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Biomedical subjects

B I Jugdutt

Publications and source records attributed to B I Jugdutt.

At least 91 records · Page 5Linked to original sources
PubMed1983

Myocardial salvage by intravenous nitroglycerin in conscious dogs: loss of beneficial effect with marked nitroglycerin-induced hypotension.

We studied the effect of nitroglycerin-induced decreases in mean arterial pressure (MAP) on myocardial salvage. Two hours after occlusion of the left anterior descending coronary artery, 65 conscious dogs were randomly allocated to receive 4 hr intravenous infusions of saline (group 1, 19 dogs), or nitroglycerin in doses to decrease MAP by 10% (group 2, 18 dogs), 25% (group 3, 14 dogs), and 50% (group 4, 14 dogs), respectively. At 7 days, 41 dogs were killed for measurement of infarct size; 24 dogs, given 7 to 10 micron radioactive microspheres for flow calculations, were killed 6 hr after occlusion. Boundaries of the occluded bed were defined by postmortem coronary arteriography. Infarct and occluded bed masses were measured by planimetry of weighed transverse sections of the left ventricle. Compared with saline infusions in group 1, nitroglycerin infusions produced sustained reductions (p less than .001) in mean left atrial pressure and MAP in all dogs, but heart rate was unchanged. The decreases in MAP achieved in groups 2, 3, and 4 were 10% (range, 5% to 19%), 23%, and 39%, respectively, with average levels of 96 (range, 83 to 113), 83, and 64 mm Hg, respectively. Despite similar masses of the occluded bed and left ventricle among the four groups, infarct size was significantly smaller (p less than .025) in group 2 compared with groups 1, 3, or 4, expressed both as percent of the left ventricle (6% vs 14% vs 13% vs 15%) and as percent of the occluded bed (13% vs 37% vs 34% vs 44%). Myocardial salvage (expressed as percent of the occluded bed) with nitroglycerin correlated inversely with the percent of decrease in MAP (r = -.77, p less than .001). Collateral blood flow increased (p less than .005) throughout the occluded bed in group 2 compared with group 1 but was unchanged in groups 3 and 4. In contrast, coronary vascular resistance decreased (p less than .025) in all nitroglycerin groups. These results suggest that perfusion pressure is an important determinant of myocardial salvage during nitroglycerin therapy. An increase in the dose of nitroglycerin to decrease MAP by more than 10%, and to levels below 96 mm Hg, might offset its potential for myocardial salvage in the conscious dog.

Animals↗
PubMed1983

Persistent reduction in left ventricular asynergy in patients with acute myocardial infarction by intravenous infusion of nitroglycerin.

Intravenous nitroglycerin (NG) infusion in patients with acute myocardial infarction (AMI) has been shown to improve left ventricular function and myocardial perfusion and to decrease ischemic injury and creatine kinase (CK) indexes of infarct size. To determine whether early NG infusions in patients with AMI decreases the extent of left ventricular asynergy, we used two-dimensional echocardiography to measure asynergic segments (akinesis and/or dyskinesis) at four serial short-axis levels from base to apex (mitral, M; chordal, C; midpapillary, MP; low papillary, LP) in 22 patients with a first anterior AMI. Patients were randomized between infusions of NG (n = 11) or 5% dextrose in water (controls, n = 11) within 5.6 hr after the onset of pain. NG infusion rates were titrated to lower mean arterial pressure to an average level of 7% below control (but not below 80 mm Hg) and were maintained at this level for the duration of the infusions (39 hr). After NG, left ventricular function improved as left ventricular filling pressure decreased (p less than .005), and sigma ST on precordial ST segment mapping decreased (p less than .001). These parameters did not change in control subjects. Computed CK infarct size was smaller in the NG group than in the control group (p less than .05). Before the infusions, the mean extent of left ventricular asynergy (% left ventricular circumference) were similar in both groups: M, 18% vs 21%; C, 22% vs 23%; MP, 26% vs 24%; LP, 32% vs 29%. In addition, the computed total left ventricular asynergy (% surface area) was also similar for these two groups before therapy (25% vs 25%). There was no change in left ventricular asynergy from pretreatment values by 1 hr and 10 days among control subjects: M, 18% vs 18% vs 17%; C, 22% vs 22%; MP, 26% vs 26% vs 22%; LP, 32% vs 33% vs 33%; total 25% vs 25% vs 24% (multiple measures analysis of variance). In contrast, there was a significant decrease (p less than .001) in left ventricular asynergy from pretreatment values by 1 hr and 10 days with NG: M, 21% vs 10% vs 8%; C, 23% vs 12% vs 10%; MP, 24% vs 13% vs 9%; LP, 29% vs 14% vs 10%; total, 25% vs 12% vs 9%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1983

Effect of doxorubicin on [omega-I-131]heptadecanoic acid myocardial scintigraphy and echocardiography in dogs.

The effects of serial treatment with doxorubicin on dynamic myocardial scintigraphy with [omega-I-131]heptadecanoic acid (I-131 HA), and on global left-ventricular function determined echocardiographically, were studied in a group of nine mongrel dogs. Total extractable myocardial lipid was compared postmortem between a group of control dogs and doxorubicin-treated dogs. A significant and then progressive fall in global LV function was observed at a cumulative doxorubicin dose of 4 mg/kg. A significant increase in the myocardial t1/2 of the I-131 HA was observed only at a higher cumulative dose, 10 mg/kg. No significant alteration in total extractable myocardial lipids was observed between control dogs and those treated with doxorubicin. Our findings suggest that the changes leading to an alteration of myocardial dynamic imaging with I-131 HA are not the initiating factor in doxorubicin cardiotoxicity.

Animals↗
PubMed1983

Right ventricular involvement in transmural inferior wall infarction: two-dimensional echocardiographic and clinical correlations.

We used two-dimensional echocardiography to assess asynergy in the right (RV) and left (LV) ventricles in 34 selected patients with electrocardiographic evidence of acute transmural inferior myocardial infarction (IMI) 40 +/- 3 (SE) h from the onset of pain. We measured the extent of asynergy, defined as akinesis and/or dyskinesis, for RV and LV in 4 short axis sections and computed asynergy for both ventricles. The incidence of asynergy was 100% in the inferior LV, 76% in the inferior ventricular septum and 76% in the inferior RV. We found a direct correlation between peak creatine phosphokinase levels and LV asynergy (R = 0.71) or (RV + LV) asynergy (R = 0.72). The asynergy and right heart catheterization data correlated with clinical findings in 4 subgroups identified on the basis of hypotension (systolic blood pressure less than 100 mmHg) and pulmonary congestion, (confirmed radiographically): 1A, extensive biventricular asynergy (32% RV, 32% LV) with hypotension and congestion (N = 10); 1B, predominant RV asynergy (49% RV, 26% LV) with hypotension but no congestion (N = 5); 2A, predominant LV asynergy (7% RV, 26% LV) with congestion (N = 10); 2B less extensive biventricular asynergy (15% RV; 16% LV) and uncomplicated IMI (N = 9). Hypotension identified a high risk group (N = 15) prone to complications and death. The extent of RV asynergy was the third strongest discriminator for hypotension, next to systolic blood pressure and jugular venous pressure. The extent of LV asynergy was the strongest discriminator for pulmonary congestion. Among hypotensive patients, the RV/LV asynergy ratio was the strongest discriminator for pulmonary congestion, being significantly greater in those without congestion than in those with congestion (2.2 vs 1.0, P less than 0.001). The increased RV/LV asynergy ratio may be a useful index for predicting predominant RV infarction in IMI.

Aged↗
PubMed1981

Prostaglandin inhibition and myocardial infarct size.

In parallel with experimental research into methods for salvage of ischemic myocardium after acute myocardial infarction (AMI) over the last decade, there has been a growing interest in prostaglandins (PG) and their inhibition by aspirin-like drugs or nonsteroidal anti-inflammatory drugs (NSAID). The finding of enhanced PG release during myocardial ischemia and its blockade by the NSAID indomethacin led to the hypothesis that PG might influence the infarction process. Because PG differ in vasoactive, cellular, and metabolic properties, and PG inhibitors also differ in their ability to inhibit synthesis of different PG and their metabolites, some PG inhibitors might be expected to reduce myocardial ischemic injury and infarct size. In addition, the NSAID may directly modify cellular events during infarction. Experiments with NSAID in the anesthetized and conscious animals have demonstrated a reduction of myocardial infarct size with ibuprofen, but an increase in infarct size with indomethacin. The opposite effects of these agents on infarct size might have been related to the different doses used, different degrees of inhibition of PG and their metabolites, and different effects on factors influencing myocardial oxygen supply and demand, metabolic and cellular events during infarction. It has recently been suggested that some of these agents might also influence the healing process after AMI and, therefore, late complications.

Acute Disease↗
PubMed1981

Ischemic ventricular fibrillation: the importance of being spontaneous.

Although the energy level required to defibrillate normal myocardium is low and constant, as determined from studies of induced ventricular fibrillation, little is known of the specific energy requirements in regionally ischemic hearts for spontaneous or induced ventricular fibrillation. In this study the lowest energy threshold for defibrillation was determined in 10 open chest dogs with reversible 10 minute coronary occlusions at various sites for each of 44 events of ventricular fibrillation, using apical and superior vena caval electrodes with a generator providing variable output of 1 to 30 watt seconds. The ischemic mass, quantitated from postmortem angiographic and planimetric data, was 52 +/- 9 percent (mean +/- standard deviation) of the left ventricle in dogs with induced ventricular fibrillation (Group I), 52 +/- 12 percent in dogs with spontaneous ventricular fibrillation after occlusion (Group II) and 54 +/- 9 percent in dogs with spontaneous ventricular fibrillation after reperfusion (Group III). Defibrillation thresholds in watt seconds were 9 +/- 7 in Group I (n = 12), 19 +/- 10 in Group II (n = 13) and 18 +/- 10 in Group II (n = 19). (Group I versus Groups II and III, probability [p] less than 0.025). In nonischemic hearts, the defibrillation threshold was 3 +/- 2 (n = 32) (p less than 0.001 compared with values in Group I, II or III). Thus, despite similar masses of ischemia, twice as much energy was required for defibrillation of spontaneous ventricular fibrillation (whether after occlusion or reperfusion) as for induced ventricular fibrillation, suggesting that these conditions are caused by different metabolic or pathologic derangements. Such differences should be considered in assessing interventions such as drug therapy designed to inhibit the repetitive ventricular response and in design of implantable defibrillators.

Animals↗
PubMed1981

Effect of PGE1, PGE2 and PGI2 on ventricular arrhythmias during myocardial infarction in conscious dogs: relation to infarct size.

The relation between the effect of vasodilator prostaglandins on ventricular arrhythmias during myocardial infarction and infarct size was studied in conscious dogs. Two infarct-limiting drugs, nitroglycerin and ibuprofen, were also studied for comparison. Infusions were given between 20 and 380 minutes after occlusion of the left circumflex coronary artery: intravenously for saline (N = 27), ibuprofen (N = 14), and nitroglycerin (N = 14); left atrially for PGE1 (N = 11), PGE2 (N = 12) and PGI2 (N = 18). Doses of prostaglandins and nitroglycerin were adjusted to decrease mean arterial pressure by 5%. Pathologic infarct size was measured 2 days post-occlusion. During the infusion period, ventricular fibrillation (VF) deaths were nil with PGI2 (p less than 0.05) and nitroglycerin (p less than 0.1), ventricular premature beats (VPB's) were less (p less than 0.01) with PGI2, PGE2 and nitroglycerin, and collateral blood flow (microspheres) increased with PGE1, PGI2 and nitroglycerin but did not change with saline, PGE2 and ibuprofen. Infarct size, as percent of left ventricle or occluded bed, was less (p less than 0.05) with PGE1, PGI2, nitroglycerin and ibuprofen but similar with PGE2 and saline. Thus, PGE2 diminished VPB's despite no effect on flow or infarct size. In contrast, both PGE1 and PGI2 diminished VPB's, increased flow and decreased infarct size, but PGI2 also reduced VF mortality.

Alprostadil↗
PubMed1981

Prostaglandins in myocardial: with emphasis on myocardial preservation.

Various therapies during early hours of acute myocardial infarction (AMI) have been suggested to protect ischemic myocardium and reduce infarct size. Despite reports that prostaglandins (PGs) are released during myocardial ischemia, and that prostacyclin (PGI2) and thromboxane A2 (TXA2) have opposing effects on vasomotion and platelet aggregation, the physiologic roles of PGs, PGI2 and TXA2 in AMI have not been clearly defined. However, in pharmacologic doses, experimental evidence suggests that vasodilator PGs might be beneficial, and vasoconstrictor PGs might be deleterious, in AMI. Recent recognition that coronary spasm is frequent in AMI has led to the notion that an increased PGI2/TXA2 ratio might be desirable. Thus, exogenous PGE1, exogenous PGI2 or tis more stable analogs, drugs that stimulate PGI2 release, and inhibitors of TXA2 and harmful PGs are potential agents for protective therapy in AMI.

Alprostadil↗
PubMed1981

Salvage of ischemic myocardium by dipyridamole in the conscious dog.

We investigated the effect of i.v. dipyridamole, a potent small-vessel coronary vasodilator, on myocardial infarct size in conscious dogs. Dipyridamole, 7-9.7 microgram/kg; 15 dogs) or saline (15 dogs) was infused for 6 hours beginning 10 minutes after acute permanent occlusion of the mid-circumflex coronary artery. After sacrifice, 48 hours after occlusion, stereoscopic postmortem angiography was used to define the mass of the occluded coronary bed. Infarct size was determined by planimetry of weighed, unstained left ventricular slices. Dipyridamole produced a striking reduction in mean infarct mass compared with control (3.1 g vs 13.2 g, p less than 0.001), while mean occluded bed mass was similar (30.3 g vs 32.7 g, NS). As a percentage of the occluded bed, mean infarct size was reduced from 36.8% to 8.6% ( p less than 0.001). Mean arterial blood pressure declined approximately 10% after dipyridamole. Heart rate and left atrial pressure did not change significantly. Collateral blood flow, measured with 8- mu radioactive microspheres, increased in all regions during dipyridamole infusion. The infarct center and border regions had sustained increases over 6 hours of 23-80%, while nonischemic regions demonstrated a diminishing response over time, with a large (98-125%) increase 10 minutes after infusion and a smaller (22-25%) increase 6 hours later. Although antiplatelet or local metabolic effects cannot be excluded, the myocardial salvage produced by dipyridamole was most likely due to the increase in collateral blood flow.

Animals↗
PubMed1979

Early changes in collateral blood flow during myocardial infarction in conscious dogs.

We studied the early changes in collateral blood flow (CBF) after acute coronary artery occlusion and the relation of these changes to subsequent necrosis. We measured CBF with 7--9 microns radioactive microspheres before and at various times after circumflex artery occlusion in 42 conscious dogs that were killed 48 h later. CBF increased from 20 s postocclusion to later measurements (5 min, 15 min, 1 h, or 6 h) and did so in both necrotic and nonnecrotic areas of the occluded bed. However, the increase in CBF over time was not gradual, but appeared to occur between 20 s and 5 min, with no further changes for up to 6 h. There was a gradation of CBF in the occluded bed, from periphery to center and subepicardium to subendocardium. Central and subendocardial regions with CBF less than 0.40 ml-min-1-g-1 at 5--15 min postocclusion subsequently showed necrosis whereas epicardial and lateral regions with CBF greater than 0.50 ml/min did not. Thus CBF increases very early throughout the occluded coronary bed, and the level of CBF by 5 min appears to determine whether necrosis ultimately occurs.

Animals↗