transdiaphragmatic pressure (Pdimax), tidal volume (VT), and inspiratory time fraction during 74 spontaneous breathing trials in nine patients. Diaphragmatic performance was poor in all patients. The Pdi, Pdimax, and VT improved significantly, but values for Pdi and Pdimax remained low even after weaning. Improvement in Pdimax was the best predictor of recovery (r = 0.48; p less than 0.001). Maximal inspiratory force correlated with Pdimax (r = 0.48; p less than 0.005), but FVC did not. The TTdi rarely exceeded the expected fatigue threshold of 0.15 in spite of the patient's inability to sustain ventilation. Although our patients demonstrated diaphragmatic weakness, TTdi did not demonstrate diaphragmatic fatigue.

Acute Disease↗
PubMed1990

Long-term cognitive sequelae of acyclovir-treated herpes simplex encephalitis.

Survival from untreated herpes simplex type 1 encephalitis is well known to be accompanied by severe cognitive impairments. Recently, acyclovir has been proven to be the most effective available treatment for this disease, with the expectation that it would appreciably reduce morbidity. We performed detailed assessments of four consecutive patients who received acyclovir in the early stages of biopsy-proven herpes encephalitis and who now have been followed up for 1.5 to 4 years. All four patients showed definite residual on either clinical or formal neuropsychological testing, most commonly dysnomia and impaired new learning for both verbal and visual material, even though three had normal performance on a standard clinical mental status test. All four patients were unable to function at their prior level of achievement. Therefore, despite early administration of acyclovir in herpes encephalitis, long-lasting neuropsychological residua are likely. Furthermore, cognitive deficits of prognostic importance may not be detected by clinical screening.

Acyclovir↗
PubMed1990

A continuing controversy: magnesium sulfate in the treatment of eclamptic seizures.

It would appear from the above that Pritchard agrees with the use of some agents other than magnesium sulfate that have known anticonvulsant properties. We believe that the subject at issue is whether magnesium sulfate should be used in treating the seizures of eclampsia. In our "Controversies" article, we do not address the issue of whether magnesium sulfate modifies pathophysiological factors leading to preeclampsia, but restrict ourselves to the treatment of the seizure per se, once seizures supervene, and the avoidance of their recurrence. The pathophysiological mechanisms and optimal treatment of preeclampsia and of eclampsia (excepting seizures) remain to be determined, as does the use of magnesium sulfate in this condition. Eclamptic seizures are clinically and electroencephalographically indistinguishable from generalized tonic-clonic seizures. Whether seizures arise in or out of the setting of preeclampsia, they should be treated as are other seizures, with known anticonvulsants. Controlled clinical trials are needed to address the effectiveness of alternative antiseizure regimens.

Eclampsia↗