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Biomedical subjects

D P Becker

Publications and source records attributed to D P Becker.

At least 127 records · Page 7Linked to original sources
PubMed1984

Evidence for involvement of cholinoceptive cells of the parabrachial region in environmentally induced nociceptive suppression in the cat.

We have previously observed that activation of muscarinic receptors within the pontine parabrachial region (PBR) of cats produces potent analgesia. This study demonstrated that bilateral microinjections of the muscarinic antagonist atropine (each 4.0 micrograms in 1.0 microliter) into PBR attenuated nociceptive suppression elicited by exposure of cats to novel environmental changes without affecting general responsiveness to environmental stimulation. This observation suggests that muscarinic cholinoceptive cells in PBR function physiologically to modulate nociceptive responsiveness in response to certain environmental stimuli.

Animals↗
PubMed1984

Behavioral evidence for a cholinoceptive pontine inhibitory area: descending control of spinal motor output and sensory input.

Earlier studies have shown that microinjection of the cholinergic agonist carbamylcholine (carbachol) into the rostral pontine tegmentum of the cat elicits postural atonia. However, conflicting reports exist regarding other concomitant behavioral changes. The present study has demonstrated that a variety of functions supporting animals' responsiveness to external stimuli including postural somatomotor, sympathetic visceromotor and nociceptive somatosensory functions are differentially affected depending upon the injection sites. Sites associated with maximal effects on each of these functions are clustered in the dorsal pontine tegmentum, i.e. cholinoceptive pontine inhibitory area (CPIA). In a medial area of CPIA, which corresponds to an area caudal to the ventral tegmental nucleus of Gudden and ventromedial to the principal nucleus of locus coeruleus, postural somatomotor and sympathetic visceromotor functions were maximally suppressed. In a laterally adjacent area ventral to the principal nucleus of locus coeruleus, somatomotor function was predominantly suppressed. Nociceptive somatosensory function was primarily suppressed following microinjections into a more lateral area surrounding the lateral half of the brachium conjunctivum. Several lines of evidence suggest that each of these phenomena ultimately involves descending influences on the spinal motor output and/or sensory input. There was no correlation between maximal suppression of these spinal cord functions and signs of desynchronized sleep such as rapid eye movement. Carbachol microinjection into wide areas of CPIA also suppressed orienting behaviors. Taken together, these data suggest that CPIA is a system which primarily regulates animals' responsiveness to external stimuli, in part by influencing segmentally organized behaviors.

Animals↗
PubMed1984

Non-opiate analgesia induced by carbachol microinjection into the pontine parabrachial region of the cat.

These studies investigated the effect of microinjection of the cholinergic agonist carbamylcholine (carbachol) into various sites of the dorsolateral pontine tegmentum of the cat. Carbachol microinjection into an area surrounding the lateral half of the brachium conjunctivum (parabrachial region, PBR) produced profound suppression of nociceptive responses. In the dorsal part of PBR, carbachol microinjection produced no generalized sensory, emotional or motor deficits, indicating that nociceptive transmission was primarily affected. Carbachol microinjection into the ventral part of PBR resulted in slight suppression of motor responses in addition to profound nociceptive suppression. Carbachol-produced analgesia (CPA) observed within PBR blocked supraspinally as well as spinally integrated responses normally elicited by either phasic or tonic noxious stimuli. Atropine sulfate, but not mecamylamine hydrochloride, significantly antagonized CPA, indicating that muscarinic receptors mediate this phenomenon. The opiate antagonist naloxone, systemically administered either prior to or after carbachol microinjection, did not reliably attenuate CPA. Microinjection of morphine into the sites from which CPA had previously been obtained did not produce significant effects on nociceptive responses. Thus, opiate mechanisms appear not to be necessary either for the activation of this system or for the production of the resultant analgesia. These findings indicate that the neural population examined in the present study is anatomically and pharmacologically distinct from previously identified opiate-mediated pain inhibitory systems. Results are discussed in light of other recent evidence indicating the existence of endogenous non-opiate pain inhibitory systems.

Animals↗
PubMed1984

Activation of pontine cholinergic sites implicated in unconsciousness following cerebral concussion in the cat.

Low levels of cerebral concussion in the cat produce reversible behavioral suppression presumably associated with unconsciousness. This injury is also associated with increased rates of glucose utilization in regions within the dorsomedial pontine tegmentum. Microinjection of carbachol into these regions produced behavioral suppression resembling that following concussion. These data, together with previously published observations on cholinergic responses to brain injury, suggest that concussive unconsciousness may be attributable in part to activation of cholinergic pontine sites.

Animals↗
PubMed1984

Nutrition and the neurosurgical patient.

There has been a rapid expansion of knowledge in the field of nutrition and metabolism with regard to the general surgical patient. However, only recently has there been greater appreciation of the benefits of adequate nutrition and appropriate metabolic care of the neurosurgical patient. In this review, the authors attempt to outline 1) the metabolic response to stress in general, and how it applies to the neurosurgical patient; 2) how best to provide adequate nutritional support for the neurosurgical patient; 3) the effects of nutrition on neurotransmitters; and 4) the effect of diet and nutrition on patients with malignant brain tumors.

Acetylcholine↗
PubMed1984

Origin and evolution of plateau waves. Experimental observations and a theoretical model.

Laboratory observations made in cats with fluid-percussion head injuries have suggested that plateau waves or Lundberg "A-waves" are not independent of systemic circulatory events. Four distinct phases in the evolution of the plateau wave have been identified, and each related to a circulatory change in a causal manner. The first phase is the premonitory drift phase where intracranial pressure (ICP) gradually increases prior to the plateau proper. This phase is caused by a slow gradual decline in systemic arterial blood pressure (SABP) which increases ICP by autoregulatory vasodilation and reduces cerebral perfusion pressure (CPP) to a range of 70 to 80 mm Hg. The second phase is the plateau phase initiated at a CPP of about 70 to 80 mm Hg, and is characterized by a rapid increase in ICP as CPP falls further to 40 to 50 mm Hg. The plateau lasts as long as the CPP remains stable and above ischemic levels. The third phase is the ischemic response, characterized by CPP being returned toward normal by increases in SABP in response to very low CPP's. The fourth phase is the resolution, characterized by a rapid decline in the ICP to baseline levels with stabilization of the SABP and CPP, and is best explained by autoregulatory vasoconstriction. Plateau waves appear to occur as the result of intact or mostly intact autoregulation responding to changes in CPP. The series of events that follow are best explained by what is known of normal autoregulation; the various properties of plateau waves are viewed and explained as the expected and logical consequences of an unstable CPP acting upon a generally intact cerebrovascular bed in the face of elevated ICP and decreased compliance.

Animals↗
PubMed1984

Experimental brain injury: successful therapy with the weak base, tromethamine. With an overview of CNS acidosis.

The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p less than 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p less than 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.

Acidosis↗
PubMed1984

Mechanical brain injury: the sympathoadrenal response.

Catecholamine release was studied in cats as a function of injury severity in the fluid-percussion model of brain injury. Hyperglycemia was also studied as a function of catecholamine response and injury severity. Epinephrine (E) and norepinephrine (NE) increased as a function of injury. This increase was maximal at about a 3.0-atmosphere (atm) injury level and amounted to a 500-fold increase for E and 100-fold increase for NE. Both catecholamines increased maximally by 10 seconds postinjury. Glucose increased to about 350% of baseline at 500 seconds postinjury and also increased as a function of injury severity. Results suggested that the sympathoadrenal discharge was capable of a graded response which was maximal at about 3.0 atm. Associated with this increase were hypertensin, bradyarrhythmias, tachyarrhythmias, and hyperglycemia.

Adrenal Glands↗
PubMed1984

Residual anterior pituitary function following transsphenoidal resection of pituitary macroadenomas.

A series of 84 patients with pituitary adenomas greater than 1 cm in diameter is presented. Full preoperative and postoperative endocrine evaluations were carried out, and the effects of transsphenoidal surgery on remaining anterior pituitary function were analyzed. Of the patients who had normal anterior pituitary function before surgery, 78% retained normal function after surgery. Thirty-three percent of those patients with pituitary deficits who did not have panhypopituitarism before surgery had improved function after surgery; 33% had worsened function after surgery. None of the patients with panhypopituitarism before surgery regained function after surgery. Transsphenoidal surgery carries an acceptable risk for sacrificing anterior pituitary function, but the risk is greater in patients with larger tumors and preoperatively compromised pituitary function.

Adenoma↗
PubMed1984

Effect of mannitol on ICP and CBF and correlation with pressure autoregulation in severely head-injured patients.

In a previous paper, the authors showed that mannitol causes cerebral vasoconstriction in response to blood viscosity decreases in cats. The present paper describes the changes in intracranial pressure (ICP) and cerebral blood flow (CBF) after mannitol administration in a group of severely head-injured patients with intact or defective autoregulation. The xenon-133 inhalation method was used to measure CBF. Autoregulation was tested by slowly increasing or decreasing the blood pressure by 30% and measuring CBF again. Mannitol was administered intravenously in a dose of 0.66 gm/kg; 25 minutes later, CBF and ICP were measured once again. In the group with intact autoregulation, mannitol had decreased ICP by 27.2%, but CBF remained unchanged. In the group with defective autoregulation, ICP had decreased by only 4.7%, but CBF increased 17.9%. One of the possible explanations for these findings is based on strong indications that autoregulation is mediated through alterations in the level of adenosine in response to oxygen availability changes in cerebral tissue. The decrease in blood viscosity after mannitol administration leads to an improved oxygen transport to the brain. When autoregulation is intact, more oxygen leads to decreased adenosine levels, resulting in vasoconstriction. The decrease in resistance to flow from the decreased blood viscosity is balanced by increased resistance from vasoconstriction, so that CBF remains the same. This might be called blood viscosity autoregulation of CBF, analogous to pressure autoregulation. Vasoconstriction also reduces cerebral blood volume, which enhances the effect of mannitol on ICP through dehydration of the brain. When autoregulation is not intact there is no vasoconstriction in response to increased oxygen availability; thus, CBF increases with decreased viscosity. With the lack of vasoconstriction, the effect on ICP through dehydration is not enhanced, so that the resulting decrease in ICP is much smaller. Such a mechanism explains why osmotic agents do not change CBF but decrease ICP in normal animals or patients with intact vasoconstriction, but do (temporarily) increase CBF in the absence of major ICP changes after stroke.

Brain Injuries↗
PubMed1984

Intracranial pressure variations associated with activation of the cholinoceptive pontine inhibitory area in the unanesthetized drug-free cat.

Intracranial pressure (ICP) was recorded continuously in chronically prepared, unanesthetized cats in order to investigate the effects on ICP of the cholinergic agonist, carbamylcholine (carbachol), injected by microsyringe needles into the dorsal pontine tegmentum. As reported previously, carbachol microinjections into the medial part of the cholinoceptive pontine inhibitory area (CPIA) located ventromedially to the locus coeruleus produced a comatose state characterized by a profound unresponsiveness to external stimuli, desynchronized electroencephalograms (EEG's), and suppression of postural somatomotor and sympathetic visceromotor functions. Four of six ICP records following carbachol microinjections into the CPIA showed small but significant increases which occurred in association with these carbachol effects. Tracings of ICP increases ranged up to 3.2 mm Hg and were similar in shape to plateau waves. The start and resolution of these carbachol-induced ICP variations were closely associated with the onset and termination of EEG desynchronization and signs of reduced cervical sympathetic tone, but not with changes in systemic arterial blood pressure or arterial pCO2. Temporal associations between ICP increases, desynchronized EEG's, and signs of reduced sympathetic tone were repeatedly confirmed during recovery periods associated both with recurrent comatose states following wakefulness produced by various intensities of external stimulation and with spontaneously occurring states resembling rapid eye movement sleep. The authors infer that carbachol-induced ICP variations may be produced by increased cerebral blood volume in response to accelerated cerebral metabolism and reduced vasoconstrictor tone of cervical sympathetic nerves. The simultaneous occurrence of continuously accelerated cerebral metabolism and reduced cervical sympathetic tone can neither be seen in physiologically normal, awake organisms nor produced by other known experimental manipulations of the central nervous system. Such a paradoxical relationship appears to be a unique consequence of activity within the CPIA. These data suggest that episodic activity within the CPIA may provide at least one endogenous neural basis for plateau waves seen during certain pathological conditions such as disturbed cerebrospinal fluid (CSF) absorption or with reduced equilibrium volume of CSF space.

Animals↗
PubMed1983

Axonal change in minor head injury.

Anterograde axonal transport of horseradish peroxidase (HRP) in selected cerebral and cerebellar efferents was studied in cats subjected to minor head injury. After trauma, the animals were allowed to survive from one to 24 hours, when they were perfused with aldehydes and processed for the light and electron microscopic visualization of the peroxidase reaction product. By light microscopy, the brain injury elicited an initial intra-axonal peroxidase pooling. With longer post-traumatic survival, HRP pooling increased in size, demonstrated frequent lobulation, and ultimately formed large ball- or club-like swellings which suggested frank axonal separation from the distal axonal segment. Ultrastructural examination revealed that the initial intra-axonal peroxidase pooling was associated with organelle accumulation which occurred without any other form of axonal change or related parenchymal or vascular damage. This accumulation of organelles increased with time and was associated with conspicuous axonal swelling. Ultimately these organelle-laden swellings lost continuity with the distal axonal segment and the axonal swelling was either completely invested by a thin myelin sheath or protruded without myelin investment into the brain parenchyma. This study suggests that axonal change is a consistent feature of minor head injury. Since these axonal changes occurred without any evidence of focal parenchymal or vascular damage, minor brain injury may ultimately disrupt axons without physically shearing or tearing them.

Animals↗
PubMed1983

An improved method for in situ freezing of cat brain for metabolic studies.

This study introduces a new method for rapid freezing of the cat brain. The method employed a Styrofoam box which was fitted around the head of the animal. Liquid nitrogen was poured into the box until the head was submerged. Temperature changes in three brain sites (ventral hypothalamus, the fourth ventricle, and the corpus callosum) and levels of labile carbohydrate metabolites (glycogen, glucose, ATP, P-creatine, and lactate) in five brain regions (cortex, thalamus, midbrain, cerebellum, and pons) frozen by the box method were compared with those frozen by a conventional cup method in which liquid nitrogen was poured into a hollow Styrofoam cup placed on top of the skull. The box method shortened the time of arrival of the freezing front and improved the freezing rate. The time required to bring the tissue to -20 degrees C was shortened, from 20 min at the ventral hypothalamus and 10-12 min at the fourth ventricle with the cup method, to less than 5 min at both sites with the box technique. Continued perfusion of brainstem prior to freezing was demonstrated. Levels of metabolites frozen by either method were similar. Lactate levels in any of the five brain regions studied by either method were not elevated, indicating no ischemic change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effect of changes in magnesium ion concentration on cat cerebral arterioles.

The effect of changes in cerebrospinal fluid (CSF) concentration of magnesium ion ([Mg2+]) on pial arterioles was investigated in anesthetized cats equipped with acutely implanted cranial windows for the observation of the pial microcirculation. Increased [Mg2+] caused vasodilation, whereas decreased [Mg2+] caused vasoconstriction. The effect of [Mg2+] was dose dependent and was the same in small and larger arterioles. There was an interaction between CSF [Mg2+] and calcium ion concentration ([Ca2+]), such that the vasodilator effect of Mg2+ was greater when the [Ca2+] was lower, especially in larger vessels. The vasodilator effect of Mg2+ on pial arterioles was enhanced in the presence of the calcium antagonist verapamil (0.5 micrograms/ml), despite the fact that verapamil by itself caused a 12-13% arteriolar dilation. These results show that the vasodilator effect of Mg2+ is probably related to an interaction at the cell membrane resulting in reduction in the influx of Ca2+ into vascular smooth muscle.

Animals↗
PubMed1983

Gastric secretory and mucosal injury response to severe head trauma.

The problem of gastric secretory and mucosal injury response was evaluated in 19 patients who had suffered a severe head injury. Fifteen of 19 patients had some evidence of gastrointestinal hemorrhage. In 7 cases, this was marked. The mean volume of gastric secretions ranged from 36.4 ml/hour on Day 1 to 47.6 ml/hour on Day 6. The mean value of titratable acidity ranged from 3.4 meq/hour on Day 1 to 3.9 meq/hour on Day 6. Possible risk factors were analyzed as a means of predicting specific subgroups of severely injured patients who would be more prone to have gastrointestinal complications. During the first 6 days after injury, there was no significant association (correlation coefficient not significant at the 0.05 level of significance) of the presence of an intracranial mass lesion, elevated intracranial pressure, brain stem dysfunction or prior episodes of hypotension or hypoxia, sepsis, shock, or the requirement for pressor agents with elevated gastric acid output, mucosal erosion, or hemorrhage. Because no specific risk factor or factors could be identified, all severely brain-injured patients should be on some form of therapy for the prevention of gastrointestinal complications.

Adult↗