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H Ting

Publications and source records attributed to H Ting.

9 recordsLinked to original sources
PubMed2005

GABAergic modulation of ventilatory response to acute and sustained hypoxia in obese Zucker rats.

OBJECTIVE: To determine whether altered central and/or peripheral gamma-aminobutyric acid (GABA)ergic mechanisms acting in GABA(A) receptors contribute to the abnormal ventilatory response to acute and sustained hypoxia in obese Zucker rats. METHODS: In all, 10 lean and 10 obese Zucker rats were studied at 12 weeks of age. Ventilation (V(.-)(E)), tidal volume (V(T)), and breathing frequency (f) during room air breathing and in response to sustained (30 min) hypoxic (10% O(2)) challenges were measured on three separate occasions by the barometric method following the randomized blinded administration of equal volumes of DMSO (vehicle), bicuculline methiodide (B(M), 1 mg/kg, peripheral GABA(A) receptor antagonist), or bicuculline hydrochloride (B(HCl), 1 mg/kg, peripheral and central GABA(A) receptor antagonist). RESULTS: Administration of B(M) and B(HCl) in lean animals had no effect on ventilation either during room air breathing or 30 min of sustained exposure to hypoxia. Similarly, B(M) failed to alter ventilation in obese rats. In contrast, B(HCl) significantly (P<0.05) increased V(.-)(E) and V(T) during room air breathing and 10-30 min of hypoxic exposure in obese rats. During 5 min of acute hypoxic exposure, V(T) remained elevated with B(HCl) in obese rats, but the V(.-)(E) appeared not to be increased with B(HCl) due to a decrease in f. CONCLUSION: Thus, endogenous GABA modulates both ventilation during room air breathing and ventilatory response to sustained hypoxia in obese, not in lean, Zucker rats by acting specifically on GABA(A) receptors located within the central, not peripheral, nervous system. However, endogenous GABA does not modulate ventilation but the pattern of breathing during acute hypoxia in obesity in a different manner from that during sustained hypoxia.

Acute Disease↗
PubMed2001

Use of sonography and radioisotope renography to diagnose hydronephrosis in patients with spinal cord injury.

OBJECTIVE: To study the accuracy of sonography and radioisotope renography in detecting hydronephrosis in patients with spinal cord injury (SCI). DESIGN: Prospective, blinded comparison study. SETTING: Rehabilitation hospital affiliated with a medical college. PARTICIPANTS: One hundred and nine patients with SCI (21 women, 88 men) participated. INTERVENTIONS: Comprehensive urologic examinations including clinical evaluation, laboratory tests, intravenous urography (IVU), sonography, radioisotope renography (renal scan), voiding cystourethrography, and cystometry. The findings at sonography and renal scan were separately compared with the final diagnosis interpreted by IVU and clinical findings. MAIN OUTCOME MEASURES: Effective renal plasma flow, pyelocaliectasis, and positive and negative predictive value. RESULTS: A total of 235 kidneys were analyzed. Sonography correctly excluded the presence of hydronephrosis in 173 of 192 nonobstructed kidneys. Sonograms were interpreted as positive in 41 of 43 kidneys with documented hydronephrosis. Renal scan correctly excluded 161 nonobstructed kidneys. The renal scan detected 39 of 43 kidneys with hydronephrosis. The sensitivity of sonography was.96 with a specificity of.90. Renal scan reached a sensitivity of.91 with a specificity of.84. CONCLUSION: Sonography and renal scan are safe, sensitive, and specific for detecting hydronephrosis. Combined use of both methods appears to be a reliable alternative to IVU in the long-term follow-up for patients with SCI with neurogenic bladder dysfunction.

Adolescent↗
PubMed2001

Carbon dioxide pressure-concentration relationship in arterial and mixed venous blood during exercise.

To calculate cardiac output by the indirect Fick principle, CO(2) concentrations (CCO(2)) of mixed venous (Cv(CO(2))) and arterial blood are commonly estimated from PCO(2), based on the assumption that the CO(2) pressure-concentration relationship (PCO(2)-CCO(2)) is influenced more by changes in Hb concentration and blood oxyhemoglobin saturation than by changes in pH. The purpose of the study was to measure and assess the relative importance of these variables, both in arterial and mixed venous blood, during rest and increasing levels of exercise to maximum (Max) in five healthy men. Although the mean mixed venous PCO(2) rose from 47 Torr at rest to 59 Torr at the lactic acidosis threshold (LAT) and further to 78 Torr at Max, the Cv(CO(2)) rose from 22.8 mM at rest to 25.5 mM at LAT but then fell to 23.9 mM at Max. Meanwhile, the mixed venous pH fell from 7.36 at rest to 7.30 at LAT and to 7.13 at Max. Thus, as work rate increases above the LAT, changes in pH, reflecting changes in buffer base, account for the major changes in the PCO(2)-CCO(2) relationship, causing Cv(CO(2)) to decrease, despite increasing mixed venous PCO(2). Furthermore, whereas the increase in the arteriovenous CCO(2) difference of 2.2 mM below LAT is mainly due to the increase in Cv(CO(2)), the further increase in the arteriovenous CCO(2) difference of 4.6 mM above LAT is due to a striking fall in arterial CCO(2) from 21.4 to 15.2 mM. We conclude that changes in buffer base and pH dominate the PCO(2)-CCO(2) relationship during exercise, with changes in Hb and blood oxyhemoglobin saturation exerting much less influence.

Adult↗
PubMed2001

A noninvasive assessment of pulmonary perfusion abnormality in patients with primary pulmonary hypertension.

STUDY OBJECTIVES: The ventilatory equivalent for CO(2) (ie, the ratio of minute ventilation [VE] to carbon dioxide output [VCO(2)]) is increased in patients with primary pulmonary hypertension (PPH) consequent to an increase in physiologic dead space and alveolar ventilation. We wished to see whether the VE/V(2) ratio correlated with the abnormality in pulmonary hemodynamics in PPH patients and whether it changed in response to prostacyclin infusion. METHODS: Following right-sided heart catheterization, 10 patients with severe PPH were studied in the coronary-care unit while hemodynamic and gas exchange measurements were measured simultaneously before and after infusion with epoprostenol (Epo), a prostacyclin analog. Studies were performed at baseline and during IV infusion of two to three increasing dosages of Epo in 10 PPH patients (NYHA class III-IV). Four patients had radial artery catheters for simultaneous blood gas measurements. Nine healthy subjects who were matched by sex, height, and weight underwent gas exchange analyses only. RESULTS: The mean (+/- SD) VE/VCO(2) ratio was higher in PPH patients than in control subjects (50.7 +/- 9.7 vs 30.6 +/- 3.8; p < 0.001). Thirteen measurements made in four patients showed that the VE/VCO(2) ratio correlated with the physiologic dead space/tidal volume ratio (r = 0.78; p = 0.002). The VE/VCO(2) ratio measurement at baseline correlated significantly with total pulmonary vascular resistance (TPVR) (r = 0.70; p = 0.02) but not with mean pulmonary artery pressure (mPAP) or cardiac index. During Epo infusion, the VE/VCO(2) ratio decreased with increasing dosage in 6 of 10 patients, with no change or slight increases in the 4 remaining patients. Considering all doses, the VE/VCO(2) ratio decreased significantly in response to the short-term administration of Epo. The decrease tended to parallel the pattern of decrease in TPVR, but the changes in both variables were too small to provide a statistically significant correlation. The mPAP did not change significantly in response to Epo infusion, although TPVR did change at the highest dosage. CONCLUSIONS: In patients with severe PPH, the VE/VCO(2) ratio correlated significantly with TPVR but not with mPAP or cardiac index. The VE/VCO(2) ratio decreased systematically from baseline with the dose of Epo in some but not all patients. The VE/VCO(2) ratio and TPVR decreased significantly in response to Epo when all doses were considered. Further studies are needed to elucidate whether noninvasive gas exchange measurements may be clinically useful in the evaluation of the severity of pulmonary vascular disease and the effectiveness of pulmonary vasodilator therapy.

Cardiac Catheterization↗
PubMed2000

Comparison of exercise cardiac output by the Fick principle using oxygen and carbon dioxide.

BACKGROUND AND STUDY OBJECTIVE: Theoretically, cardiac output (CO) calculated by the Fick principle should be the same using O(2) (CO[O2]) or CO2 (CO[CO2]) as the test gas. However, agreement depends on the accuracy of gas exchange and blood gas measurements and the validity of the equations to convert measured variables into blood gas contents. Considering the widespread use of indirect estimates of pulmonary artery blood PCO2 and CO2 content to measure Fick principle CO during exercise, we wished to determine whether CO[O2] and CO[CO2] were equal during exercise and whether CO[CO2] could be accurately and precisely determined using direct measures of pulmonary artery blood. PREPARATION AND METHODS: Five healthy young nonsmoking volunteer men performed incremental exercise from rest to peak exercise on two separate occasions with intervening rest. Catheters were placed in brachial and pulmonary arteries to allow repeated blood sampling every minute during concurrent breath-by-breath gas exchange measurements from rest to peak exercise. CO[O2] was compared with CO[CO2] at multiple levels of exercise. Using standard equations, arterial and mixed venous O2 contents were calculated from hemoglobin concentration (Hb), oxyhemoglobin saturation (SO2), and PO2, whereas CO2 contents were calculated from PCO2, pH, Hb, and SO2. Blood gas analyzers were used for measurement of pH, PCO2, and PO2, and a co-oximeter was used for measurement of Hb and SO2. Initial calculations suggested that exercise CO[CO2] was 14% higher than CO[O2] and helped disclose small systematic measurement errors in PCO(2) for values > 45 mm Hg detected by proficiency testing surveys and documented with blood tonometry in the blood gas analyzer. RESULTS: After correcting PCO2 for the small systematic measurement error found, the measures and equations used to calculate arterial and mixed venous O2 and CO2 contents were adequate to provide mean CO values that are reasonably similar. However CO[CO2] values were more than twice as variable as CO[O2]. CONCLUSIONS: The increased variability of Fick principle CO[CO2] compared with CO[O2] is attributable to the much lower extraction ratio for CO2 and the greater complexity in calculation of blood CO2 than O2 contents. These results raise concerns about the accuracy and precision of estimating CO and stroke volume using CO2 as a test gas, even with direct measurement of blood CO2 contents in normal subjects.

Adult↗
PubMed1999

Clopidogrel versus ticlopidine after intracoronary stent placement.

OBJECTIVES: The study compared the safety and efficacy of ticlopidine with clopidogrel in patients receiving coronary stents. BACKGROUND: Stent thrombosis is reduced when ticlopidine is administered with aspirin. Clopidogrel is similar to ticlopidine in chemical structure and function but has fewer side effects; few data are available about its use in stent patients. METHODS: We compared 30-day event rates in 500 consecutive coronary stent patients treated with aspirin and clopidogrel (300 mg loading dose immediately prior to stent placement, and 75 mg/day for 14 days) to 827 consecutive stent patients treated with aspirin and ticlopidine (500 mg loading dose and 250 mg twice daily for 14 days). RESULTS: Patients treated with clopidogrel had more adverse clinical characteristics including older age, more severe angina, and more frequent infarction within the prior 24 h. Nonetheless, mortality was 0.4% in clopidogrel patients versus 1.1% in ticlopidine patients; nonfatal myocardial infarction occurred in 0% versus 0.5%, stent thrombosis in 0.2% versus 0.7%, bypass surgery or repeat angioplasty in 0.4% versus 0.5%, and any event occurred in 0.8% versus 1.6% of patients, respectively (p = NS). Based on the observed 30-day event rate of 1.6% with ticlopidine, the statistical power of the study was 43% to detect an even rate of 0.5% with clopidogrel, and 75% to detect an event rate with of 4% with clopidogrel, with a p value of 0.05. CONCLUSIONS: These data indicate that clopidogrel can be safely substituted for ticlopidine in patients receiving coronary stents.

Aged↗
PubMed1999

Aerobically generated CO(2) stored during early exercise.

Previous studies have shown that a metabolic alkalosis develops in the muscle during early exercise. This has been linked to phosphocreatine hydrolysis. Over a similar time frame, the femoral vein blood pH and plasma K(+) and HCO(-)(3) concentrations increase without an increase in PCO(2). Thus CO(2) from aerobic metabolism is converted to HCO(-)(3) rather than being eliminated by the lungs. The purpose of this study was to quantify the increase in early CO(2) stores and the component due to the exercise-induced metabolic alkalosis (E-I Alk). To avoid masking the increase in CO(2) stores by CO(2) released as HCO(-)(3) buffers lactic acid, the transient increase in CO(2) stores was measured only for work rates (WRs) below the lactic acidosis threshold (LAT). The increase in CO(2) stores was evident at the airway starting at approximately 15 s; the increase reached a peak at approximately 60 s and was complete by approximately 3 min of exercise. The increase in CO(2) stores was greater, but the kinetics were unaffected at the higher WR. Three components of the change in aerobically generated CO(2) stores were considered relevant: the carbamate component of the Haldane effect, the increase in CO(2) stores due to increase in tissue PCO(2), and the E-I Alk. The Haldane effect was calculated to be approximately 5%. Physically dissolved CO(2) in the tissues was approximately 30% of the store increase. The remaining E-I Alk CO(2) stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O(2) uptake correlated with the time course of the increase in CO(2) stores; the size of the O(2) deficit correlated with the size of the E-I Alk component of the CO(2) stores. We conclude that a major component of the aerobically generated increase in CO(2) stores is the new HCO(-)(3) generated as phosphocreatine is converted to creatine.

Adult↗
PubMed1985

N-terminal amino acid sequence and some properties of isopenicillin-N synthetase from Cephalosporium acremonium.

Isopenicillin-N synthetase (IPNS) was purified to homogeneity from Cephalosporium acremonium C0728. The enzyme existed in two states during purification; an oxidised state with a disulphide linkage and its reduced state. These two forms can be interconverted in the presence or absence of thiol agents, and separated by fast protein liquid chromatography (FPLC) with the strong anion exchange Mono-Q column. The enzyme is a monomer with a molecular mass of 38 kDa and pI 5.05. The first 50 amino acid N-terminal sequence of the enzyme was determined. The purified enzyme has an absolute requirement of Fe2+ and a 2-electron donor for activity.

Acremonium↗