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Biomedical subjects

A H Li

Publications and source records attributed to A H Li.

9 recordsLinked to original sources
PubMed1991

Acetazolamide on the ventral medulla of the cat increases phrenic output and delays the ventilatory response to CO2.

1. Acetazolamide (0.1 mM) applied to the surface of the rostral ventrolateral medulla or microinjected beneath the medullary surface in chloralose-urethane-anaesthetized, vagotomized, carotid-denervated, paralysed, servo-ventilated cats produced a long-lasting increase in integrated phrenic nerve activity. 2. Extracellular pH measured beneath the rostral ventrolateral medulla exhibited a long-lasting decrease after surface acetazolamide but was not a good predictor, in each individual animal, of changes in phrenic activity. 3. Medullary carbonic anhydrase inhibition reduced the slope and the half-time of the phrenic response to rapid step CO2 increases. Conversely, acetazolamide did not affect the phrenic response to steady-state CO2 increases. 4. These data indicate that localized inhibition of medullary carbonic anhydrase causes a centrally mediated increase in ventilation that we attribute to medullary tissue hypercapnia and acidosis. In addition, these data indicate that medullary carbonic anhydrase may play a role in central CO2 chemotransduction.

Acetazolamide↗
PubMed1991

Lesions in retrotrapezoid nucleus decrease ventilatory output in anesthetized or decerebrate cats.

Kainic acid (KA) injections into the retrotrapezoid nucleus (RTN) of anesthetized deafferented cats profoundly decreased phrenic activity (PA) and CO2 sensitivity (J. Appl. Physiol. 68: 1157-1166, 1990). In this study small electrolytic lesions of the RTN produced the same results, indicating that the KA destroyed cells. We then asked whether anesthetic depression or the absence of peripheral chemoreceptors could explain the degree of respiratory depression observed. In decerebrate cats electrolytic lesions of the RTN resulted in a decrease in PA similar to that seen under anesthesia. CO2 sensitivity was decreased by RTN lesions that extended into the caudal RTN but less so than under anesthesia. KA injections resulted in an initial increase in PA followed by a continuous decrease, a pattern similar to that seen under anesthesia but with a slower time course. CO2 sensitivity was essentially absent. Peripheral chemodenervation produced a small further decrease in PA and a downward shift of the CO2 response without change in slope. Blood pressure was unaffected by RTN lesions but was decreased by more-caudal lesions without respiratory effects. The RTN appears to be necessary for the maintenance of eupneic phrenic activity and CO2 sensitivity even in decerebrate cats with intact peripheral chemoreceptors.

Anesthesia↗
PubMed1990

Fluorescence location of RVLM kainate microinjections that alter the control of breathing.

Kainic acid (4.7 mM) applied to the rostral ventrolateral medulla (RVLM) surface decreases phrenic output, CO2 sensitivity, and blood pressure in chloralose-urethan-anesthetized, vagotomized, paralyzed, glomectomized, servoventilated cats. In this study using the same preparation, bilateral 50- to 100-nl kainate injections just below the RVLM surface better localized these responses topographically. The physiological responses to unilateral 10-nl kainate injections were then correlated with anatomic location determined by fluorescent microbeads (0.5 micron diam). Many sites were associated with no effect, a few rostral and caudal sites with increased phrenic activity, and cluster of sites with decreased phrenic activity often to apnea, decreased CO2 sensitivity, and decreased responses to carotid sinus nerve stimulation. Blood pressure was unaffected. These sites, within 400 microns of the surface, were ventral to the facial nucleus, ventrolateral to the nucleus paragigantocellularis lateralis, caudal to the superior olive, and rostral to the retrofacial nucleus. They appeared to be within the recently described retrotrapezoid nucleus, which contains cells with respiratory-related activity and projections to the dorsal and ventral respiratory groups. Cells within this site appear able to provide tonic input to respiration and to affect peripheral and central chemoreception.

Animals↗
PubMed1990

Ventral medulla sites of muscarinic receptor subtypes involved in cardiorespiratory control.

Bilateral 10-nl injections of the muscarinic (M1) receptor antagonist pirenzepine (PZ) and the M3-antagonist 4-diphenylacetoxy-N-methylpiperidine (DAMP) just below the surface of the rostral ventrolateral medulla (VLM) in anesthetized, paralyzed, vagotomized, glomectomized, servo-ventilated cats decreased base-line phrenic activity and CO2 sensitivity but not blood pressure. Unilateral 10-nl injections of PZ, DAMP, or the M2-antagonist AFDX-116 resulted in the following. AFDX-116 greater than PZ greater than DAMP decreased blood pressure. DAMP greater than PZ greater than AFDX-116 decreased base-line phrenic activity and the CO2 response slope. Many injections had no effect, and some affected only one variable. The injection sites were within 700 microns of the VLM surface extending from the caudal aspect of the superior olive through a region ventromedial to the facial nucleus to the rostral aspect of the inferior olive. In a small number of experiments the response to carotid sinus nerve stimulation was affected by some injections of each antagonist. In the rostral VLM cardiovascular regulation involves M2-receptors, whereas respiratory regulation involves predominantly the M3-subtype. Neurons with these receptors appear to be closely intermingled.

Animals↗
PubMed1989

Changes of plasma amino acids in total parenteral nutrition-supported patients with intraabdominal infection.

Plasma aminogram changes were prospectively studied in 95 patients with external enteric fistula and intraabdominal infection who were under total parenteral nutrition (TPN) therapy with anfuming 14s. Plasma amino acids and albumin were determined before the administration of TPN, weekly and at the end of the therapy or 2 to 5 days before death of patients. In patients with sepsis and starvation, the aminogram showed remarkably low total free amino acids before TPN therapy. In survivors, free amino acids increased gradually to normal in 2 weeks after use of TPN and in the dead increased rapidly to a significantly high peak at the terminal stage. In both survivors and deceased, phenylalanine level remained high during the study. In response to infection, proline was also elevated but to a lesser degree; the ratio of branched chain amino acid (BCAA) to aromatic amino acid (AAA) was lower than normal and the decrease of arginine was parallel to the severity of infection. We conclude that the ideal amino acid preparation for the starved, septic patients should be high in BCAA and arginine but low in phenylalanine; the administration of inappropriate exogenous amino acids in metabolically decompensated septic patients may bring about more harm than benefit; and in septic patients the persistently elevated level of plasma phenylalanine and proline along with decrease of arginine is a useful prognostic sign.

Amino Acids↗