SUMMARY To better define the mechanisms of blood pressure control in states of catecholamine excess, we infused norepinephrine for 28 days using subcutaneously implanted osmotic pumps in dogs previously instrumented for monitoring left ventricular dynamics and cardiac output. Plasma norepinephrine rose from 238 ± 27 to 4346 ± 952 pg/ml at 21 days, while epinephrine and dopamine levels did not change. Heart rate fell from 85 ± 4 to 63 ± 6 beats/min, while arterial pressure was unchanged from baseline. Total peripheral resistance rose 0.011 ± 0.003 mm Hg/ml/min from a control value of 0.029 ± 0.002 mm Hg/ml/min, and cardiac output decreased 1093 ± 292 ml/min from a baseline level of 3575 ± 156 ml/min. Since stroke volume did not change, the maintenance of arterial pressure is related to decreases in cardiac output secondary to bradycardia. Buffering mechanisms are responsible for maintenance of systemic arterial pressure because hexamethonium and atropine caused hypertension. Although left ventricular end-diastolic pressure, end-diastolic diameter, shortening, rate of change of pressure, velocity of myocardial shortening, cardiac work, stroke work, and the double product did not change significantly during the study, postmortem examination demonstrated biventricular hypertrophy. Thus, despite markedly elevated catecholamine levels and no elevation of systemic arterial pressure, myocardial hypertrophy developed. These studies lend support to the hypothesis that norepinephrine may be a direct myocardial tropic hormone and suggest that intense activation of reflex buffering mechanisms maintains blood pressure in the normal range during chronic catecholamine infusion. (Hypertension 9: 582-590, 1987) KEY WORDS • bradycardia • hypertension • hypertrophy • catecholamines • total peripheral resistance • atropine E LEVATIONS in catecholamine levels may be associated with a number of disease states, including mitral valve prolapse (MVP), 1 -2 chronic myocardial failure, 3 " 6 and pheochromocytoma. 7 These disease states may be characterized by sustained or episodic hypertension, myocardial dysfunction, and cardiomyopathy.Recently, it has been noted that certain patients with MVP, chronic myocardial failure, or pheochromocytoma have dysautonomia, manifested by abnormalities in heart rate or blood pressure response (or both) to orthostatic change or exercise. 8 " 12 Some investigations of patients with MVP having dysautonomia are consistent with evidence of hyperadrenergic states and some with simultaneous hypervagatonia. 9 -13 Significant elevations in serum catecholamine levels have been observed in a group of symptomatic patients with MVP 1 ' l4 ; these results have been confirmed by other workers. 2 ' 8> l5 Patients with chronic myocardial failure, regardless of etiology, have elevated plasma norepinephrine (NE) levels. 16 In addition, defects in baroreceptor reflex-mediated vasoconstrictor responses have been noted in dogs 17 and in patients 18 -19 with marked myocardial dysfunction.Several studies, summarized by Ec...
SUMMARY The contractile state of the noninfarcted myocardium was examined in adult cats after myocardial infarction produced by ligation of several branches of the left coronary artery. At 2 days, 7 days, and 6 weeks after infarction, and after determination of intracardiac pressures, papillary muscles were excised from the noninfarcted segment of the right ventricle and attached to a myograph for analysis of contractile function. One week after infarction there was a decline in actively developed force at L msx , caused by a decrease in the rate of force development. In addition, the response to procedures that augment myocardial contractility, such as paired stimulation and increasing the frequency of electrical stimulation, was significantly depressed. Two days after infarction, changes were less significant, although similar in direction. Six weeks after infarction, developed force at L max had returned to normal values. The response to procedures augmenting contractility also had returned to normal. There appears to be a distinct, reversible loss of contractility in the remaining viable myocardium in the early phase after experimental infarction.AFTER MYOCARDIAL infarction, the uninvolved portion of the heart generally is thought to maintain function and metabolism, unless coexisting stenosis of additional vessels causes ischemia of the noninfarcted segments. However, after experimental myocardial infarction, the clearly nonischemic portion of the heart muscle shows changes in its energy metabolism as well as a reversible decline in norepinephrine content.1 * 3 The functional significance of these changes, however, remains largely unknown because determinations of ventricular function after infarction fail to differentiate the infarcted and the surviving areas. Theroux et al. 4 demonstrated an increased extent of shortening of noninfarcted areas early after infarction which was caused by regional operation of the Frank-Starling mechanism; an alternate explanation could be that unloading of the ischemic segment permits increased active shortening as well. In the present study we analyzed myocardial function after isolation of the surviving heart muscle, to exclude any effect of the infarct itself. To avoid the ill-defined changes which occur in the zone which borders the infarct, we studied right ventricular papillary muscles after left ventricular infarction. We thus attempted to determine the effect of an acute myocardial infarction on the contractile properties of surviving, noninfarcted heart muscle. MethodsMyocardial infarction was produced in adult cats by ligation of several branches of the left coronary artery. Under general anesthesia (halothane, N 2 O, and O 2 ), the cats were intubated, and a thoractomy was performed through the 5th left intercostal space. After opening the pericardial sac, we ligated between three and five branches of the left coronary artery which lead to the free wall of the left ventricle. Infarctions produced in this way were comparable in extent and location in different cat...
Perioperative blood usage during 172 heart transplants (HTs) and 100 heart-lung transplants (HTLs) performed at the same center during 1986 and 1989 was reviewed. In 1986, 79 HTs were performed with a median (interquartile range) blood component use of 12 (range, 8-20) units, of which 6 (range, 4-8) constituted red cell components. The use of blood components was significantly reduced (p less than 0.05 by the Mann-Whitney U test) in 1989 to 10 (range, 8-20) units, of which red cell components constituted 5 (range, 3-7) units. Fifty HLTs in 1986 used a median (interquartile range) of 25.5 (range, 11.5-53) units of blood components. This use was significantly reduced (p less than 0.05) to a median of 18 (range, 9-29) units in 1989, of which 8 (range, 5-11) were red cell components, 4 (range, 2-8) were units of fresh-frozen plasma, and 5 (range, 0-10) were units of platelets. More blood components were used in patients who had previous cardiothoracic surgery and/or previous transplants; this reached significance in the 1986 HTs (p less than 0.001). Fresh blood was used in only one HT but in 12 (24%) of 1086 HLTs and 4 (8%) of 1989 HLTs. As the indication for fresh blood was excessive bleeding, there was a significantly greater use of blood components in 1989 HLT patients receiving fresh blood than in those not receiving fresh blood (median [range] of 163.5 [62-251] units compared to 15.5 [3-126]).(ABSTRACT TRUNCATED AT 250 WORDS)
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