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Biomedical subjects

F L Gold

Publications and source records attributed to F L Gold.

6 recordsLinked to original sources
PubMed1984

Adrenergic coronary vasoconstriction in acute right ventricular hypertension.

This study tested the hypothesis that alpha-adrenergically mediated coronary vasoconstriction during the haemodynamic stress of right ventricular hypertension antagonises the effect of adenosine. Myocardial blood flow and plasma catecholamines were measured in 12 awake, but mildly sedated, chronically instrumented dogs during acute pulmonary artery constriction (PAC) before and during an infusion of adenosine (1 mg X kg-1 iv), with and without prior alpha blockade with phenoxybenzamine (10 mg/kg iv). PAC was performed by gradual inflation of a pulmonary artery hydraulic occluder until aortic pressure began to fall, after which aortic pressure was restored to control levels by aortic constriction. Heart rate was held constant by pacing. Two distinct patterns of response to adenosine during PAC were observed. Six dogs (group A) demonstrated attenuation of adenosine induced coronary vasodilatation; left ventricular (LV) myocardial flow fell from 7.35 +/- 1.14 ml X min-1 . g-1 (+/- SE) during adenosine to 3.63 +/- 0.81 during PAC and adenosine (p less than 0.05). In the six remaining dogs (group B) attenuation was not observed (LV flow = 6.51 +/- 0.92 during adenosine; 8.14 +/- 1.11 during PAC and adenosine). During PAC, both the severity of RV hypertension and levels of circulating catecholamines were greater in group A than in group B. Alpha-blockade partially restored adenosine responsiveness in group A during PAC, and LV flow increased to 6.23 +/- 0.80 (p less than 0.05). We propose that attenuation of the coronary flow response to adenosine infusion during PAC is related to the severity of PAC and alpha-adrenergically mediated coronary vasoconstriction.

Adenosine↗
PubMed1982

Influence of systolic intracavity pressure on right ventricular perfusion in the awake dog.

This study tested the hypothesis that an acute increase in right ventricular pressure would result in selective impedance of blood flow into the right ventricular subendocardium (ENDO) similar to that seen normally in the left ventricle. Since tachycardia (reduces diastolic time) and vasomotor paralysis will reveal impedence to blood flow by a decrease in ENDO to subepicardial (EPI) myocardial blood flow (MBF) ratio, MBF was measured with microspheres in eight awake dogs during rapid pacing at 176 +/- 2 beats . min-1 (mean +/- SE) after acute pulmonary artery constriction (PAC) before and during adenosine (A) infusion (1.00 mg . kg-1 . min-1). AP was held constant by aortic constriction. During control pacing the ENDO/EPI ratios were 1.38 +/- 0.08 and 1.46 +/- 0.12 in the RV and LV, respectively. During adenosine infusion the ENDO/EPI decreased to 0.85 +/- 0.08 (P less than 0.05) in the LV but did not change in the RV (1.17 +/- 0.10). During PAC and pacing alone the RV ENDO/EPI was 1.24 +/- 0.05 (NS vs control), but during adenosine fell to 0.88 +/- 0.07 (P less than 0.05). Transmural blood flow to the interventricular septum (IVS) was also affected by increased RV pressure. During control the ratio of blood flow to the left and right side (LV/RV) of the IVS was 1.32 +/- 0.12. PAC alone caused a redistribution of MBF toward the right side and the LV/RV fell to 0.66 +/- 0.06 (P less than 0.05). During PAC and adenosine, however the LV/RV rose to 1.38 +/- 0.08. These data demonstrate that increased RV systolic pressure produces systolic impedance to blood flow to the right ventricular ENDO and the right side of the interventricular septum.

Adenosine↗
PubMed1982

Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve.

Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 microM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 +/- 0.09 ml/min per g (mean +/- SEM) during control conditions to 1.69 +/- 0.27 ml/min per g during moderate pulmonary artery occlusion (P less than 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-to-subepicardial blood flow ratio fell from 1.36 +/- 0.14 to 0.77 +/- 0.06 (P less than 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 +/- 0.18 (P less than 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 +/- 0.10 to 2.25 +/- 0.30; P less than 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted.

Adenosine↗
PubMed1980

Alternating bundle branch block.

Mechanisms postulated for alternating bundle branch block are incomplete- and cycle-length-dependent-block in both the right and left bundle branches. A patient with severe longstanding cardiac conduction disease who developed alternating bundle branch block during treatment for advanced ischemic heart disease and malignant ventricular arrhythmia is presented. In this patient alternation was induced by atrial premature beats as well as spontaneous and pacemaker induced premature ventricular beats. Right bundle branch block which followed a premature atrial beat resulted from the longer refractory period of the right bundle. The maintenance of right bundle branch block at long cycle lengths was presumed to be due to continuous retrograde reentry. This was terminated when a pause following a premature beat allowed functional recovery of the right bundle branch. This patient died suddenly at home with a functioning pacemaker, demonstrating the high risk of death from ventricular dysrhythmia in the post myocardial infarction patient with a new conduction defect.

Aged↗
PubMed1980

Combined left ventricular aneurysmectomy, mitral valve replacement and aortocoronary bypass grafting: results of surgery.

Eighteen patients with ischemic heart disease who underwent left ventricular aneurysmectomy (LVA) and concomitant mitral valve replacement (MVR) for severe mitral regurgitation during 1973-1978 were identified. Eleven patients (61%) underwent aortocoronary bypass procedures (CABG) at the same operation. All patients had New York Heart Association class III or IV symptoms of congestive heart failure; six (33%) had disabling angina pectoris and four (22%) had had life-threatening ventricular tachycardia. Surgical mortality was 11%. The survival rate at 2 and 3 years was 80% and 57%, respectivey, with a mean follow-up of 21 months (range 4-56 months). At follow-up all patients had improved symptomatically by at least one functional clas; four patients were class II and six were class 1. The mean values (+/ SEM) for preoperative cardiac index, left ventricular end-diastolic pressure and ejection fraciton were 2.0 +/- 0.1 l/min/m2, 22 +/- 2.3 mm Hg, and 30 +/- 3.5%, respectively. Postoperative right-heart catheterization in seven patients revealed no difference between preoperative and postoperative resting cardiac index and pulmonary wedge pressure, although all seven patients claimed significant improvement. Thus, although resting hemodynamics may not be altered, combined LVA, MVR and CABG can be performed with acceptable surgical risk in these seriously ill patients and can provide excellent symptomatic improvement with good long-term survival.

Aged↗