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Biomedical subjects

H Ha

Publications and source records attributed to H Ha.

90 records · Page 5Linked to original sources
PubMed1989

Difficult tracheal extubation.

We describe a case of nasotracheal tube fixation with a screw. A second case is described in which a broken drill bit was found to impinge on the wall but not penetrate into the lumen of a nasotracheal tube. Possible sequelae of this complication include airway leak, aspiration, tube obstruction, and trauma from attempts at forceful extubation. We recommend the routine intraoperative testing for tracheal tube movement and routine fibreoptic bronchoscopy through the tube when blind surgical procedures occur in the vicinity of a tracheal tube.

Adolescent↗
PubMed1987

Limited capacity for renal vasodilatation in anesthetized diabetic rats.

Studies were conducted to determine whether reduced renal blood flow (RBF) exhibited by rats with uncontrolled streptozotocin (STZ)-induced diabetes is attributable to diabetes-induced structural changes in the renal vasculature. Vehicle-treated control rats (CR) and rats that were injected with STZ (STZR) after pretreatment with 3-O-methylglucose (3-OMG), an agent that prevents STZ-induced hyperglycemia, were also studied. Basal values of total RBF (ml.min-1.g kidney wt-1, electromagnetic flow probe), systemic arterial pressure (BP, mmHg), and renal vascular resistance (RVR, BP/RBF) in pentobarbital-anesthetized rats during a control period were 5.4 +/- 0.3 (P less than 0.01 vs. CR), 116 +/- 3, and 21.9 +/- 1.0 (P less than 0.01 vs. CR) in STZR (n = 12) and 8.2 +/- 0.4, 121 +/- 2, and 15.3 +/- 1.0 in CR (n = 11), respectively. Basal values of RBF, BP, and RVR in 3-OMG-pretreated STZR were identical to CR. The relative capacity of STZR and CR kidneys for vasodilatation in situ in response to intrarenal arterial infusions of acetylcholine (ACh) and bradykinin (BK) and systemically administered sodium nitroprusside (NP) was evaluated. The capacity of STZR to exhibit active renal vasodilatation in response to intrarenal arterial ACh and BK was significantly less than that of CR (P less than 0.01). The minimum level to which RVR was suppressed after 50 micrograms NP/kg iv was higher in STZR than in either CR or 3-OMG-pretreated STZR (14.8 +/- 1.5 vs. 9.0 +/- 0.7 and 9.3 +/- 1.5 mmHg.ml-1.min.g kidney wt, respectively; P less than 0.05). This dose of NP exerted effective functional antagonism of renal vasoconstriction induced by exogenous norepinephrine and angiotensin II. These in vivo studies suggest that the elevated RVR in STZR might be attributable in part to structural changes in the renal vasculature that are associated with the diabetic state and limit the capacity for renal vasodilatation. However, there was no difference in pressure-flow relationships between the two groups in maximally dilated isolated kidneys perfused with Krebs buffer containing 5% albumin, and the RBF deficit in STZR kidneys was corrected by perfusion with blood from CR. Thus the decreased RBF exhibited by STRZ in vivo cannot be attributed solely to renal vascular structural changes associated with diabetes. These findings suggest that undefined humoral factors or abnormal interaction of formed blood elements with vessel walls may account for elevated RVR in STZR.

3-O-Methylglucose↗
PubMed1984

The dexamethasone suppression test in adolescent psychiatric patients.

The authors administered a structured psychiatric interview, the Kiddie-SADS, and the dexamethasone suppression test (DST) to 42 adolescent psychiatric inpatients. Of the 26 adolescents diagnosed as depressed, nine (36.4%) failed to suppress cortisol, and of the 16 nondepressed adolescents, three (18.8%) also failed to suppress cortisol. There was no significant association between the diagnosis of depression and the failure to suppress cortisol during the DST. The use of the DST to diagnose endogenous major depressive illness in adolescents seems to be a premature clinical application of an important investigative finding.

Adolescent↗
PubMed1975

The role of the medial lemniscal and spinocervicothalamic pathways on tactile reactions in cats.

The role of dorsal column (DC)-medial lemniscus and spinocervicothalamic systems on tactile reactions, placing and tactile localization (turning to localize a point touched on the body) was studied in cats with spinal and bulbar lesions. The cats with vision occluded were trained preoperately on horizontal bars for tactile localization. The bulbar lesions of cervicothalamic tract (CTT), which anatomically overlaps with gracile nuclear efferent projection, resulted in permanent loss of tactile placing and localization in contralateral hindlimb. Section of dorsal half of lateral funiculus at C3, which interrupts afferents to lateral cervical nucleus but also involves descending motor pathways, gave loss of tactile placing without impairment of tactile localization. However, combined lesions of both systems abolished tactile placing and localization permanently. Results suggest that tactile placing and localization persists after CTT lesion alone; temporarily loss after DC section but permanently abolished after destruction of both systems. It. is also noted that cats after lesions of both systems without involving motor pathways could walk on bars without vision. The deficits following combined lesions are suggested to be primarily sensory in nature.

Animals↗
PubMedDate not supplied

Platelet glycoprotein IIb/IIIa inhibitor attenuates complement activation during in vitro ventricular assist circulation.

Complement activity and platelet glycoprotein (GP) IIb/IIIa dysfunction have been demonstrated during in vitro ventricular assist device circulation. Platelets contain C1 serine protease inhibitor (C1 INH) in secretory granules, which normally regulates complement. Complement activity may result from a loss of platelet regulation on complement during ventricular assist device circulation as platelets lose viability. The purpose of this study was to assess the ability of a platelet GP IIb/IIIa receptor inhibitor to attenuate ventricular assist device associated complement activation during in vitro ventricular assisted circulation. Eight in vitro nonpulsatile centrifugal ventricular assist device circuits were simulated for 4 days using 450 ml fresh human whole blood. Cardiac index, temperature, pH, PO2, PCO2, Ca, glucose, and activated clotting time were maintained at physiologic levels. Levels of C1 INH and C3a were measured with and without a reversible glycoprotein IIb/IIIa inhibitor (MK-383). Concentrations of C1 INH increase on exposure to ventricular assist device, and decrease to a plateau within 12 hr. The decrease in circulating unbound C1 INH was attenuated with pre treatment with MK-383. Concentrations of C3a increase 34 fold within 4 hr of exposure to a ventricular assist device with and 22 fold without pre treatment with MK-383. These findings suggest that protection of the platelet GP IIb/IIIa complex delays complement activation during in vitro ventricular assist device circulation.

Complement Activation↗