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Biomedical subjects

L Miao

Publications and source records attributed to L Miao.

68 records · Page 4Linked to original sources
PubMed1994

Cocaine-induced microvascular spasm in Yucatan miniature swine. In vivo and in vitro evidence of spasm.

The purpose of the present study was to determine the maximal coronary flow reserve (CFR) before and after the administration of successive cocaine doses (0.1, 0.5, 3, and 7 mg/kg IV) for 2 minutes at 10-minute intervals in eight miniature swine. CFR was assessed by the administration of adenosine (0.03, 0.3, and 3 mg IC). Hemodynamic and flow measurements were performed 3 minutes after each dose. Coronary flow (CF) was measured with a Doppler-tipped wire in the proximal left anterior descending coronary artery (LAD). Also, microvessels were dissected, and vessel diameters were measured by a videoelectronic dimension analyzer. In vivo, LAD CF increased fourfold, CFR increased twofold, and coronary vascular resistance (CVR) decreased fourfold after the administration of adenosine. In contrast, LAD CF decreased threefold, CFR decreased onefold, and CVR increased sixfold 3 minutes after the administration of cocaine. Adenosine (3 mg) was repeated 4 minutes after the administration of cocaine, and LAD CF increased 1.4-fold, CVR increased 2.5-fold, and CFR decreased onefold. Thus, adenosine partially reversed the potent cocaine constrictor effect. In vitro, 10(-9) mol/L cocaine decreased the diameter of the coronary microvessels from 129 +/- 12 to 127 +/- 12 microns, and 10(-4) mol/L cocaine decreased coronary microvessel diameter to 114 +/- 15 microns (P < .05). In conclusion, cocaine in vivo decreases CFR, and consistent with the in vivo effect, cocaine in vitro produced constriction of vessels < 200 microns. These results indicate that cocaine can produce profound microvascular spasm. This may contribute to the ischemia/infarction reported in patients who abuse cocaine and who are subsequently found to have normal epicardial coronary arteries.

Adenosine↗
PubMed1994

Effects of cocaine on carotid vascular reactivity in swine after balloon vascular injury.

BACKGROUND AND PURPOSE: The use of cocaine has been associated with stroke. To evaluate carotid vasospasm as a potential mechanism of cocaine-induced stroke, we studied 12 swine immediately and 10 weeks after angioplasty. METHODS: We compared the short- and long-term vasoconstrictor responses of normal and injured arterial segments to nitroglycerin, histamine, and cocaine in vivo by carotid angiography. We also compared the isometric contractile force responses to different vasoactive substances in normal and injured vascular rings in vivo, and we tested the direct action of cocaine on both arterial segments. RESULTS: In in vivo studies, immediately after angioplasty, luminal diameter in the control segment decreased by 30% with histamine 30 micrograms/kg and by 23% with cocaine 10 mg/kg (P < .001). In contrast, neither histamine nor cocaine produced vasoconstriction in the angioplasty segment. Thus, a transient loss of vasoconstriction occurred at the angioplasty site. Ten weeks later, histamine 30 micrograms/kg significantly (P < .001) decreased luminal diameter by 34% in the control and by 33% in the angioplasty segment; similarly, cocaine 10 mg/kg significantly (P < .001) decreased luminal diameter by 26% in the control and by 34% in the angioplasty segment. Thus, 10 weeks after angioplasty, the transitory loss of carotid vasoconstriction in response to histamine and cocaine reverted, and a moderate generalized vasoconstriction occurred in both segments without localized vasospasm. In vitro, the maximal isometric tension responses to KCl, acetylcholine, histamine, and phenylephrine were similar in vascular rings from normal and angioplasty segments. The median effective doses to histamine and phenylephrine were similar. In contrast, cocaine in concentrations from 10(-7) to 10(-3) mol/L failed to produce any isometric contraction in vitro. CONCLUSIONS: Cocaine in vivo produced a generalized carotid vasoconstriction without evidence of localized vasospasm; since there was no response to cocaine in vitro, the in vivo effect was most likely mediated by neurohumoral factors rather than by a direct action of cocaine on vascular smooth muscle.

Angioplasty, Balloon↗
PubMed1993

Cellular mechanism of the positive inotropic effect of hydralazine in mammalian myocardium.

1. The purpose of this study was to elucidate the cellular mechanism of the positive inotropic effect of hydralazine, a vasodilator widely used for afterload reduction in patients with heart failure that has also been reported to have positive inotropic effects on the heart. After isolation, right ventricular papillary muscles from the ferret were maintained in bicarbonate-buffered salt solution (30 degrees C). A concentration-response relationship was obtained for hydralazine (10(-6) to 10(-3) M). In order to mimic different levels of catecholamine release found in heart failure, we utilized two methods of stimulation: (a) threshold punctate pulses and (b) suprathreshold punctate stimulation with voltage approximately 10% above threshold. 2. In a first group of muscles (n = 16), a maximally effective concentration of hydralazine (10(-3) M) increased peak isometric tension by 39 +/- 9% (P < 0.05). Doses lower than 10(-5) M had no significant effect. The bioluminescent Ca2+ indicator, aequorin, was loaded into a subset of these muscles (n = 7). A significant increase in peak light (i.e., intracellular Ca2+) developed, concurrently with an increase in peak tension (38 +/- 5% to 66 +/- 8%). This inotropic response was associated with a decrease in time to peak tension (ms), 221 +/- 7 to 186 +/- 5 (P < 0.05), and time to peak light, 65 +/- 4 to 52 +/- 2 (P < 0.05). These effects were markedly attenuated by pretreatment with autonomic blocking agents. 3. In a second group of muscles (n = 12), histamine was used to stimulate cyclic AMP production in the presence of propranolol. Hydralazine (3 x 10-4 M) led to a shift in the pD2 (i.e. the negative log of the concentration of histamine producing 50% of the maximal response) from 6.1 +/- 0.1 to 5.9 +/- 0.1(P <0.05), thus increasing the sensitivity of the muscles to histamine. Hydralazine also increased maximum tension from 160 +/- 77% to 195 +/- 57% (P <0.05) above baseline. Thus, hydralazine altered the potency and efficacy of histamine despite the presence of beta-adrenoceptor blockade.4. A third group of muscles were chemically skinned to examine the effects of hydralazine on myofilament Ca2+ responsiveness. Pretreatment of ferret papillary muscles with hydralazine (10-3 M)before skinning did not shift the force-pCa curve after skinning (n = 16). However, hydralazine added to previously skinned fibres desensitized the myofilaments, as indicated by a rightward shift of the force-pCa curve (n = 12). Maximum tension development was not changed.5. The pharmacological effects of hydralazine are characteristic of inotropic drugs that act mainly via cyclic AMP; however, the increase in peak tension demonstrated with histamine in the presence of hydralazine also suggests an effect on cyclic AMP-independent second messenger pathways. These data are consistent with reports that large doses of hydralazine may increase cellular levels of cyclic AMP, as well as other second messengers, by direct cardiac and indirect neuronal mechanisms.

Actin Cytoskeleton↗
PubMed1993

[Effect of different preparation crafts on the content of baicalin in shuanghuanglian (SHL) injection].

The content of baicalin is stable when baicalin is added quantitatively in preparation. The time of extraction of the effective components of SHL with alcohol and the concentration of alcohol have little effect on the content of baicalin. The components can be extracted once, and the content of alcohol is preferably 85%. The pH level has greater influence on the content of baicalin, and should be controlled between 7.0 to 8.0. 0.2% activated carbon is suitable in preparation.

Charcoal↗
PubMed1982

Randomized clinical trial of perioperative cefoxitin in preventing maternal infection after primary cesarean section.

To determine the efficacy of perioperative cefoxitin in preventing infections after primary cesarean section, a randomized placebo-controlled, double-blind clinical trial was performed. Among 266 participants, those who received three perioperative 2 gm doses of cefoxitin (138) had significantly fewer serious infections (19.5% vs. 4.3%), fewer urinary tract infections (10.7% vs. 4.4%), less standard febrile morbidity (9.4% vs. 3.6%), and fewer courses of antibiotics postoperatively (23.4% vs. 11.6%). There was no reduction in the length of hospitalization. Use of perioperative cefoxitin umbilical cord is clamped are safe and efficacious in preventing infection after primary cesarean section.

Cefoxitin↗
PubMed1982

Bacteriuria and subsequent mortality in women.

The relation of bacteriuria to subsequent mortality was investigated in population-based cohort data from women living in Jamaica and Wales. Three surveys were done in each location over a 13-year period. Women with 10(5) or more gram-negative bacilli per millilitre of urine in three consecutive cultures over a 3-week span were considered bacteriuric for that survey. Mortality was determined at the second and third surveys. Bacteriuria was associated with increased mortality both in the crude data and in life-table analyses adjusted for the confounding effects of age and weight. The adjusted risk ratio for death between the first and third surveys was 1.5 for women bacteriuric at the first survey compared with non-bacteriuric women. For deaths between the second and third surveys, the adjusted risk ratio was highest (2.0) in women who were bacteriuric at both of the first two surveys. The adjusted risk ratio for death between the second and third surveys for women who were bacteriuric at one of the first two surveys but not at the other was 1.6.

Adolescent↗
PubMed1978

Bacteriuria in a population-based cohort of women.

A survey for bacteriuria was conducted in a community-wide, unselected population of women 16--69 years old. The overall prevalence of bacteriuria was 3.5%. The prevalence of bacteriuria increased with age with a linear trend, but with a significant nonlinear component as well. Bacteriuria was associated with parity after correction for the effects of age. Current symptoms of dysuria and a history of previous urinary tract infection were slightly but significantly more common in women with bacteriuria. The population described should serve as an adequate base for continuing studies of the possible consequences of bacteriuria.

Adolescent↗
PubMedDate not supplied

Rationale and methods for a statewide, prospective surveillance system for the identification and prevention of nosocomial infections.

Review of current methods of surveillance for nosocomial infection indicates that prospective surveillance of patients on a daily basis is the most accurate and valid method. In this paper, we detail such a method. Samples of hospitalized patients for surveillance are based on a fixed period of observation in each patient-care area. Data are collected on a detailed, standardized daily log that emphasize the recording of primary clinical data. Such a system is practical and is acceptable to infection control practitioners. Representative samples of patients are obtained. The utility of such a system for identifying preventable risk factors for the development and evaluation of programs of prevention is being tested in 12 acute-care hospitals in Rhode Island.

Cross Infection↗
PubMedDate not supplied

Enhanced lipolysis in normal mice expressing liver-derived human lipoprotein lipase after adenoviral gene transfer.

The authors previously demonstrated that the gene for human lipoprotein lipase (hLPL), an enzyme crucial to the breakdown of triglyceride (TG)-rich dietary fats, corrects the hypertriglyceridemia in lipoprotein lipase (LPL)-deficient knockout mice after adenoviral (Ad)-mediated LPL gene transfer. They have now extended their observations to primary cultured mouse hepatocytes and intact animals of normal LPL genotype, and confirm effective overexpression of hLPL from the liver and a sustained TG-lowering effect in plasma over 60 days. A typical first-generation Ad-vector containing the hLPL cDNA (Ad-LPL) resulted in efficient gene transfer into isolated mouse hepatocytes and significant de novo synthesis of active hLPL protein. In this experiment, 5 x 10(9) viral particles (5 x 10(7) pfu) of either Ad-LPL or an Ad-LacZ control vector were injected into CD1 mice of normal LPL genotype. Hepatic expression of hLPL was confirmed at Day 7 postinjection by in situ hybridization and direct measurement of LPL in the liver. This correlated with a total LPL activity (human + mouse) in postheparin plasma (PHP) of 1020.5 standard deviation [SD] 93.6 mU/mL, versus 479.5 SD 129.7 mU/mL (p < 0.001) in Ad-LacZ controls at Day 7. Respective hLPL activity comprised 49% of the total. Significantly raised levels of hLPL protein mass persisted until Day 60. Corresponding plasma TGs decreased to 39% of Ad-LacZ controls at Day 7, and, despite absent hLPL activity from Day 28 on, serum TGs remained significantly lower in Ad-LPL mice up to Day 42. Fast phase liquid chromatography analysis showed a dramatic depletion in TG-rich lipoproteins, mainly very low density lipoproteins (VLDL) and chylomicron fractions. Therefore, Ad-mediated overexpression of hepatic LPL was found to significantly decrease plasma TG levels unrelated to primary LPL deficiency.

Adenoviridae↗