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Biomedical subjects

B M Hegde

Publications and source records attributed to B M Hegde.

At least 37 records · Page 2Linked to original sources
PubMed1999

Principles of drug therapy in hypertension.

The most difficult diagnosis in medicine is the diagnosis of hypertension. Since this label encompasses many maladies both known (secondary hypertension), and the unknown, the office recording of blood pressure alone will not suffice to warrant treatment with drugs right away. There are more than 6 major guidelines in the world about the rules of the game of drug therapy in hypertension. The present preoccupation with newer drugs as first line antihypertensive drugs would ruin any economy, if the exchequer is to foot the bill. The stress in drug treatment has been the step-care mode of drug therapy where one starts with one drug in small doses, building the dose gradually, adding the next drug to get cumulative power to lower the pressure. Since the early seventies, the need to step-down therapy is being stressed wherein the doctor starts cutting down the drugs and the dosage, once he achieves the desired blood pressure levels. Diuretics and beta-blockers should be the first choice when drugs are indicated, unless there are positive indications for other drugs, or the first line drugs are contra-indicated. Routine treatment with drugs is recommended by the American JNC for people with sustained blood pressure above 140/90 mm Hg, but the British recommendations put the cut off at the pressure level of 160/100 mm Hg. Indian patients respond to very small doses in the beginning. The Hypertension Optimal Treatment (HOT) study failed to demonstrate a significant difference between the 3 randomised target blood pressure groups for the majority of cardiovascular events, although it did prove the theoretical hypothesis, that more vigorous treatment could certainly bring down the measured blood pressure to greater extent in 90% of patients I Greater importance will be given in the future for the non-pharmacological approaches, as well as to baseline blood pressure values, at which drug treatment should be started.

Adrenergic beta-Antagonists↗
PubMed1999

Grudgitis.

Explore the source record for details and available documents.

Hostility↗
PubMed1998

Serum estradiol and testosterone levels following acute myocardial infarction in men.

The present study examined serum testosterone and estradiol levels on the day of admission, 5th and on 10th day following acute myocardial infarction in men. Controls were matched for age and body mass index. Testosterone levels were low on the day of admission and remained statistically unchanged on 5th and 10th day as compared to controls. On the contrary, estradiol levels were significantly higher on the day of admission. A significant decrease in estradiol concentration in comparison to the levels on the day of admission was observed on 10th day post myocardial infarction. However, the estradiol levels on 10th day were significantly higher than control subjects. The results of the study suggest that in acute myocardial infarction, hyperestrogenemia is associated with hypotestosteronemia.

Aged↗
PubMed1998

Effect of N-acetylcysteine on myocardial infarct size following ischemia and reperfusion in dogs.

The present study was designed to examine the role of N-acetylcysteine (NAC) on free radical mediated reperfusion injury in canine model. Fourteen dogs underwent 90 min of left anterior descending coronary artery (LAD) occlusion followed by 4 h of reperfusion. Treated animals received loading dose of NAC (250 mg/kg) at the time of reperfusion upto 1 h followed by maintenance dose (70 mg/kg) for remaining 3 h through left atrial line. Infarct size, myocardial tissue lipid peroxidation, superoxide dismutase (SOD) and glutathione (GSH) levels were measured at the end of reperfusion in treated (n = 7) and untreated animals (n = 7). Left ventricular end diastolic pressure was significantly lower in treated animals compared to untreated group. SOD and GSH levels in myocardial tissue at risk and in infarcted zone were similar in both groups. However, in NAC treated animals the lipid peroxidation was significantly lower in comparison to untreated control animals. Infarct size in the area at risk, percent left ventricular necrosis and myocardial tissue preservation were not significantly different in treated and untreated animals. These results suggests that N-acetylcysteine infusion at the time of reperfusion following 90 min of ischemia and 4 h of reperfusion fails to offer significant cardioprotection against free radical damage but it can improve ventricular performance by decreasing pre load.

Acetylcysteine↗
PubMed1998

Clinical implications of hypocalcemia in malaria.

Total serum calcium levels were estimated in 60 adult patients with malaria to know the prevalence of hypocalcemia in different types of malaria and its clinical implications. As hypocalcemia is known to cause Q-Tc interval prolongation, electrocardiograms were obtained in all patients with low calcium levels. Twenty seven (45%) patients with malaria had hypocalcemia. Majority (88.24%) of the complicated malaria patients had hypocalcemia as against uncomplicated malaria (27.91%). Mean calcium levels were significantly lower in complicated malaria (7.4 +/- 0.98 mg/dl) when compared to uncomplicated malaria (8.4 +/- 0.44 mg/dl). There was an inverse relation between calcium levels and parasite load (P < 0.05). Significant correlation was also seen between the degree of hypocalcemia and Q-Tc prolongation (P < 0.01). Return of calcium levels to normal coincided with clinical recovery and parasite clearance. Three patients who had low calcium levels and prolonged Q-Tc died of hypotension, bradycardia and heart block after quinine therapy. The exact cause of hypocalcemia could not be ascertained but renal failure, hypomagnesemia and parathyroid failure could have been contributary. In conclusion, hypocalcemia is not uncommon in complicated malaria. It can be of prognostic value as it may indicate complicated malaria or heavy parasitemia and its return to normal may indicate clinical recovery and parasite clearance.

Adult↗
PubMed1997

Effect of alpha-tocopherol pretreatment on infarct size following 90 minutes of ischemia and 4 hours of reperfusion in dogs.

The present study was designed to evaluate the effects of pretreatment with antioxidants on free radical mediated reprefusion injury. Five dogs were fed with alpha-tocopherol (1000 IU/kg, bw) for ten days prior to 90 min of left anterior descending coronary artery occlusion followed by 4 hours of reperfusion. Infarct size, serum and myocardial lipid peroxidation were measured in pretreated and in untreated animals. Infarct size, as percentage of myocardial tissue at risk in alpha-tocopherol pretreated animals was 5.86+/-0.83 and was 39.35+/-7.58 in the untreated animals. Following reprefusion in untreated group, the values of serum and myocardial tissue lipid peroxidation were significantly higher than observed values in alpha-tocopherol treated animals. alpha-tocopherol pretreatment significantly reduced the myocardial infarct size and percent necrosis in the left ventricular mass in comparison to the untreated animals. These results suggest that alpha-tocopherol pretreatment possibly helps in reducing infarct size.

Animals↗
PubMed1997

Effect of superoxide dismutase and acidified sodium nitrite on infarct size following ischemia and reperfusion in dogs.

The effects of superoxide dismutase (SOD) alone or in combination with acidified sodium nitrite (NaNO2), a liberator of nitric oxide were examined in dogs after ischemia and reperfusion. Animals were divided into five groups. Left anterior descending coronary artery was occluded for 90 min followed by 4 hours of reperfusion with or without therapeutic interventions given preceding reperfusion. Left ventricular end diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP) and ECG changes were monitored throughout the study. Area at risk was defined by Evans blue and area of infarction by incubation in triphenyltetrazolium. Myocardial tissue lipid peroxidation was measured in ischemic and non-ischemic zones. There was no evidence of infarction until ninety minutes of ischemia. Percentage area of necrosis vis-a-vis area at risk percentage necrosis in left vertricular mass was significantly low in animals treated with combination of SOD and NaNO2 in comparison with isolated treatment with saline, SOD or NaNO2. LVEDP increased significantly following ischemia and remained unchanged during saline reperfusion. Treatment with SOD, NaNO2 in isolation or its combination significantly lowered LVEDP. Maximum increase in tissue lipid peroxidation was observed in saline and NaNO2 treated animals. SOD alone or in combination with NaNO2 significantly lowered the lipid peroxidation. The results clearly demonstrate that reperfusion can cause necrosis in ischemic myocardium. Combined treatment with SOD and NaNO2 offers significant cardioprotection against oxidative stress.

Animals↗