摘要:

SUMMARYThe heart and lungs contain numerous receptors that, when activated, can modulate the behavior of the heart and blood vessels. However, the separate roles of these two organs in causing the reflex circulatory adjustments are difflicult to assess. Present evidence indicates that the lungs can tonically inhibit the vasomotor center and that lung inflation causes a reflex decrease in blood pressure as a result of dilatation of systemic vessels, bradycardia and a negative inotropic effect on the ventricles. This lung inflationvasodepressor reflex is due to activation of low-threshold pulmonary stretch receptors, subserved by vagal afferents. The inhibition exerted by the lungs on the limb and kidney vessels is similar during normocapnia but, in certain species, the inhibition of the renal vessels becomes much greater during hypercapnia. Thus, receptors in the lungs may preserve renal blood flow during respiratory acidosis and therefore contribute to the restoration of acid-base balance. The lung inflation reflex also modulates the response to activation of the arterial chemoreceptors by attenuating the chemoreceptor-induced bradycardia and peripheral vasoconstriction. During diving, the annulment of the pulmonary depressor reflex by the reflex respiratory arrest permits the full expression of the trigeminal reflex and chemoreflex so that the arterial blood pressure is maintained by constriction of systemic vessels and the available oxygen is distributed to the mnost vulnerable systems, the brain and lungs.Other lung receptors can also affect the cardiovascular system in abnormal circumstances. Juxtapulmonary capillary receptors linked to nonmedullated vagal afferents can he activated by pulmonary congestion to cause reflex bradycardia, tachypnea and depression of the somatic nervous system. Mechanoreceptors in the pulmonary arteries, when activated with pressure up to 60 mm Hg, cause systemic hypotension and occasional bradycardia; with higher pressures, the systemic pressure increases. Some mechanoreceptors in the lung parenchyma, which increase their discharge with lung inflation, are subserved by medullated fibers that pass in the sympathetic nerves to the spinal cord. Their function is unknown.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYThe effects of brief and sustained pharmacologic alpha-adrenergic stimulation on the coronary arterial circulation were compared in awake pigs. Phenylephrine was administered into the left anterior descending coronary artery (LAD) either as a bolus (eight pigs) or as a 15-minute infusion (eight pigs), with myocardial blood flow measured by the radioactive microsphere technique. Flow in the distribution in the LAD was compared with flow in myocardium perfused by the left circumflex coronary artery (LCF) as the ratio LAD/LCF. This technique corrects for systemic factors capable of modifying oxygen demand, and hence myocardial blood flow, in both zones. After a phenylephrine bolus (50–100 μg), LAD/LCF fell significantly, whereas no change was observed after the sustained infusion (5–10 and 50–100 μg/min). Four additional pigs were pretreated with i.v. adenosine to raise myocardial blood flow in excess of demand before sustained stimulation. In this setting LAD/LCF fell significantly during the sustained phenylephrine infusion.Brief alpha-adrenergic stimulation could overcome normal flow regulatory mechanisms and resulted in constriction of coronary resistance vessels. Such changes did not occur after sustained stimulation and suggest an ability of the coronary circulation to offset chronic vasoconstrictive effects. When the myocardium is overperfused, sustained alpha-adrenergic stimulation does not jeopardize myocardial oxygenation and its vasoconstriction potential is unmasked.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYThis study was performed to determine whether nitroglycerin (NG) can increase collateral flow to ischemic myocardium and reduce ultimate infarct size. Permanent occlusion of the mid-circumflex coronary artery was produced in 43 previously instrumented conscious dogs and within 3 minutes, 6-hour intravenous infusions were begun of saline (controls, n = 18), NG in doses to reduce mean arterial pressure by 10% but not below 90 mm Hg (n = 15), or NG followed by methoxamine (MX) to correct the NG-induced fall in blood pressure (n = 10). After sacrifice 2 days later, the occluded coronary bed was defined by postmortem coronary arteriography and masses of infarct and occluded bed were measured by planimetry of weighed rings of the left ventricle (LV). Infarct size was significantly less with NG than saline, both as a percent of LV (12.1 vs 6.4%,p< 0.05) and as a percent of occluded bed (32.0 vs 15.9%,p< 0.005). NG plus MX did not reduce infarct size more than NG alone: 6.6 vs 6.4% of LV, and 16.0 vs 15.9% of occluded bed. Masses of LV and occluded bed did not differ significantly among the three groups. Coronary blood flow (CBF), measured by 7–10-μm radioactive microspheres, increased by more than 50% throughout the occluded bed (p< 0.005) after NG, and was more than the spontaneous increase seen in controls (p< 0.05), but MX had no additional effect on CBF over NG alone. Six-hour infusions of NG therefore decreased infarct size and improved CBF, and addition of MX to reverse the systemic effects of NG did not lessen the benefit. The results suggest that under the conditions of this study, myocardial protection by NG did not depend on a decrease in myocardial oxygen demands, but rather on an increase in collateral flow resulting from a direct vasodilating action of NG on the coronary bed.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYThe purposes of this investigation were (1) to develop an in vivo method of determining the myocardium at risk after experimental coronary occlusion; (2) to define the spatial geometry of the salvageable ischemic border zone; and (3) to assess the ability of flurbiprofen, an antiinflammatory agent, to protect ischemic myocardium from necrosis. Twenty-two open-chest dogs underwent left anterior descending coronary artery occlusion and were randomized to treated (flurbiprofen 1 mg/kg i.v. at 30 minutes and 4 hours after occlusion; n = 11) or control (saline; n = 11) groups. Six hours after occlusion, methylene blue, 3 mI/kg, was injected into the left atrium, and immediately thereafter the hearts were removed and sliced transversely. Areas not perfused by methylene blue (area at risk [Ar]) were traced, planimetered, and compared to the area of necrosis (An) after incubation in triphenyltetrazolium chloride. The Arfor the two groups were similar (control 28.2 ± 2.6%; treated 25.2 ± 2.3% of total left ventricle; NS). In control dogs, An/Arwas 96.2 ± 0.7%, with similar values for the epicardium and endocardium. In treated dogs, An/Arwas 66.9 ± 8.9% (p< 0.001), with greater epicardial than endocardial salvage. Topographic superimposition of the An on the Ar showed that salvage occurred both on the epicardial and lateral aspects of the infarct.We conclude that (1) the in vivo methylene blue method of assessing myocardium at risk is useful in standardizing experimental infarct size; (2) flurbiprofen, administered 30 minutes and 4 hours after occlusion, is a potent agent for reducing infarct size; and (3) salvage of myocardium occurs both at the lateral and epicardial borders of the infarct in dogs treated with flurbiprofen.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYLittle information is available relating the extent of coronary atherosclerosis and myocardial infarct size measured at autopsy to clinical information. We correlated data from 85 patients who died 1 day to 6 months after a myocardial infarction. Of 70 patients who had coronary artery analysis at the time of autopsy,67 had significant (greater than 70%) occlusion of one or more major coronary arteries. The number of vessels with significant occlusion was not greater in patients with a history of hypertension, diabetes or lipid abnormalities, but patients with these risk factors died at a younger age. The extent of atherosclerosis did not correlate with functional or clinical class, length of survival, or heart weight at autopsy. Almost all patients (84%) with a clinical history of two or more infarctions had two or more vessels with greater than 70% occlusion.Gross and microscopic myocardial infarct size was measured at autopsy. There was an inverse relation between the percentages of old and new infarct. Total infarct size was related to the number of vessels with significant occlusion in the four major coronary arteries. The total percentage of old infarct was increased in patients with a history of prior myocardial infarction. Left ventricular and septal rupture occurred in patients with a significantly greater amount of recent necrosis, whereas patients with left ventricular aneurysm had more old myocardial infarct with a smaller amount of new necrosis.We concluded that myocardial infarct size at autopsy is closely related to the number of vessels with greater than 70% occlusion. In addition, patients with a history of myocardial infarction or with left ventricular aneurysm have a greater extent of old infarct and total necrotic tissue than patients with only new infarcts, who more frequently die of left ventricular or septal rupture.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYSixteen patients with exercise-induced ST-segment elevation and without a history of myocardial infarction or left ventricular aneurysm were studied. Fourteen complained of angina at rest, which was associated with ST-segment elevation in the same leads where it was recorded during exercise, and two patients had only exertional angina. Exercise-induced ST-segment elevation was generally reproducible in subsequent exercise tests performed in different hours of the day, but exercise tests repeated a mean of 15 months later did not induce this electrocardiographic abnormality. All patients had a marked susceptibility to coronary spasm, as shown by the response to the ergonovine test (12 positive tests in 12 patients) and by the occurrence of spontaneous spasm during coronary arteriography in two patients. In addition, coronary arteriography, performed in seven patients at the time of exercise-induced ST-segment elevation, revealed spasm of a major coronary vessel in all. In two patients we documented that exercise-induced ST-segment elevation was accompanied by a decreased coronary blood flow and increased coronary vascular resistance. We conclude that exercise-induced ST-segment elevation in patients without a history of myocardial infarction or left ventricular aneurysm is caused by coronary spasm of a major coronary vessel.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYSixteen diabetic males, 32–60 years old (mean 48.7 ± 8.9 years), without clinical or electrocardiographic evidence of heart disease and 12 normal volunteers, mean age 48.9 ± 8.8 years, participated in maximal exercise testing combined with thallium-201 myocardial scintigraphy. A motorized treadmill was used with the Bruce protocol. A standard 12-lead ECG and systolic blood pressures were recorded every minute during exercise and for at least 8 minutes in the postexercise period. Echocardiograms were obtained at rest for chamber dimensions and myocardial function.At maximal stress the heart rate attained by the normal controls was higher (174.5 ± 17.4 beats/min) than that of the diabetic males (163.1 ± 9.9 beats/min) (p< 0.05). Although the maximal systolic blood pressure for both groups was comparable (215.9 ± 32.5 mm Hg for the diabetics vs 209.6 ± 21.6 mm Hg for the normal controls), maximal systolic blood pressures > 210 mm Hg occurred in only three of 12 normal subjects (25%) but was noted in nine of 16 diabetics (56.2%).The duration of exercise was longer in controls (663.0 ± 92.1 seconds) than in the diabetics (519.0 ± 127.2 seconds) (p< 0.005). The estimated maximal oxygen consumption was also increased in controls vs diabetics (p< 0.005). Functional aerobic impairment was greater in the diabetics (10.4 ± 19.1%) compared with normal controls (−7.8 ± 9.0%). Significant ST-segment changes were present in two diabetics and one control subject. Of the 12 diabetic subjects who underwent exercise testing with thallium-201, five (41.7%) had abnormal perfusion during stress or with both stress and rest. Such abnormalities were present only once in the 11 perfusion studies in healthy subjects.Echocardiographic findings were similar in both groups. However, the percent of myocardial fractional shortening was smaller in diabetics than in controls (p< 0.05).Of the 12 subjects who underwent myocardial scintigraphy, an abnormal exercise ECG or a myocardial perfusion defect appeared in seven (58.3%) of the diabetics without overt cardiac disease and in only one normal subject. This suggests that asymptomatic subjects in this high-risk category of middle-aged diabetic males should be under close and repeated surveillance.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYTen-hour electrocardiographic (ECG) monitoring was performed on 289 survivors of myocardial infarction (MI) at 2 weeks, at monthly intervals for 6 months and then at 9 and 12 months after MI. Four hundred thirty episodes of ventricular runs were recorded on 88 patients (30%). The clinical features during the acute phase of MI of these 88 patients were evaluated prospectively and compared with those of patients who did not have runs. Both groups were similar with respect to age, sex and preexisting coronary risk factors. However, patients with runs had higher peak serum enzyme levels and a higher prevalence of congestive heart failure, cardiomegaly and left ventricular hypertrophy. They also had more frequent atrial premature complexes, premature ventricular complexes at a rate of 6/minute or more, and ventricular conduction defects during the acute infarction. The presence of runs within 3 months after the MI was predictive of the presence of runs during the period 4–12 months after MI. Using a multivariate logistic analysis patients could be divided into quartiles of risk for posthospital runs on the basis of features noted during the acute phase. The prevalence of runs ranged from 4% in the lowest quartile to 49% in the highest one. Although the rate of sudden death was not different in each quartile of risk of having ventricular runs, patients in the highest quartile had a significantly higher mortality rate (16.7%) than those in the lowest one (5.6%). We conclude that severe cardiac disease manifested by poor left ventricular function, high serum enzyme levels, and certain types of cardiac arrhythmias during acute MI are associated with an increased prevalence of ventricular runs during the posthospital phase. Our study suggests that the higher mortality rate in the highest quartile of risk of having ventricular runs is related to severe cardiac disease rather than to the presence of the runs.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYNinety-nine adult mongrel dogs underwent acute ligation of the proximal left anterior descending coronary artery. Thirty minutes later, the occlusion was released to evaluate the effectiveness of five antiarrhythmic protocols in eliminating reperfusion ventricular fibrillation. The five protocols included: protocol 1 — i.v. lidocaine, preligation and prerelease (n = 19); protocol 2 — i.v. lidocaine, prereperfusion only (n = 22); protocol 3 — chronic, oral, daily amiodarone for 2 weeks preligation (n = 19); protocol 4 — i.v. procainamide, preligation and prereperfusion (n = 21); and protocol 5 — i.v. verapamil, prereperfusion (n = 18). Each regimen was evaluated with respect to the incidence of reperfusion ventricular fibrillation in dogs that survived to reperfusion, and the results were compared to 77 control dogs that underwent identical coronary artery occlusion and release procedures without drug therapy. The incidence of reperfusion ventricular fibrillation was as follows: protocol I - seven of 15 dogs (47%); protocol 2 — six of 18 (33%); protocol 3 — 11 of 16 dogs (69%); protocol 4 — eight of 17 dogs (47%); and protocol 5 — 10 of 17 dogs (59%), compared with 36 of 60 (60%) in control dogs.Using chi-square analysis, protocol 2 was beneficial (p< 0.05). The dogs were then stratified into high- and low-risk subgroups based on the arrhythmic events of the antecedent coronary artery ligation periods, and predictive risk indexes for the occurrence of reperfusion ventricular fibrillation were developed. The Mantel-Haenszel method of statistical analysis revealed that none of these protocols resulted in a statistically significant reduction in the incidence of reperfusion ventricular fibrillation. Thus, use of these predictive indexes plus appropriate statistical methods has revealed, unexpectedly, limitations in the efficacy of a spectrum of antiarrhythmic agents in preventing reperfusion ventricular fibrillation.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SUMMARYA 58-year-old man with hypertensive cardiovascular disease and atrial flutter underwent electrophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surface ECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-like rhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was protected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrillation of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, with predominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, we could assess sinus node function by overdrive stimulation of the area of sinus node activity. Sinus node function studies revealed an underlying sick sinus syndrome.

ISSN:0009-7322    

出版商:OVID    

年代:1981

数据来源: OVID