The authors used the scanning electron microscope to study the surface ultrastructure of the ependyma in six control rabbits and six rabbits subjected to bilateral jugular vein ligation four to five days previously. Whereas in the control rabbits the mean CSF pressure was 27 mm H2O, it rose to 71.5 mm H2O in the experimental animals. The ependymal lining of the fourth ventricle, third ventricle and the inferior horn of the lateral ventricle was examined. In the experimental animals, clusters of cilia emanating from ependyma were separated. This appeared secondary to ingrowth of cell processes covered with microvilli. Remarkable alterations were seen in the dorsal and infundibular regions of the third ventricle. While a marked reduction in ciliary density and appearance of pits were noticeable in the former, almost total replacement of globular excrescences by pleomorphic microvilli was noted in the infundibular region. The morphological alterations in the ependyma that occurred in experimental animals suggested a modification in its function from a surface capable of propelling cerebrospinal fluid by ciliary movement to one capable of increased ependymoabsorption. Increased incidence of macrophage-like supraependymal cells was noted in the experimental rabbits.

Animals↗

PubMedDate not supplied

"Left ventricular function in mitral stenosis by systolic time intervals".

Explore the source record for details and available documents.

Adult↗

PubMedDate not supplied

Beneficial effects of long-term metoprolol therapy on cardiac haemodynamics in patients with mitral stenosis in sinus rhythm--a randomised clinical trial.

We conducted a placebo controlled randomised clinical trial to evaluate the effects of 6 months therapy with metoprolol on resting and exercise haemodynamics in 31 patients with isolated mitral stenosis in sinus rhythm. Twenty six of them (placebo n = 13, metoprolol n = 13) completed the study protocol. Their mean age was 23.1 +/- 7.9 years and the mean mitral valve area was 0.93 +/- 0.25 cm2. The dose of metoprolol ranged between 50-100 mg per day. The primary outcome variables for the study were the resting and exercise mean pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) and the secondary outcome variables consisted of resting and exercise heart rate, mean pulmonary artery pressure (PAP), mean pulmonary vascular resistance (PVR) and clinical improvement on visual analog scale. These outcome variables were assessed blindly. The resting and exercise mean PCWP (mmHg) increased by 9.1 +/- 3.1 and 16.4 +/- 6.4 on placebo and 2.5 +/- 2.1 and -4.6 +/- 2.3 on metoprolol after 6 months therapy. These differences were statistically significant (p < 0.01). The resting and exercise CI (liters/min/m2) decreased by 0.2 +/- 0.1 and 0.1 +/- 0.1 on placebo and 0.3 +/- 0.5 and 0.3 +/- 1.0 on metoprolol. These haemodynamic effects were accompanied with much better symptomatic improvement in patients treated with metoprolol. The differences in change in mean PAP and PVR in two groups were statistically not significant. Our results suggest that the symptomatic patients with MS, waiting for definitive intervention for 6 months or less, would benefit if given beta blockers during this period.

Adult↗

PubMedDate not supplied

A study of platelet aggregation, thromboxane A2 and prostacyclin in central aortic and coronary sinus blood in ischemic heart disease.

Aortic and coronary sinus platelet aggregation, thromboxane A2 (TXA2) and prostacyclin (PG12) levels were studied in fourteen patients of stable angina (SA), six of vasopastic angina (VA) and six control subjects (C). Patients of SA were studied at rest and during incremental atrial pacing and patients with VA were studied at rest and during various stages of vasospasm. Platelet aggregation was studied with different working concentrations of ADP, epinephrine and collagen. TX A2 and PGI2 concentrations were estimated by measuring levels of their stable metabolites viz. thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (PGF1 alpha) respectively. Platelet aggregation was increased in SA and VA patients (p < 0.01) and further increase was seen during vasospasm (p < 0.001). However, it failed to increase on incremental atrial pacing. Similarly, TXB2 and PGF1 alpha levels were raised in SA and VA patients. While TXB2 further increased during vasospasm but not during atrial pacing. PGF1 infinity failed to rise with either. Thus platelets are in an activated state in SA and VA. This activated state is a cause and not an effect in SA and VA. An imbalance in the levels of TXA2 and PG12 could account for the vasospasm.

Age Factors↗

PubMedDate not supplied

Intestinal malabsorption presenting with night blindness.

Night blindness from vitamin A deficiency was observed in a patient with intestinal malabsorption, which in turn was attributable to duodenal diverticulosis and bacterial growth. Monthly supplementation with vitamin A and correction of bacterial overgrowth with tetracycline resulted in a normalisation of plasma retinol levels and resolution of the night blindness.

Aged↗

PubMedDate not supplied

Predischarge dobutamine induced distant wall motion abnormalities after acute myocardial infarction predict multivessel disease.

Presence of multivessel coronary artery disease (MVD) identifies a high risk subgroup after acute myocardial infarction (AMI). Dobutamine stress echocardiography (DSE) has recently emerged as a promising non invasive test to detect the presence and extent of coronary artery disease. Forty six consecutive patients (38 males, 8 females; mean age 48.6 +/- 10.4 years) of Q-wave acute myocardial infarction were subjected to submaximal treadmill test (TMT) and dobutamine stress echocardiography to see their ability to predict multivessel coronary artery disease as detected by coronary angiography before hospital discharge. Dobutamine infusion was started at 5 micrograms/kg/min to a maximum of 40 micrograms/kg/min, to achieve 70 percent of the age predicted heart rate. Appearance of new regional wall motion abnormality was interpreted as positive DSE for MVD. Mean peak infusion dose of dobutamine used in the study was 28.56 +/- 5.67 micrograms/kg/min. In none of the patients, the test had to be terminated due to side effects. The sensitivity and specificity of DSE to predict MVD was 80 percent and 93.7 percent, respectively as compared to 45 percent and 86 percent for submaximal TMT. Thus, DSE in patients of AMI before hospital discharge is a safe procedure with fairly accurate prediction of multivessel coronary artery disease.

Adult↗

PubMedDate not supplied

Improvement in contractility of infarct zone after dobutamine infusion predicts good (TIMI II or III) flow in infarct related artery.

Eighteen patients of 'Q' wave acute myocardial infarction (AMI) (age 50 +/- 6.2 years), underwent dobutamine stress echocardiography (DSE) before hospital discharge (7.2 +/- 1.3 days after AMI) to find out the correlation between response of infarct zone to dobutamine infusion and TIMI grade flow in infarct related artery (IRA). The aim of study was to test the hypothesis that infarct zone which shows improvement in contractility after dobutamine infusion has viable myocardial tissue and would have good flow (TIMI II or III) in IRA. Echocardiographically, improvement in contractility in the centre of infarct zone by at least 1 grade (on a scale of 4) was termed as positive response on DSE. The mean dose of dobutamine was 19.4 micrograms/kg/min. Ten patients had positive response on DSE; 8 of them had good antegrade flow in IRA. Eight patients had no improvement in contractility of infarct zone on DSE; 6 of them had poor flow in IRA. Clinical markers of reperfusion (relief of chest pain, early ST settlement, peak CPK-MB levels), age of patient, site of AMI, time to thrombolysis, resting left ventricular ejection fraction, wall motion score of the infarct zone and presence of collaterals were not significantly different in patients with good or poor flow in IRA. Thus, improvement in contractility of infarct zone after dobutamine infusion can predict good flow (TIMI II or III) in IRA with 80 percent sensitivity, 75 percent specificity, 80 percent diagnostic accuracy, 80 percent positive predictive value and 75 percent negative predictive value.

Adult↗

PubMedDate not supplied

Antitubercular treatment does not prevent constriction in chronic pericardial effusion of undetermined etiology: a randomized trial.

Patients of chronic exudative pericardial effusion are frequently treated with antitubercular treatment on presumptive grounds in developing countries, in a hope to prevent constrictive pericarditis. To assess the impact of antitubercular treatment on development of constrictive pericarditis in chronic large exudative pericarditis effusion of undetermined etiology, 25 patients above 12 years of age, with large pericarditis effusion beyond 12 weeks duration, were randomized in a prospective 2:1 fashion, to receive either 3-drug antitubercular treatment (group A) or placebo (group B) for six months. End points studied were, development of pericardial thickness as diagnosed by CT scan and constrictive pericarditis as diagnosed by cardiac catheterization. Twenty-one patients (14 in group A and 7 in group B) completed the study protocol. In all, five (23.8%) patients developed constrictive pericarditis/pericardial thickening. Histopathological examination of pericardiectomy specimens in over five patients were negative for tubercular pathology. Pericardial effusion resolved completely in another 10 (47.8%) patients. There was no significant difference in both the groups in development of constrictive pericarditis/pericardial thickening (group A: n = 3, 21.4% and group B: n = 2, 29.6%, p = NS). On multivariate analysis, development of constrictive pericarditis/pericardial thickening was associated with recurrent tamponade (p = 0.01), presence of tamponade at admission (p = 0.07) and haemorrhagic pericardial effusion (p = 0.08). Thus, antitubercular treatment does not prevent the development of constrictive pericarditis in patients of large chronic pericardial effusion of undetermined etiology.

Adult↗