PubMed Health⌕ Search

Biomedical subjects

W K Hass

Publications and source records attributed to W K Hass.

At least 19 recordsLinked to original sources
PubMed1989

A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. Ticlopidine Aspirin Stroke Study Group.

We report the results of the Ticlopidine Aspirin Stroke Study, a blinded trial at 56 North American centers that compared the effects of ticlopidine hydrochloride (500 mg daily) with those of aspirin (1300 mg daily) on the risk of stroke or death. The medications were randomly assigned to 3069 patients with recent transient or mild persistent focal cerebral or retinal ischemia. Follow-up lasted for two to six years. The three-year event rate for nonfatal stroke or death from any cause was 17 percent for ticlopidine and 19 percent for aspirin--a 12 percent risk reduction (95 percent confidence interval, -2 to 26 percent) with ticlopidine (P = 0.048 for cumulative Kaplan-Meier estimates). The rates of fatal and nonfatal stroke at three years were 10 percent for ticlopidine and 13 percent for aspirin--a 21 percent risk reduction (95 percent confidence interval, 4 to 38 percent) with ticlopidine (P = 0.024 for cumulative Kaplan-Meier estimates). Ticlopidine was more effective than aspirin in both sexes. The adverse effects of aspirin included diarrhea (10 percent), rash (5.5 percent), peptic ulceration (3 percent), gastritis (2 percent), and gastrointestinal bleeding (1 percent). With ticlopidine, diarrhea (20 percent), skin rash (14 percent), and severe but reversible neutropenia (less than 1 percent) were noted. The mean increase in total cholesterol level was 9 percent with ticlopidine and 2 percent with aspirin (P less than 0.01). The ratios of high-density lipoprotein and low-density lipoprotein to total cholesterol were similar in both treatment groups. We conclude that ticlopidine was somewhat more effective than aspirin in preventing strokes in this population, although the risks of side effects were greater.

Aspirin↗
PubMed1988

Comparative protective effects of nicardipine, flunarizine, lidoflazine and nimodipine against ischaemic injury in the hippocampus of the Mongolian gerbil.

1. Morphological changes characterizing delayed neuronal death (DND) of selectively vulnerable CA1 pyramidal cells in the hippocampus of the Mongolian gerbil brain occurred 72 h after transient (5 min) bilateral occlusion of the common carotid arteries. 2. Different groups of animals were treated 15 min before carotid artery occlusion and twice daily during the 72 h post-ischaemia period with either saline alone, nicardipine, flunarizine, lidoflazine or nimodipine at doses of 500 micrograms kg-1 intraperitoneally. 3. At 72 h the animals were killed and their brains examined histologically. Absolute cell counts were made from 5 sites distributed linearly throughout the hippocampal CA1 subfield in each hemisphere to determine the percentage DND in each group. Normal brains and those of sham-operated animals were included in the study for comparison. 4. Features of DND were distributed evenly throughout the CA1 subfield in both hemispheres in all groups of gerbils. Nicardipine, lidoflazine and flunarizine, but not nimodipine, were protective. This protection extended linearly throughout the hippocampus without altering the pattern of neuronal damage. 5. Compared to saline-treated (78.3 +/- 2.9% DND) and nimodipine-treated (76.5 +/- 3.4% DND) gerbils, the overall protection afforded by nicardipine (41.8 +/- 3.8% DND) was statistically significant. The effects of lidoflazine (53.6 +/- 7.1%) and flunarizine (55.8 +/- 3.9% DND) were of borderline significance. 6. Abnormal neurones appeared in normal and sham-operated brains to the extent of 4.5 +/- 1.0% and 4.6 +/- 0.4%, respectively. Such changes can be attributed to fixation artefacts. 7. The results demonstrate that overall protection is conferred on ischaemic hippocampal CA1 neurones by nicardipine and to a lesser extent by flunarizine and lidoflazine, but not by nimodipine.

Animals↗
PubMed1987

The potential beneficial effect of nicardipine in a rat model of transient forebrain ischemia.

In a rat 3-day survival model of 10-minute four-vessel occlusion, halothane anesthesia was used to attenuate the ictal blood pressure elevation of the cerebral ischemic response and thereby maintain an isoelectric EEG. Selectively vulnerable regions of the brain were protected by preischemia plus postischemia maintenance treatment with the calcium entry blocker nicardipine. Compared with untreated animals, repeated doses at 500 micrograms/kg IP were markedly more effective than doses of 50 micrograms/kg. Ongoing studies demonstrate a neurocytoprotective action of nicardipine when deferred treatment is given postischemia.

Animals↗
PubMed1983

The cerebral ischemic cascade.

The author reviews the major biochemical events that follow in the wake of a significant brain ischemic insult. Evidence is presented that establishes lactic acidosis as a significant accelerant of the ischemic cascade and that proposes that uncontrolled entry of calcium into the vulnerable neuron triggers cell death.

Animals↗
PubMed1980

Unsymmetrical alkyl aryl thiourea compounds for use as cerebral blood flow tracers.

The synthesis and characterization of an homologous series of inert nonvolatile 14C-labeled unsymmetrical alkyl aryl thiourea compounds is described for their use as regional blood flow (rCBF) tracers employing autoradiographic procedures. In alert normocapnic rats the single-pass extraction values into brain for these thioureas were found to be dependent on their respective lipid solubilities ranging from 0.497 for 1-methyl-3-phenylthiourea to 0.730 for 1-butyl-3-phenylthiourea. The commonly used rCBF tracers [14C]antipyrine and [14C]iodoantipyrine had single-pass extraction values of 0.451 and 0.553, respectively. The single-pass extraction value for n-butanol was found to be the same as that for 1-butyl-3-phenylthiourea indicating that both n-butanol and 1-butyl-3-phenylthiourea are mildly diffusion limited at normal rates of flow in rat brain. Since 1-butyl-3-phenylthiourea diffused most readily into rat brain it was chosen as a potentially valuable rCBF tracer. Its brain-blood partition coefficient was found to be 1.09. The plasma distribution of this thiourea in blood varied inversely with the hematocrit, and the compound was freely exchangeable between plasma and erythrocytes. Employing 1-butyl-3-phenylthiourea to measure rCBF and its empirically derived brain extraction values the following flow rates in normocapnic rats were found: 3.2 ml . g-1 . min-1 for cochlear nucleus: 3.0 for inferior colliculus; 2.5 for medical geniculate; 1.9 for pontine gray and hypothalamus; 1.7 for caudate and cerebral cortex; and 1.2 for cerebellar gray and 0.41-0.50 for white matter structures. It was concluded from these studies that 1-butyl-3-phenylthiourea is more advantageous than iodoantipyrine for measuring rCBF, especially in those areas that possess very rapid rates of flow.

Animals↗