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Biomedical subjects

W B Hood

Publications and source records attributed to W B Hood.

At least 91 records · Page 5Linked to original sources
PubMed1977

Effects of sympathetic blockade and splenectomy on cardiac output response to muscular work in dogs.

The effects of splenectomy and sympathetic blockade on cardiac output (Q) response to mild to moderate exercise were studied in chloralose-anesthetized vagotomized dogs during electrically-induced muscular work, which increased oxygen consumption (VO2) 4- to 5-fold. Splenectomy reduced the exercise factor (deltaQ/deltaVO2 ratio) from 5.86 +/- 0.43 (SE) to 3.30 +/- 0.34 (p less than 0.001), while left nephrectomy had no effect. The exercise factor was not affected by beta-adrenoceptor blockade produced by propranolol or practolol, but was reduced by mecamylamine. The spleen did not increase cardiac output by displacing blood into the general circulation because pulmonary artery wedge pressure did not change during exercise in normal dogs. Furthermore, cardiac output was increased 35 +/- 6% after intraportal infusion of splenic venous blood obtained during exercise, whereas arterial blood infusion increased cardiac output only 10%. We conclude that the cardiac output rise during exercise in part is caused by the inotropic action of a splenic noncatecholamine substance, which is released by sympathetic stimulation.

Animals↗
PubMed1977

Graded global ischemia and reperfusion. Cardiac function and lactate metabolism.

The effect of global ischemia of different degrees of severity and reperfusion was studied in the isolated working rat heart. Four degrees of ischemia were induced by reducing the control total coronary flow of 8 ml/min to 0, 0.04, 0.4, or 0.8 ml/min for 30 minutes, after which the coronary flow was returned to the control level. After severe ischemia (0 and 0.04 ml/min ischemic coronary flow groups), recovery of contractility was to less than 30% of the control, pre-ischemic value of ventricular developed pressure and dP/dt, and irreversible cardiac contracture and an increased pacing threshold occurred. After moderate ischemia (0.4 and 0.8 ml/min ischemic coronary flow groups), contractile function recovered completely, ischemic contracture was rapidly reversible and the pacing threshold did not increase. The moderately ischemic groups were able to function at a stable, low level of contractility for the 30 minute ischemic period, whereas the severely ischemic groups had no contractile activity. The amount of calculated tissue lactate accumulation correlated with the occurrence of irreversible ischemic injury; the severely ischemic groups which failed to recover with reperfusion accumulated 3-5 times as much lactate as the moderately ischemic groups which recovered completely. The results suggest that relatively small differences in the severity of the ischemic condition can markedly affect the degree of tissue injury.

Animals↗
PubMed1976

Coronary turncoat.

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Angina Pectoris↗
PubMed1976

Experimental myocardial infarction: XII. Dynamic changes in segmental mechanical behavior of infarcted and non-infarcted myocardium.

The mechanical behavior of ischemic myocardium was studied in anesthetized open chest dogs. In each animal, a small well localized myocardial infarction was produced by ligation of a single ventricular branch of the left circumflex coronary artery. Serial in situ measurements of segment length were made by mercury-in-Silastic gauges sutured directly to the left ventricular surface. After coronary ligation, systolic aneurysmal bulging of the ischemic segment was uniformly noted. This was quantified as follows: normalized segment length change in this region, expressed in muscle lengths (where muscle lengths = phasic segment length amplitude/end-diastolic segment length), immediately increased from 0.06 +/- 0.01 (standard error of the mean) to 0.10 +/- 0.02 muscle lengths (+67 percent, P less than 0.02). Over a 6 hour period, muscle lengths progressively declined to near control values, but retained an aneurysmal contour. End-diastolic segment length increased 5 percent above control values after coronary occlusion and remained fixed at this level for 6 hours. In contrast, noninfarcted myocardium exhibited no significant changes in muscle length or end-diastolic segment length. These studies demonstrate that the degree of systolic aneurysmal bulging in infarcted myocardium, although initially great, resolves within 6 hours but retains an aneurysmal contour. These findings are consistent with either partial return of contractility or diminished local compliance, but persistence of an aneurysmal shape favors the latter mechanism. The fixed increase in end-diastolic segment length suggests that "stress-relaxation" takes place in the infarcted region. It is possible that diminished compliance in zones of infarction, previously noted after several days, begins within a few hours after the onset of ischemia.

Animals↗
PubMed1976

Precordial ST-segment mapping. 4. Experience with mapping of ST-segment depression in anterior transmural myocardial infarction.

In order to assess the relative significance of precordial ST-segment elevations and depressions, 32 patients with anterior transmural myocardial infarction were studied utilizing serial 49-lead precordial maps. Theoretically, zones of ST-segment depression adjacent to major zones of ST-segment elevation might represent border areas of mild ischemia, and hence could be more readily amenable to intervention therapy. As expected, an extensive zone of ST-segment elevation was observed precordially in each of these patients. However, zones of ST-segment depression in adjacent areas were noted to occur inconsistently, were limited in distribution and magnitude, and bore no fixed relationship to zones of ST-segment elevation. Thus, mapping of precordial ST-segment depression in anterior transmural infarction probably has a limited role in assessing evolution of ischemic injury or therapy in these patients. This finding does not, however, vitiate the significance of ST-segment depressions in angina, intermediate coronary syndrome, or non-transmural infarction, conditions which may deserve further study using mapping techniques.

Adult↗
PubMed1976

Diagnosis of high anterolateral and true posterior myocardial infarction by chest wall ECG-mapping.

Precordial and posterior chest wall ST-mapping has been utilized in a patient with high anterolateral and true posterior myocardial infarction. In this patient evolution of the anterolateral component of the infarct was accurately delineated by changes in the precordial map which were not detected in the standard precordial leads. The true posterior component of the infarct was clearly diagnosed by detection of pathological Q waves and ST elevations in posterior chest wall maps, whereas right precordial standard leads had shown only suggestive reciprocal changes. The study illustrates the superiority of localized chest wall mapping over conventional 12-lead electrocardiography in detecting transmural infarction in high anterolateral and posterior regions of the left ventricle.

Electrocardiography↗
PubMed1976

Persistence of myocardial injury following brief periods of coronary occlusion.

Transient (20 min) occlusion of the left anterior descending coronary artery in open-chest anaesthetized dogs caused immediate aneurysmal bulging of the ischaemic segment, which preceded epicardial ST-segment elevation. Reperfusion after 20 min restored epicardial electrograms to normal, wheras mechanical dysfunction persisted for a least 45 min therafter. The study shows that there is temporal disparity between electrical and mechanical events both at the inception of myocardial ischaemia and during recovery from transient myocardial ischaemia.

Animals↗
PubMed1976

Precordial ST-segment mapping. 2. Effects of oxygen inhalation on ischemic injury in patients with acute myocardial infarction.

Precordial ST-segment mapping was serially applied in the Coronary Care Unit for the study of the effect of oxygen inhalation on the ischemic injury in 17 patients with acute anterior transmural myocardial infarction. A 49-lead ECG system was used. The sum of all ST elevations (sigmaST) recorded was taken as an index of magnitude of ischemic injury and the number of recording sites showing ST elevation (NST) was taken as an index of extent of ischemic damage. Stability of the precordial maps was observed over a period of one hour while the patients were on ambient air. Oxygen inhalation for a mean of 66 min resutled in a fourfold increase of PaO2 and a mean of 16% reduction of both sigmaST and NST. When the patients were returned to ambient air breathing, a mean of 13% increase of sigmaST and 19% of NST from the levels recorded during oxygen inhalation were observed. Levels of sigmaST and NST on ambient air following discontinuation of oxygen inhalation were not significantly different from the corresponding values from maps recorded before onset of oxygen breathing. Blood pressure and heart rate remained unchanged throughout the study. Clinical status of the patients was unchanged during the study period save for two patients who showed changes in intensity of their chest pain.

Acute Disease↗
PubMed1976

Experimental myocardial infarction. XIII. Sequential changes in left ventricular pressure-length relationships in the acute phase.

Diastolic pressure-length relationships of an ischemic region of the canine left ventricle were measured over a six-hour period following left anterior descending coronary artery ligation, and their evolution was compared with the extent of systolic aneurysmal bulging. Normalized ischemic segment length excursion, which after coronary artery ligation may be taken as a measure of systolic aneurysmal bulging, increased during the first hour after ligation but thereafter declined toward control values. Concurrently, reciprocal changes were demonstrated in the slope of the end-diastolic pressure-length curves obtained during transient pressure loading of the left ventricle. These data show that the magnitude of acute systolic aneurysmal bulging followed experimental coronary artery ligation is determined not only by loss of contractile function, but also by changes in passive pressure-length relationships of the myocardium. Moreover, the results indicate that development of akinesis in experimental ischemia, heretofore demonstrated only in the chronic phase of infarction, may begin within hours of the onset of myocardial ischemia.

Acute Disease↗
PubMed1976

Afferent neural pathway in the regulation of cardiopulmonary responses to tissue hypermetabolism.

We studied the role of neural transmission from hypermetabolic peripheral tissues in the regulation of cardiac output and pulmonary ventilation in chloralose-anesthetized dogs. Cross-circulation techniques with femoral-femoral or femoral-aortic anastomoses were used to produce a vascularly isolated, but normally innervated, hindlimb or lower half-body, 2,4-Dinitrophenol (DNP) was infused into the arterial side of the perfusion circuit to triple oxygen consumption and to increase lactate production by the cross-perfused area. After infusion of DNP, cardiac output and mean systemic arterial blood pressure increased, but neither heart rate nor pulmonary artery wedge pressure changed significantly. Pulmonary minute ventilation and arterial pH also increased, while arterial PCO2 fell. These changes were abolished when the nerve connections between the perfused limb and its parent body were severed. Normal saline, when administered in a similar manner, did not increase either ventilation or cardiac output, and simple denervation without previous infusions of DNP also had no effect. These results indicate that there are receptors sensitive to metabolic changes in the tissue, and that neural transmission is an important afferent link in regulating the cardiopulmonary responses to increased tissue metabolism.

Afferent Pathways↗
PubMed1976

Effects of ischemia and reperfusion on myocardial uptake of tritiated digoxin.

The effect of coronary reperfusion on the uptake of cardiac glycosides by ischemic myocardium was studied in 17 open chested dogs undergoing anterior wall infarction produced by snaring confluent branches of the left coronary system. Epicardial electrograms delineated ischemic zones of S-T elevation, border, and nonischemic zones. Animals were reperfused by snare release 1, 2, and 6 hr after occlusion. After 15 min of reperfusion, 1.0 mg of [3H] digoxin was given intravenously, and 2 hr later the hearts were excised and endocardial (endo) and epicardial (epi) samples from each zone were analyzed for [3H] digoxin concentration. In five dogs occluded for 1 hr and reperfused, [3H] digoxin uptake was comparable in endo and epi layers of all three zones. In six dogs reperfused after 2 hr of occlusion, mean (+/-S.E.) [3H] digoxin concentrations (nanograms per gm) were significantly reduced by 54 percent in endo (111 +/-18) and 35 percent in epi (151 +/- 23) layers of the ischemic zone as compared with the mean nonischemic concentration (endo249 +/- 34; epi 239 +/- 34). Border zone endo and epi [3H] digoxin uptake was reduced by 21 and 17 percent, respectively. In six dogs reperfused after 6 hr of occlusion, [3H] digoxin uptake in the ischemic zone was markedly reduced by 85 percent in endo (34 +/- 4) and 60 percent in epi (86 +/- 12) layers as compared with the nonischemic concentration (endo 232 +/- 19; epi 217 +/- 15). Border zone uptake was decreased by 54 percent in endo and 38 percent in epi regions. We conclude that coronary reperfusion between 2 and 6 hr of coronary occlusion is associated with markedly reduced myocardial digoxin uptake, more pronounced in subendocardial regions of ischemic tissue. This alteration in digoxin binding by reperfused ischemic myocardium is consistent with ischemia-induced structural or functional alterations in the putative digitalis receptor, (Na++K+)-ATPase.

Animals↗