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Biomedical subjects

J Ochoa

Publications and source records attributed to J Ochoa.

At least 37 records · Page 2Linked to original sources
PubMed1995

High doses of dietary arginine during repletion impair weight gain and increase infectious mortality in protein-malnourished mice.

There is considerable evidence for the beneficial effects of dietary arginine, a conditionally-essential amino acid that enhances anabolism and T-cell function. However, the safety and efficacy of higher doses of arginine supplementation following infection have not been investigated completely. These issues were explored therefore, in a murine model of malnutrition and infection. Severe protein malnutrition was induced by feeding mice for 6 weeks on an isoenergetic diet containing only 10 g protein/kg. Mice were then allowed to consume diets with normal amounts of protein (200 g/kg) with 50 g/kg provided as amino acid mixtures of glycine and arginine in which the arginine content ranged from 0 to 50 g/kg. During the repletion period a significant weight gain was noted in the groups fed on diets with either 10 or 20 g arginine/kg, but not in the group fed on the diet with 50 g arginine/kg, compared with the diet with 0 g arginine/kg. Mortality rates after infection with Salmonella typhimurium were not decreased by the addition of 10 or 20 g arginine/kg to the diet, and were in fact worsened by supplementation with 50 g arginine/kg. The results of the present study showed that not only are the beneficial effects of arginine supplementation after infection lost when high doses are administered, but also that these high doses become toxic. Mice fed on higher doses showed significant impairment of weight gain and an increase in mortality rates.

Animals↗
PubMed1993

Painful nerve injuries: bridging the gap between basic neuroscience and neurosurgical treatment.

Pain which followed suspected nerve injury was comprehensively evaluated with detailed examination including history, neurologic exam, electrodiagnostic studies, quantitative sensory testing, thermography, anesthetic and sympathetic nerve blocks. Forty two patients treated surgically fell into four discrete groups: 1) Distal sensory neuromas treated by excision of the neuroma and reimplantation of the proximal nerve into muscle or bone marrow, 2) Suspected distal sensory neuromas in which the involved nerve was sectioned proximal to the injury site and reimplanted, 3) Proximal neuromas-incontinuity of major sensorimotor nerves treated by external neurolysis, and 4) Proximal major sensorimotor nerve injuries at points of anatomic entrapment treated by external neurolysis and transposition, if possible. Patient follow up was possible in 40/42 patients (95%) from 2-32 months (average F/U = 11 mo.). Surgical success was defined as: > or = 50% improvement in pain (VAS) or pain relief subjectively rated as good or excellent, and no postoperative narcotic usage. Overall, 40% (16/40) of patients met those criteria. Success rates varied as follows: Group 1 (n = 18) 44%, Group 2 (n = 10) 40%, Group 3 (n = 5) 0%, and Group 4 (n = 7) 57%. A total of 12 of 40 patients (30%) were employed both pre- and postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Electromyography↗
PubMed1993

The surgical treatment of painful traumatic neuromas.

Pain following suspected nerve injury was comprehensively evaluated with detailed examination including history, neurological evaluation, electrodiagnostic studies, quantitative sensory testing, thermography, anesthetic agents, and sympathetic nerve blocks. Forty-two surgically treated patients fell into four discrete groups: Group 1 patients had distal sensory neuromas treated by excision of the neuroma and reimplantation of the proximal nerve into muscle or bone marrow; Group 2 patients had suspected distal sensory neuromas in which the involved nerve was sectioned proximal to the injury site and reimplanted; Group 3 patients had proximal in-continuity neuromas of major sensorimotor nerves treated by external neurolysis; and Group 4 patients had proximal major sensorimotor nerve injuries at points of anatomical entrapment treated by external neurolysis and transposition, if possible. Patient follow-up monitoring from 2 to 32 months (average 11 months) was possible in 40 (95%) of 42 patients. Surgical success was defined as 50% or greater improvement in pain using the Visual Analog Scale or pain relief subjectively rated as either good or excellent, without postoperative narcotic usage. Overall, 16 (40%) of 40 patients met those criteria. Success rates varied as follows: 44% in 18 Group 1 patients, 40% in 10 Group 2 patients, 0% in five Group 3 patients, and 57% in seven Group 4 patients. Twelve (30%) of 40 patients were employed both pre- and postoperatively. It is concluded that: 1) neuroma excision, neurectomy, and nerve release for injury-related pain of peripheral nerve origin yield substantial subjective improvement in a minority of patients; 2) external neurolysis of proximal mixed nerves is ineffective in relieving pain; 3) surgically proving the existence of a neuroma with confirmed excision may be preferable; 4) traumatic neuroma pain is only partly due to a peripheral source; 5) demographic and neurological variables do not predict success; 6) the presence of a discrete nerve syndrome and mechanical hyperalgesia modestly predict pain relief; 7) ongoing litigation is the strongest predictor of failure; and 8) change in work status is not a likely outcome.

Humans↗
PubMed1992

Inhibition of nitric oxide synthesis during endotoxemia promotes intrahepatic thrombosis and an oxygen radical-mediated hepatic injury.

Corynebacterium parvum-treated mice produce large amounts of circulating nitrogen oxides and develop a severe liver injury in response to lipopolysaccharide (LPS). Concurrent administration of NG-monomethyl-L-arginine not only suppresses nitric oxide synthesis in these animals but also profoundly increases the hepatic damage following LPS. In this report, we present evidence that the increased hepatic damage from inhibition of nitric oxide synthesis is mediated in part by superoxide and hydroxyl radicals. The hepatic damage induced by suppressing nitric oxide production during endotoxemia could be reduced by treating mice with superoxide dismutase and deferoxamine, scavengers of superoxide and hydroxyl radicals, respectively. This damage could also be prevented by treating mice with the anticoagulant heparin sodium. The results suggest that nitric oxide synthesis during endotoxemia is important in preventing hepatic damage by reducing oxygen radical-mediated hepatic injury and preventing intravascular thrombosis.

Animals↗
PubMed1992

Sigmoid volvulus in the high altitude of the Andes. Review of 230 cases.

Sigmoid volvulus (SV) is uncommon in the United States. Little has been published in the English literature about the high incidence of SV among rural areas of the Bolivian and Peruvian Andes at 13,000 feet above sea level. A review of 230 cases of SV in a Bolivian hospital is presented. SV accounted for 79 percent of all intestinal obstructions. Nonoperative reduction was attempted in all patients except those with peritonitis. Nonoperative reduction alone was performed in 31 percent of the patients, and 69 percent underwent surgical intervention, 66 percent as an emergency and 3 percent electively. Surgical treatment consisted of sigmoidectomy and primary anastomosis (50 percent), Hartmann's procedure (12 percent), and operative detorsion with sigmoid plication (38 percent). Overall mortality was 13.5 percent. Fifty-seven of the surgically treated patients developed significant complications. The etiology of SV is unclear. High altitude, along with other etiologic factors, may play an important role in SV. To our knowledge, this series represents the highest incidence of SV in bowel obstruction.

Adolescent↗
PubMed1991

Argon beam coagulation is superior to conventional techniques in repair of experimental splenic injury.

Present management of splenic trauma focuses on splenic preservation. However, conventional operative techniques for splenic salvage are time consuming and frequently ineffective. The purpose of this study was to assess the efficacy of the argon beam coagulator (ABC) in the management of experimental splenic injury. Ten adult miniature pigs were randomized to treatment with either conventional surgical techniques (topical Surgicel, electrocautery, suture-ligation, digital pressure) or splenic repair with the ABC. Three standard splenic injuries were made in each pig: capsular avulsion, splenic laceration, and hemisplenectomy. The ABC was more effective in treating all three types of splenic injury. The time required to achieve hemostasis and total operative time were significantly less in the group treated with the ABC for all three types of splenic injuries (p less than 0.05, Student's t-test, two sided). Operative blood loss was significantly less in the group treated with ABC for avulsion and hemisplenectomy (p less than 0.05, Student's t-test, two sided). Recurrent bleeding was significantly higher in the group treated with conventional techniques (p less than 0.001, Fisher's exact test, two-sided). We conclude that the argon beam coagulator is more effective than conventional techniques in treating experimental splenic injuries. The ABC provides more rapid and reliable hemostasis. Clinical trials using the ABC for splenic injury are warranted.

Animals↗
PubMed1991

Bacterial translocation in trauma patients.

Sepsis and multiple system organ failure (MSOF) are major causes of morbidity and mortality in trauma patients. Bacterial translocation induced by hypotension, endotoxemia, or burns is a reproducible phenomenon in the laboratory. The incidence of bacterial translocation to mesenteric lymph nodes (MLNs) in 29 critically ill patients was evaluated to determine its relationship to subsequent sepsis and MSOF. Bacterial translocation was documented in 3 of 4 patients who underwent laparotomy for gastrointestinal (GI) disease. No trauma patient (25 patients), even at second exploration 3-5 days after injury, had a positive MLN culture. Five patients died; 4 trauma patients, one with GI disease. Forty percent of the trauma patients had major complications, predominantly pulmonary infections with gram-negative bacteria. However, infectious complications and outcome were not related to MLN culture results. The classical progression of bacteria from the gut to the bloodstream via the MLNs may require time and gut mucosal injury. The data suggest that bacterial translocation to the MLNs is not a common occurrence in acutely injured trauma patients.

Bacterial Physiological Phenomena↗
PubMed1990

Sympathetic neural outflow directly recorded in patients with primary autonomic failure: clinical observations, microneurography, and histopathology.

We evaluated 2 patients with primary autonomic failure, without clinical peripheral neuropathy. One had primary autonomic failure alone (PAF), and the other had autonomic failure and multiple system atrophy (MSA). Direct intraneural recordings demonstrated a marked reduction of sympathetic efferent nerve impulse activity in the PAF patient. The patient with MSA had spontaneous bursts of sympathetic nerve impulses that confirmed the functional integrity of post-ganglionic sympathetic efferent neurons. Neurosecretory activity of these neurons correlated with the electrophysiologic findings. The PAF patient had markedly reduced supine norepinephrine (NE) levels that did not rise upon standing. The supine NE level in the MSA patient was normal. Morphometric study of biopsied sural nerve in the MSA patient showed that unmyelinated fibers were normal, whereas the nerve of the PAF patient showed clear evidence of past degeneration. We suggest that the primary preganglionic sympathetic defect in MSA releases viable postganglionic sympathetic efferents from central control. Decentralized postganglionic elements may fire spontaneously, thus activating peripheral effectors and providing potentially useful signs and symptoms for differential diagnosis.

Autonomic Fibers, Postganglionic↗
PubMed1989

Chronic hyperalgesia and skin warming caused by sensitized C nociceptors.

A patient suffering from an acquired painful syndrome, due to injury to primary somatic afferent units, was studied. Clinical features included chronic spontaneous burning pain in one hand, abnormal painful response to nonnoxious cutaneous stimuli, and deviation of temperature and dystrophic changes in symptomatic skin. Diagnostic stellate ganglion blocks did not improve spontaneous or stimulus-induced pains, and observation of sympathetic efferent neural activity and vasomotor effector responses revealed no abnormality, failing to support an autonomic contribution to the pathogenesis of the pains. A quantitative psychophysical assessment documented exaggerated magnitude of pain in response to noxious stimuli in symptomatic skin, together with abnormal painful quality and prolongation of sensation induced by nonnoxious tactile or warm stimuli. Such mechanical and thermal hyperalgesia persisted during A fibre blocks, suggesting transmission by primary afferents with unmyelinated C fibres and implying sensitization of C polymodal nociceptors. Direct microneurographic recordings of single, identified C polymodal nociceptors from symptomatic skin confirmed the presence of units with pathologically enhanced receptor responses: lowered threshold and very prolonged afterdischarges. While bypassing skin receptors, strongly intraneural microstimulation in fascicles supplying symptomatic or control skin evoked equivalent magnitudes and temporal profiles of pain from both sides. Thus secondary CNS dysfunction need not be postulated to explain the painful syndrome. Skin grafted onto the affected region partially recovered tactile and thermal sensation (but not pain) without expressing the painful syndrome. This supports the overall conclusion that in this patient A fibres are not involved as primary carriers of input decoded as pain. Sensitization of C polymodal nociceptors is consistent with the features of hyperalgesia in this patient: pain evoked by nonnoxious stimuli, exaggerated pain magnitude, and abnormally prolonged aftersensation of pain. This is the first documentation of chronic sensitization of human C polymodal nociceptors as a symptom of disease. In the context of sensitized C nociceptors and in the absence of sympathetic vasoconstrictor deficit, the abnormally elevated temperature in symptomatic skin is interpreted as due to antidromic vasodilatation triggered by neurosecretion from hyperactive nociceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Heat and mechanical hyperalgesia induced by capsaicin. Cross modality threshold modulation in human C nociceptors.

Quantitative thermal and mechanical algometry was studied in 4 human subjects exposed to various concentrations of capsaicin administered topically to the skin of the palm or forearm. Treated skin patches were assessed for changes in heat pain threshold and in mechanical pain threshold at various controlled temperatures. The results showed that: (1) in addition to heat hyperalgesia, capsaicin consistently induces overt mechanical hyperalgesia; (2) thermal and mechanical hyperalgesias are linearly dependent on the log of capsaicin dose; (3) mechanical hyperalgesia is increased by increasing skin temperature; (4) mechanical hyperalgesia is abolished by cooling the skin to a point about 10 degrees C below the threshold for heat pain, a temperature that does not impair touch or sharp pain sensation. These sensory effects of capsaicin are mediated by C fibres, since dissociated A fibre block established by compression-ischaemia does not abolish either spontaneous pain or mechanical hyperalgesia. In addition, abolition of mechanical hyperalgesia by cooling persists during A fibre block. Cooling thus appears to act directly, presumably decreasing hyperexcitability of the C nociceptor. Hyperalgesia is also transiently depressed for at least 30 min during the postischaemic period, well beyond the duration of paraesthesiae or overt hyperaemia. Sensory changes identical to those induced experimentally by capsaicin have been observed in patients with a particular variety of neuropathic pain (ABC syndrome) and have been termed polymodal hyperalgesia and cross modality threshold modulation (Ochoa, 1986; Ochoa et al., 1987). Based on these overall observations, it is postulated here that the sensory abnormalities induced by capsaicin and those observed in this particular variety of patients relate to primary hyperalgesia and share a common mechanism in that the excitable receptor membrane of polymodal C nociceptors behaves as if it 'misreads' temperature.

Biomechanical Phenomena↗
PubMed1989

Sensations evoked by intraneural microstimulation of C nociceptor fibres in human skin nerves.

1. Seventy-one C polymodal nociceptors supplying glabrous and hairy skin in limbs of awake human volunteers were identified on the basis of cutaneous stimulus-response characteristics recorded intraneurally by microneurography (MNG). The large majority of such units were primarily detected during intraneural microstimulation (INMS) on the basis of subjective quality and cutaneous localization of evoked painful sensation. Electrophysiological studies were supplemented with rigorous psychophysical testing during microstimulation delivered at intraneural C recording sites. 2. The conduction velocity of single C nociceptor units could be shown to become transiently slowed following repetitive INMS at threshold intensity for conscious sensation. Such 'marking' witnessed that particular C units, identified by recording, had been effectively activated during INMS and psychophysical testing. 3. Cognitive attributes of sensations evoked from C recording sites by INMS at threshold intensity for perception were estimated psychophysically for subjective quality, temporal attributes and localized projection. There was remarkable matching of physiological unit type (C polymodal nociceptor) with subjective quality of evoked sensation (dull or burning pain). Further, there was remarkable spatial matching of receptive field of given C nociceptors with projected field of the pain sensation evoked from the C recording site by INMS delivered at threshold intensity for conscious sensation. 4. Dissociated A nerve fibre blocks caused by compression-ischaemia did not abolish the sensation of burning pain projected to hairy skin, evoked by INMS delivered at C recording sites. 5. While the double matching of (a) subjective quality and spatial localization with (b) objective physiological unitary type and receptor location, coupled with the results of A blocks, provide evidence that C nociceptor fibres can be fairly selectively activated during INMS, the results also attest that C polymodal nociceptors from human skin evoke delayed dull or burning pain, accurately projected to a defined locus in skin, even after spatial summation is reduced to a minimum.

Adult↗
PubMed1989

[Complications of acute gastroenteritis caused by Salmonella no typhi].

A review was made of the histories of 125 adult patients admitted for acute gastroenteritis (GEA) due to Salmonella no typhi. The complications that appeared in the series are analyzed. A total of 16 patients (12.8%) presented complications: the most common was bacteremia, 3 had renal tubular necrosis, 2 alithiasic cholecystitis that required surgery, 2 toxic megacolon, 2 rectal hemorrhage, 1 erythema nodosum and 1 intestinal perforation. The authors review the features of each complication.

Acute Disease↗