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S Hassan

Publications and source records attributed to S Hassan.

87 records · Page 5Linked to original sources
PubMed1984

A chemically stable analogue, 9 beta-methyl carbacyclin, with similar effects to epoprostenol (prostacyclin, PGI2) in man.

The effects of 9 beta-methyl carbacyclin, a chemically stable analogue of epoprostenol (prostacyclin, PGI2) were studied, in comparison with epoprostenol, both in vitro and in vivo in man. In vitro 9 beta-methyl carbacyclin and epoprostenol inhibited platelet aggregation induced by ADP, collagen, the endoperoxide analogue U46619 and arachidonic acid. The potency of 9 beta-methyl carbacyclin relative to epoprostenol was comparable in ADP and collagen-aggregated platelet rich plasma (PRP), 9 beta-methyl carbacyclin being 0.01 times as active as epoprostenol. The anti-aggregatory potencies of the two compounds were comparable in PRP and whole blood. The phosphodiesterase inhibitor isobutyl methyl xanthine enhanced the anti-aggregatory activity of both compounds in vitro. 9 beta-methyl carbacyclin and epoprostenol elevated platelet cyclic AMP, 9 beta-methyl carbacyclin being 0.04 times as active as epoprostenol. In a placebo controlled trial both drugs produces significant headache and facial flushing when compared with placebo. Nasal stuffiness, abdominal discomfort and nausea were reported on all three treatments. Both drugs caused significant and comparable increase in heart rate and decrease in pre-ejection (PEP) and PEP/left ventricular ejection time (LVET) ratio compared with placebo. Systolic and diastolic blood pressure, LVET and QS2 index were unchanged. Platelet aggregation responses to ADP were significantly inhibited by all three doses of both drugs compared with placebo. Bleeding time was significantly longer during epoprostenol infusion than either placebo or 9 beta-methyl carbacyclin infusion. Neither drug had significant effect, compared with placebo, on kaolin activated clotting time in PPP, PRP or in PRP in the presence of heparin, prothrombin time, partial thromboplastin time, thrombin clotting time, fibrinogen, fibrinogen degradation products or euglobulin clot lysis time. The pharmacodynamic effects and duration of action of 9 beta-methyl carbacyclin and of epoprostenol are similar; 9 beta-methyl carbacyclin is approximately 100 times less potent than epoprostenol in man.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Epoprostenol (prostacyclin,PGI2) increases apparent liver blood flow in man.

When epoprostenol (prostacyclin, PGI2) is given by infusion to man, cardiac output is increased, and it appears that the gastrointestinal tract may receive a disproportionate share of this. We have used the clearance of indocyanine green dye to estimate liver blood flow in 8 healthy subjects. During an infusion of PGI2 at a dose of 5 ng/kg/min, apparent liver blood flow increased from 925 +/- 220 ml/min (Mean +/- s.d) to 1320 +/- 453 ml/min, an average increase of 41.1%. Significant changes in heart rate, headache, facial flushing, systolic blood pressure, and pulse pressure were noticed. We suggest that endogenous epoprostenol (PGI2) may be of importance in the physiological regulation of liver blood flow in man. As this dose of epoprostenol could be tolerated readily, epoprostenol therapy could prove a therapeutic advance in some liver disorders, particularly liver transplantation, and possibly in the therapy of certain drug overdoses.

Adult↗
PubMed1983

Effects of intravenous epoprostenol on platelets and the cardiovascular system are not potentiated by dipyridamole.

Normal subjects received infusions of epoprostenol (prostacyclin, PGI2) at doses of 2, 4, 6, and 8 ng/kg/min on each of two occasions after pretreatment with dipyridamole (400 mg/day for 3 days) or placebo. Baseline headache and bleeding time were increased and preejection period (PEP) shortened after dipyridamole. The baseline heart rate was increased on dipyridamole by an amount that correlated to the blood dipyridamole level. PGI2 infusion increased heart rate, systolic blood pressure (BP), pulse pressure, left ventricular ejection time index, and degree of flushing and severity of headache, and reduced diastolic BP, PEP, and T wave height. There was no apparent interaction between PGI2 and dipyridamole on these variables. PGI2 inhibited adenosine diphosphate-induced platelet aggregation and increased bleeding time. We conclude that, despite the synergism between dipyridamole and PGI2 that might be predicted and has been demonstrated in some animal experiments, no such interaction is apparent in normal humans after standard doses.

Adult↗
PubMed1983

Systolic time intervals: a review of the method in the non-invasive investigation of cardiac function in health, disease and clinical pharmacology.

Measurement of systolic time intervals is a valuable, non-invasive procedure to assess left ventricular performance, particularly when influenced by drugs. In this review, we discuss various factors affecting systolic time intervals, the therapeutic implications of the technique and its place among other non-invasive tests of cardiac function.

Adolescent↗
PubMed1982

The cardiovascular and platelet effects of epoprostenol (prostacyclin, PGI2) are unaffected by beta-adrenoceptor blockade in man.

1 Atenolol 0.2 mg/kg i.v., propranolol 0.2 mg/kg i.v. or placebo were given in a double-blind crossover study to six healthy male subjects, and the effects of a subsequent infusion of epoprostenol (prostacyclin, PGI2) 0-6 ng kg-1 min-1 monitored. 2 PGI2 caused a tachycardia, a fall in diastolic blood pressure, a rise in pulse pressure, reduction in pre-ejection period (PEP) and rise in left ventricular ejection time index (LVETI), headache and facial flushing at doses of PGI2 greater than 2 ng kg-1 min-1,, (P less than 0.05). 3 Beta-adrenoceptor blockade did not prevent the tachycardia in response to PGI2, and did not interact with any of the other dynamic effects of PGI2. 4 In vitro, PGI2 at 1 and 2 ng/ml inhibited platelet aggregation to ADP (P less than 0.01), although no significant effect on platelet aggregation was seen in the in vivo study. Atenolol and propranolol at a final concentration of 1 microgram/ml did not affect this in vitro study. Atenolol and propranolol at a final concentration of 1 microgram/ml did not affect in vitro effect of PGI2 on platelet aggregation. 5 Pretreatment with atropine 0.04 mg/kg i.v. in three subjects did not attenuate the tachycardia caused by PGI2 infusion, even though the baseline heart rate was increased. 6 Adverse effects to PGI2 infusion included sudden bradycardia, pallor and sweating, suggesting that the Bezold-Jarisch reflex seen in animals in response to PGI2 may also occur in humans. 7 Neither increased sympathetic drive nor vagal withdrawal are likely causes of the tachycardia following PGI2 infusion.

Adrenergic beta-Antagonists↗
PubMed1977

Nephrotic syndrome.

The nephrotic syndrome is clinical entity having multiple etiology. In the present study, 70 cases of nephrotic syndrome both in children and adults have been studied. The condition appears to be more common than thought of. The histological classification is helpful both in management and forecasting the prognosis. Steorid and cytotoxic drugs have been used in light negative glomerulonephritis and lupus nephritis producing nephrotic syndrome with good results. The other forms of of glomerulonephritis needs further study to be able to offer any specific therapy.

Adult↗
PubMed1971

Cervical pregnancy.

Explore the source record for details and available documents.

Abortion, Spontaneous↗
PubMedDate not supplied

Can latissimus dorsi muscle stimulation benefit heart during training period after vascular delay?

We hypothesized that a two-stage vascular delay procedure followed by 5 weeks of conditioning of the latissimus dorsi muscle (LDM) could benefit the heart during the training period and greatly increase cardiac assistance when examined with maximum potential. In mongrel dogs (n = 10), left ventricle (LV) dysfunction was induced by intracoronary injections of latex microspheres [90 +/- 2 micro diameter]. Vascular delay of the LDM was performed in one group (n = 6), whereas the other group (control, n = 4) did not undergo vascular delay. After 2 weeks, CMP was performed in all animals followed by LDM conditioning. After 5 weeks of muscle training, we examined left ventricular function at 20 Hz-4 volts, 33 Hz-4 volts, and 50 Hz-10 volts stimulation by assessing peak aortic pressure (AoP), left ventricular pressure (LVP), maximum LV +dP/dt, stroke volume (SV), stroke work (SW), stroke power (SP), and aortic flow. LDM assisted beats were compared with nonstimulated beats. LDM stimulation caused significant increases in pressure and flow in the vascular delay group. At 20 Hz-4 volts, absolute increases were LVP (10.2 +/- 0.6) mm Hg, AoP (9.8 +/- 1.7) mm Hg, SV (1.8 +/- 0.4) ml, SW (5.3 +/- 1.0) gm x m, SP (40.8 +/- 12.7) gm x m/sec, max LV dP/dt (104.8 +/- 53.2) mm Hg/sec, and peak aortic flow (0.9 +/- 0.3) L/min. At 33 Hz-4 volts, the absolute increases were LVP (13.6 +/- 1.3) mm Hg, AoP (12.1 +/- 2.4) mm Hg, SV (2.7 +/- 0.7) ml, SW (7.4 +/- 1.4) gm x m, SP (72.7 +/- 16.5) gm x m/sec, max LV dP/dt (294 +/- 19) mm Hg/sec, and peak aortic flow (1.8 +/- 0.5) L/min. At 50 Hz-10 volts, the absolute increases were LVP (17.7 +/- 0.7) mm Hg, AoP (21.1 +/- 1.9) mm Hg, SV (6.0 +/- 1.1) ml, SW (14.6 +/- 2.2) gm.m, SP (128.2 +/- 15.3) gm x m/sec, max LV dP/dt (352 +/- 62) mm Hg/sec, and peak aortic flow (3.3 +/- 0.4) l/min (p < 0.05). The percentage increases were significantly larger in the vascular delay group compared with controls at 50 Hz-10 volts LDM stimulation. By using a two-stage vascular delay procedure, LDM stimulation can provide meaningful cardiac assistance during training periods. Furthermore, brief periods of maximal potential benefit (demand cardiomyoplasty) can be achieved during the training period.

Animals↗
PubMedDate not supplied

Augmentation of water-immersion stress- induced gastric mucosal lesions in BALB/c mice infected with Helicobacter felis.

BACKGROUND AND AIMS: Inoculation of Helicobacter felis into the murine stomach has been reported to induce chronic gastric inflammation and may be a model of Helicobacter pylori-induced chronic gastritis. In this study, to characterize H. felis-induced gastritis, the gastric production of interleukin-1beta (IL-1beta) and hepatocyte growth factor (HGF) was measured in mice. METHODS: Gastric mucosal lesions were induced in H. felis-infected BALB/c mice by water-immersion stress. The severity score of gastric erosions per stomach was measured as the sum of the length of erosions. Gene expression of IL-1beta and HGF were analyzed by Northern blot analysis and production of HGF was examined using the enzyme immunoassay method. RESULTS: Water-immersion stress induced gastric mucosal lesions accompanied by increased expression of IL-1beta mRNA. H. felis infection evoked enhanced expression of IL-1beta and HGF genes. When H. felis-infected mice were stressed by water immersion, the mucosal lesions were more severe than those in non-infected mice. Moreover, IL-1beta gene expression as well as HGF production was further increased. CONCLUSIONS: Although H. felis inoculation did not cause gastric mucosal erosions by itself, it augmented the stress-induced erosions.

Animals↗
PubMedDate not supplied

Amnioinfusion in the evaluation of fetal obstructive uropathy: the effect of antibiotic prophylaxis on complication rates.

OBJECTIVE: Amnioinfusion plays an important role in the intrauterine evaluation and treatment of fetal obstructive uropathy. However, it may significantly increase the risk for chorioamnionitis, premature rupture of membranes and premature labor. We evaluated the impact of prophylactic antibiotics on postamnioinfusion complications. METHODS: Thirty pregnancies complicated by fetal obstructive uropathy, treated by amnioinfusion and with documentation of pregnancy outcome were identified from our database. Pregnancy outcomes were compared between patients who were treated with prophylactic antibiotics and those with no prophylaxis. RESULTS: Chorioamnionitis was diagnosed in 3 out of 15 (20%) patients who did not receive prophylactic antibiotics as compared to 2 (13%) in the treated group. The overall rate of serious obstetrical complication was significantly higher in the untreated group (66 vs. 20%; p = 0. 021). Patients receiving prophylactic antibiotics delivered at a significantly greater gestational age than those who did not receive antibiotics (34.0 +/- 3.7 vs. 31.3 +/- 1.9 weeks, respectively; p = 0.018). CONCLUSIONS: Our study supports the use of oral prophylactic antibiotics as being effective in reducing the previously observed significant risks associated with amnioinfusion in fetal obstructive uropathy.

Amnion↗
PubMedDate not supplied

Evaluation of fetal echogenic bowel in the second trimester.

Previous studies cite different possible etiologies for fetal echogenic bowel (FEB). The purpose of this study was to evaluate the possible etiologies for second-trimester FEB, and to provide clinical guidelines for evaluation of this finding. The study included 79 patients diagnosed with FEB in the second trimester. Fifteen cases (19%) were associated with maternal vaginal bleeding. Of these, 12 patients underwent amniocentesis, 9 of which had visible blood products in the amniotic fluid. Seven cases (8.9%) had associated severe malformation. Seven other cases (8.9%) were noted in multifetal pregnancies. Five fetuses (6.3%) had evidence of bowel obstruction or perforation not associated with cystic fibrosis (CF). Chromosomal aberrations were found in 5 fetuses (6.3%). Intrauterine infection with cytomegalovirus, herpes simplex virus, varicella-zoster virus, or parvovirus B-19 was documented in 5 patients (6.3%). Three cases (3.8%) were associated with subsequent unexplained stillbirth. Two fetuses (2.5%) were found to be affected by CF. Finally, in 30 cases (38%), no obvious reason for FEB was found. We conclude that the evaluation of second-trimester FEB should include targeted ultrasound for associated malformations, infectious studies, DNA analysis for CF mutations, amniocentesis for chromosomal analysis and evaluation of the amniotic fluid for degraded blood products, and an autopsy in cases of stillbirth. Even when no apparent reason is found, pregnancies should be considered at high risk for poor outcome.

Chromosome Aberrations↗