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Biomedical subjects

K D Davis

Publications and source records attributed to K D Davis.

At least 73 records · Page 4Linked to original sources
PubMed1991

Topical application of clonidine relieves hyperalgesia in patients with sympathetically maintained pain.

Patients with reflex sympathetic dystrophy or causalgia characteristically have ongoing pain and pain to light touch (hyperalgesia). Some of these patients obtain relief of their pain following interruption of sympathetic function to the affected area and, therefore, have sympathetically maintained pain (SMP). Evidence suggests that the pain and hyperalgesia in SMP are related to activation of peripheral adrenergic receptors. We wished to determine the contribution of alpha 1- and alpha 2-adrenergic receptors in SMP and thus examined the effects of local application of adrenergic agents in patients with SMP. The alpha 2-adrenergic agonist clonidine, available as a transdermal patch, was delivered topically to the patients' hyperalgesic skin. In four patients with SMP, clonidine eliminated or substantially reduced hyperalgesia to mechanical and cold stimuli. In three of these patients the effects were confined to the skin region beneath the patch, suggesting a peripheral and not central effect. The relief of hyperalgesia was not due to a local anesthetic effect since touch thresholds were unaffected. Topical clonidine did not relieve hyperalgesia of similar severity for two other patients whose hyperalgesia and pain were unaffected by sympathetic ganglion blocks (i.e., diagnosed as having sympathetically independent pain). In two SMP patients, intradermal injection of norepinephrine or phenylephrine (a specific alpha 1-adrenergic agonist) at a site treated with clonidine evoked intense pain and rekindled the pre-clonidine hyperalgesia at that site. It is likely that clonidine locally blocks the release of norepinephrine via activation of alpha 2 receptors on the sympathetic terminals. This study suggests, therefore, that SMP is mediated via alpha 1-adrenergic receptors located in the affected tissue.

Administration, Cutaneous↗
PubMed1991

A comparison of hospital-based and private outpatient physical therapy practices.

A paucity of data exists about the delivery of contemporary adult outpatient physical therapy services in the United States. Although many debates about this issue have taken place within the physical therapy profession, assumptions about practice patterns have generally not been studied. This article reports some of the first-year findings from a 3-year survey research effort begun in September 1988 by Mathematica Policy Research Inc for the American Physical Therapy Association. Analyses are based on survey data from national probability samples of physical therapy facilities and discharged patients from 155 hospital-based and 166 private outpatient practices. The primary goal was to compare outpatient physical therapy practice patterns in the hospital-based and private practice settings. Findings reveal considerable homogeneity in private and hospital-based outpatient physical therapy practices. Hospital-based and private practices serve predominantly young, white adults who have private health insurance and a prevalence of orthopedic impairments. In both settings, direct access to outpatient physical therapy services was the exception and not the rule. Even in states in which direct access without a physician's referral was permitted by law, the majority of outpatient physical therapy was provided with a physician's referral. Most respondents in direct-access states indicated that reimbursement requirements were the major reason for needing a physician's referral to provide outpatient physical therapy.

Adult↗
PubMed1991

Systemic alpha-adrenergic blockade with phentolamine: a diagnostic test for sympathetically maintained pain.

The diagnosis of sympathetically maintained pain (SMP) is typically established by assessment of pain relief during local anesthetic blockade of the sympathetic ganglia that innervate the painful body part. To determine if systemic alpha-adrenergic blockade with phentolamine can be used to diagnose SMP, we compared the effects on pain of local anesthetic sympathetic ganglion blocks (LASB) and phentolamine blocks (PhB) in 20 patients with chronic pain and hyperalgesia that were suspected to be sympathetically maintained. The blocks were done in random order on separate days. Patients rated the intensity of ongoing and stimulus-evoked pain every 5 min before, during, and after the LASB and PhB. Patients and the investigator assessing pain levels were blinded to the time of intravenous administration of phentolamine (total dose 25-35 mg). The pain relief achieved by LASB and PhB correlated closely (r = 0.84), and there was no significant difference in the maximum pain relief achieved with the two blocks (t = 0.19, P greater than 0.8). Nine patients experienced a greater than 50% relief of pain and hyperalgesia from both LASB and PhB and were considered to have a clinically significant component of SMP. We conclude that alpha-adrenergic blockade with intravenous phentolamine is a sensitive alternative test to identify patients with SMP.

Adult↗
PubMed1991

Central mechanisms of vascular headaches.

The intracranial blood vessels supplying the dura and brain are innervated by sensory afferents from the trigeminal nerve. These fibers are believed to be responsible for conveying the pain associated with vascular head pain such as migraines. This paper reviews recently published data describing the existence of neurons within the cat trigeminal nucleus and thalamus that respond to electrical stimulation of the middle meningeal artery and superior sagittal sinus. Almost all of these neurons receive convergent input from the facial skin and most of the receptive fields include the periorbital region. On the basis of their cutaneous inputs, most of the neurons are classified as nociceptive. The characteristics of these cerebrovascular-activated neurons are consistent with their role in mediating vascular head pains and with the typical referral of such pains in man to the orbital region. This paper also presents preliminary results of recordings from rat trigeminal ganglion neurons activated by electrical stimulation of the middle meningeal artery and sagittal sinus. The latencies of activation of these neurons are indicative of conduction in slowly conducting myelinated axons and in unmyelinated axons. Some of the neurons could also be activated by mechanical stimuli applied to the vessels.

Animals↗
PubMed1991

Management of severe hypercalcemia.

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.

Humans↗
PubMed1990

Intradermal injections of bradykinin or histamine cause a flare-like vasodilatation in monkey. Evidence from laser Doppler studies.

The spreading cutaneous vasodilatation (flare) that follows a cutaneous injury is readily visible in humans but cannot be visualized in monkey. To determine if monkeys exhibit this neurally mediated reaction, cutaneous blood flow changes after intradermal injections of bradykinin and of histamine were monitored in the hairy skin of pentobarbital anesthetized monkeys. Using a laser Doppler device, recordings of cutaneous blood flow were made at distances of 15 and 25 mm from the injection of 50 microliters of saline, bradykinin (10(-3) M) and histamine (10(-3) M). These sites were beyond the radius of the wheal caused by bradykinin (6.3 mm) or histamine (6.8 mm). At both recording sites, both drugs caused an increase in blood flow that was significantly larger than that caused by the injection of the same volume of saline. These results provide evidence that although a flare is not visible in monkey skin, a flare-like vasodilatation does occur over an area of at least 50 mm diameter.

Animals↗
PubMed1988

Effect of trigeminal subnucleus caudalis cold block on the cerebrovascular-evoked responses of rostral trigeminal complex neurons.

The technique of reversible cold block was used to explore the possibility that the trigeminal subnucleus caudalis (Vc) influences the responses of rostral trigeminal brainstem nuclear complex (TBNC) neurons to stimulation of the cerebrovasculature. Reversible cold block of Vc was found to abolish totally the responses of many rostral TBNC neurons to stimulation of the cerebrovasculature. The remaining neurons were not affected by the cold block. These data suggest that some rostral TBNC neurons may receive an indirect input from the cerebrovasculature via Vc while other rostral TBNC neurons receive a direct input from the cerebrovasculature.

Animals↗
PubMed1988

Properties of feline thalamic neurons activated by stimulation of the middle meningeal artery and sagittal sinus.

Previous studies have identified a population of neurons in the cat trigeminal brainstem complex that respond to stimulation of the middle meningeal artery (MMA) and/or superior sagittal sinus (SS). In the present study, neuronal responses to stimulation of the MMA and SS were sought in the thalamus of the cat. Sixty-one neurons excited by electrical stimulation of the MMA and/or SS were located in the ventroposteromedial (VPM) nucleus, and surrounding regions in lateral thalamus. Of these 61 neurons, 23% were excited only by MMA stimulation, 39% only by SS stimulation and 38% by both MMA and SS stimulation. The latencies to activation from MMA and/or SS stimulation suggest the involvement of small, myelinated primary afferent fibers. Most neurons (48/61) responded to electrical stimulation of the MMA or SS with a burst of 2-5 spikes. Mechanical stimulation of the MMA and SS was also an effective stimulus and in some cases evoked a burst response. Of the neurons tested for the existence of orofacial inputs, all were found to have an excitatory receptive field (RF) on the face and usually (22/26 neurons) involved the ophthalmic distribution. Twelve of these neurons were excited by a tap stimulus applied to the face, 6 by pinching (nociceptive specific), 6 by low-threshold mechanical stimuli (LTM), one by both pinch and low-threshold stimuli and one by mechanical stimulation of the cornea. The firing properties, RF and modalities of these thalamic neurons suggest that they may play a role in the appreciation of pain of cerebrovascular origin.

Action Potentials↗
PubMed1988

Cerebrovascular application of bradykinin excites central sensory neurons.

The activity of sensory neurons in the trigeminal brainstem complex and thalamus responsive to electrical stimulation of the cerebrovasculature was monitored during topical application of bradykinin to the cerebral vessels or during an intravascular injection of bradykinin into the sagittal sinus. Bradykinin was found to excite 8 of the 15 cells studied. The excited cells were usually those that were spontaneously active and received nociceptive input from the oro-facial region. These neurons may be involved in mediating vascular head pain related to the acute or pathological changes of the cerebral vessels and/or the associated trigeminovascular sensory afferents.

Action Potentials↗
PubMed1988

Responses of feline trigeminal spinal tract nucleus neurons to stimulation of the middle meningeal artery and sagittal sinus.

1. Extracellular single-unit activity was recorded from 250 trigeminal (V) spinal tract nucleus neurons that were excited by electrical stimulation of the middle meningeal artery (MMA) and/or sagittal sinus (SS) in anesthetized cats. One hundred and thirty of these neurons were located in the V subnucleus caudalis (Vc), and the remaining 120 neurons were located in the V subnucleus oralis (Vo) or rostral part of the V subnucleus interpolaris (Vi). In many cases these neurons were also examined for the existence of orofacial receptive fields (RFs) by applying mechanical stimuli to the orofacial region. 2. The mean minimum latencies to suprathreshold electrical stimulation of the MMA and the SS were similar for Vc and Vo/Vi neurons. Excitation of Vc neurons occurred at latencies of 14.3 +/- 1.0 (n = 102) and 17.4 +/- 1.6 ms (n = 36) to MMA and SS stimulation, respectively. Excitation of Vo/Vi neurons occurred at latencies of 12.4 +/- 0.9 (n = 86) and 16.4 +/- 1.1 ms (n = 58) to MMA and SS stimulation, respectively. These latencies correspond to mean conduction velocities of approximately 5.2 and 4.0 m/s to MMA and SS stimulation, respectively. 3. Mechanical stimulation of the vessels evoked neuronal responses in five of eight MMA-activated neurons tested and three of five SS-activated neurons tested. 4. Almost all of the neurons tested (127 of 131) had peripheral RFs, and all were in the orofacial region. Nearly all (95%) Vc neurons had RFs within or including the ophthalmic facial region. The RFs of most (67%) Vo/Vi neurons also had RFs within or including ophthalmic regions, but in some cases were only within maxillary and/or mandibular regions. 5. Most of the Vc neurons (87%) were classified on the basis of their cutaneous inputs as nociceptive. The incidence of nociceptive neurons in Vo/Vi was also high (61%), although less than in Vc. In both the Vc and Vo/Vi neuronal populations, MMA-activated neurons were more likely to have nociceptive peripheral inputs than SS-activated neurons. 6. Histological reconstruction of recording sites indicated that the MMA- and/or SS-activated Vc neurons were concentrated in the lateral half of laminae III-V. The responsive neurons at the level of Vo/rostral Vi were not confined to any particular portion of these subnuclei. 7. These findings indicate that sensory afferents that innervate the dural arteries and venous sinuses are capable of activating neurons throughout the V spinal tract nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Modulatory influences of red nucleus stimulation on the somatosensory responses of cat trigeminal subnucleus oralis neurons.

Little is known of the effect of red nucleus (RN) stimulation on somatosensory neurons despite its known anatomic projections to somatosensory relay nuclei. The effect of RN stimulation on the somatosensory responses of trigeminal subnucleus oralis (Vo) neurons was investigated in chloralose- or barbiturate-anesthetized cats. Arrays of bipolar stimulating electrodes were inserted into the contralateral and ipsilateral RN and the contralateral thalamus. Extracellular single-unit recordings were obtained in Vo with tungsten microelectrodes. Neurons in Vo were excited to just suprathreshold by electrical stimulation within their receptive fields. Red nucleus influences were studied by applying 100-ms, 500-Hz conditioning trains to the contralateral or ipsilateral RN 130 ms prior to the peripheral test stimulus. The effect of RN stimulation was also tested on mechanically evoked responses of Vo cells. The somatosensory responses of most cells (70/73) were inhibited after RN stimulation. Some of these cells (15/70) could be antidromically activated from the contralateral thalamus. Stimulation of the RN resulted in excitation followed by inhibition in nine Vo cells. The results suggest that the RN may modulate transmission of somatosensory information through Vo.

Animals↗
PubMed1982

Interference in a chromogenic alpha-amylase assay caused by dye-labeled oligosaccharide-induced precipitation of lipoprotein.

We examined the mechanism by which hypertriglyceridemia interferes with the Roche Diagnostics "Amylochrome" procedure for measurement of amylase in lactescent samples with normal and above-normal amylase activity. The serum blank recommended in the Amylochrome protocol to compensate for lactescence remains inappropriately turbid, compared with the test, and is partly responsible for the underestimation of amylase activity. Other major interference is seen when lipoprotein in hyperlipemic samples with above-normal amylase activity reacts with the soluble oligosaccharide-triazinyl dye product of the Amylochrome assay to form a flocculent blue precipitate. The formation of this precipitate in the test, and its removal, diminish lactescence due to lipemia, an effect that cannot be matched by any manipulation of a serum blank procedure. Oligosaccharide-dye product is removed as a component of the precipitate.

Amylases↗
PubMed1980

Human platelet acetylcholinesterase: the effects of anticholinesterases on platelet function.

Platelet acetylcholinesterase (AChE) activity was measured in gel-filtered platelet preparations. Three different anticholinesteratic agents (eserine, neostigmine, and diisopropylphosphorofluoridate) at final concentrations of 10 muM caused complete inhibition of AChE activity after 30 min incubation at room temperature with either platelet-rich plasma or gel-filtered platelets. Complete inhibition of platelet AChE had no effect on platelet aggregation, factor-3 availability, and plasma clot retraction. We conclude that platelet membrane AChE activity is not required for normal platelet function as measured by these in vitro parameters.

Acetylcholinesterase↗
PubMed1979

Posttransfusion purpura: therapeutic failure of PlAl-negative platelet transfusion.

The effect of platelet type-specific transfusion in posttranfusion purpura is reported. Seven days after receiving 4 units of whole blood during total hip replacement a 69-year-old woman developed fulminant thrombocytopenic purpura. Her undiluted serum inhibited the clot retraction of PlAl-positive but not PlAl-negative blood. Anti-PlAl titer of her serum, determined by 51Cr platelet lysis technique, was 1:64. The serum had no lytic activity against platelet-rich plasma from two PlAl-negative donors. No anti-HLA antibody was detectable in the serum by lymphocytotoxicity technique, and serum obtained prior to transfusions had no platelet lytic activity. Four units of PlAl-negative platelet concentrate were administered, the first instance in which this treatment has been used. No rise in platelet count ensued, and the patient succumbed to purpura. Exchange transfusion or plasmapheresis remain the treatments of choice.

Aged↗