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Biomedical subjects

J G Stone

Publications and source records attributed to J G Stone.

At least 55 records · Page 3Linked to original sources
PubMed1987

Propranolol increases oxygen utilization during hypoxia.

The effects of propranolol on whole body oxygen consumption and blood oxygen content were measured in the dog during extreme hypoxic conditions. At 9% inspired oxygen four of eight control animals died within 40 min. An identical second group was pretreated with propranolol and none died during the same hypoxic stress. Hypoxia decreased oxygen consumption in both groups, but the decrease was less in the propranolol-pretreated dogs. A second set of 16 dogs was ventilated with 10% oxygen and all animals survived. A similar, although less pronounced, effect on oxygen consumption was noted and propranolol once again lessened the hypoxia-induced decrease in oxygen consumption. With hypoxaemia, metabolic acidosis developed in all animals and the arterio-venous oxygen content difference decreased; however, propranolol lessened the acidosis and the decrease in arterio-venous oxygen content difference. We conclude that, during hypoxia, propranolol increases oxygen utilization by the tissues and this might account for better survival.

Animals↗
PubMed1987

The association isoflurane-verapamil causes regional left-ventricular dyssynchrony in the dog.

In ten dogs anesthetized with 1% inspired isoflurane, the effect of low-dose verapamil on global and regional myocardial function was studied. The administration of verapamil resulted in no change in heart rate or blood pressure, but left ventricular stroke work, peak power, LV dP/dt max, and aortic blood acceleration were significantly reduced, while coronary blood flow remained unchanged. End-diastolic length increased in territory supplied by both left anterior descending (LAD) and left circumflex (LC) artery, but a significant decrease in systolic shortening occurred in the LAD segment only. Dyssynchrony of wall motion, characterized by post-systolic shortening, accompanied in three animals by a small amount of systolic lengthening, appeared with the administration of verapamil and was more pronounced in the LAD segment. Such patterns of wall motion have usually been attributed to myocardial ischemia. In the absence of significant reduction in coronary blood flow, and in the presence of a delay in onset of shortening and lengthening, these patterns of wall motion are more likely to reflect dyssynchrony of regional function than ischemia.

Anesthesia, Inhalation↗
PubMed1984

Propranolol premedication blunts stress response to nitroprusside hypotension.

Hypotension was induced in sixteen patients with nitroprusside during anesthesia for surgical correction of cerebral aneurysms. Eight patients were premedicated with propranolol (180 mg orally) for one day and the other eight were not. Before the start of anesthesia, the untreated patients had a mean arterial pressure of 102 +/- 3 mm Hg, a heart rate of 76 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 114 +/- 21 and 258 +/- 34 pg/ml, respectively. The propranolol-premedicated patients came to the operating room in a significantly different clinical state with a mean arterial pressure of 92 +/- 3 mm Hg, a heart rate of 71 +/- 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 76 +/- 28 and 144 +/- 28 pg/ml. During induced hypotension, plasma epinephrine and norepinephrine concentrations increased significantly in both groups (454 +/- 42 and 730 +/- 58 pg/ml in the untreated patients, 160 +/- 48 and 419 +/- 67 pg/ml in the propranolol premedicated patients), but the increase in catecholamines was significantly greater in the untreated patients. Thirty minutes after nitroprusside was discontinued, epinephrine and norepinephrine concentrations were higher than in the awake state in untreated patients and were associated with rebound hypertension and tachycardia. In contrast, in propranolol-premedicated patients, plasma epinephrine and norepinephrine concentrations decreased towards the preanesthesia values, mean arterial pressure gradually returned to the prehypotension level, and heart rate remained unchanged. This study thus demonstrates that propranolol premedication attenuates the release of catecholamines in response to nitroprusside-induced hypotension.

Adult↗
PubMed1983

Influence of volume loading on intraoperative hemodynamics and perioperative fluid retention in patients with valvular regurgitation undergoing prosthetic replacement.

Preload and afterload were controlled intraoperatively in 2 groups of patients with valvular regurgitation and congestive heart failure in order to determine the effect of fluid loading on weight gain and subsequent recovery. As a part of their anesthetic management before cardiopulmonary bypass, 16 patients were given 1 liter of crystalloid with nitroprusside infused at 1 microgram/kg/min and 16 received 4 liters of crystalloid with nitroprusside at 4 micrograms/kg/min. Arterial and filling pressures were kept the same in both groups. Heart rate and vascular resistance became significantly lower and cardiac index and stroke volume significantly higher in the fluid-augmented group. The transition to cardiopulmonary bypass was smoother for the fluid-augmented patients. All patients survived, and 2 in each group were ventilated beyond 24 hours. The mean weight gain at surgery was the same in the 2 groups (3 kg). For the first 2 postoperative days, body weight remained unchanged and thereafter, both groups lost weight at 0.6 kg/day. Preoperative weight was reached on day 7 and discharge occurred on day 15, 2 kg below control. Thus, a modest operative weight gain in these patients is inevitable, benign, and independent of the volume of fluid infused before bypass.

Aortic Valve↗
PubMed1983

Catheter-induced pulmonary arterial trauma: can it always be averted?

Catheter-induced pulmonary arterial hemorrhage is a serious and still recurring complication. This report describes our experience with 200 cases managed successfully by a prophylactic approach to the problem. The technique involves partial withdrawal of the pulmonary arterial catheter into a sterile protective sleeve during cardiopulmonary bypass and subsequent reinsertion when the normal circulation is restored.

Adult↗
PubMed1981

Propranolol alters renin release during nitroprusside-induced hypotension and prevents hypertension on discontinuation of nitroprusside.

Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 +/- 3 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 +/- 2 torr and plasma renin activity increased to 3.5 +/- 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 +/- 0.02 mg/kg) mean arterial pressure was reduced to 53 +/- 2 torr, and plasma renin activity increased to 8.8 +/- 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.

Adult↗
PubMed1981

Catheter-induced pulmonary artery hemorrhage. Diagnosis and management in cardiac operations.

Three case reports describing catheter-induced pulmonary artery hemorrhage in patients having cardiac operations are presented--a 0.2% incidence of this complication. One patient exsanguinated and died, another survived after undergoing an emergency lobectomy, and the third escaped without surgical intervention. As a result of this experience and the recommendations in the literature, we have developed and describe herein a rational therapy for this highly lethal complication.

Aged↗
PubMed1980

Acute hemodynamic alterations after mitral valve replacement with the glutaraldehyde-treated porcine heterograft prosthesis.

Perioperative hemodynamic changes following mitral valve replacement using the porcine heterograft prosthesis were measured in 21 patients with acquired mitral valve disease. Preoperatively, a state of compensatory cardiac failure was suggested by the following: an increased heart rate (HR) (96 beats per minute); low cardiac and stroke volume (SVI) indices (2.3 +/- 0.10 L/min/m2 and 25 +/- 2 ml/beat/m2); and increased systemic vascular resistance (SVR) (1,626 +/- 116 DYNE SEC CM-5). Bothe the mean pulmonary artery PAP) and pulmonary capillary wedge pressures (PCWP) were elevated as well (32 +/- 3 and 22 +/- 2 torr). Immediate hemodynamic improvement followed valve replacement. HR, SVR, PAP, and PCWP all decreased significantly. Twenty-four hours after valve replacement, PAP (23 +/- 1 torr) and PCWP (13 +/- 1 torr) demonstrated marked declines, SVR was reduced by one-third (1,173 +/- 87 dyne sec cm-5), HR had decreased by 10 beats per minute, and SVI had increased to 30 +/- 2 ml/beat/m2. The prompt circulatory improvement of patients soon after mitral valve replacement using the porcine heterograft compares favorably with studies in which other valve types were employed and in which postoperative cardiovascular depression was encountered frequently.

Adult↗
PubMed1980

Nitroprusside and mitral stenosis.

The cardiovascular effects of an intravenous nitroprusside infusion were evaluated intraoperatively in seven patients with pure mitral stenosis and seven patients with predominant mitral stenosis. Prior to therapy the adverse hemodynamic consequences of light anesthesia and surgical stimulation were evident in all patients: systemic and/or pulmonary hypertension were present, systemic vascular resistance was twice normal, and cardiac function was depressed. Nitroprusside consistently reduced systemic vascular resistance and systemic arterial as well as pulmonary arterial and wedge pressures, but cardiac index increased only when severe pulmonary hypertension and/or some mitral regurgitation coexisted with mitral stenosis. In the group with predominant mitral stenosis, cardiac index increased from 1.8 to 2.1 L/min/m2 with nitroprusside (p < 0.05). In three individuals who demonstrated severe pulmonary hypertension (one with pure mitral stenosis and two with predominant mitral stenosis), nitroprusside induced an increase of almost 50% in cardiac index and stroke volume. In contrast, patients with pure mitral stenosis and mild pulmonary hypertension showed little change in cardiac index or stroke volume. It is concluded that nitroprusside can safely be used to control systemic or pulmonary hypertension during anesthesia and surgery in patients with mitral stenosis and that if severe pulmonary hypertension and/or mitral regurgitation coexist with mitral stenosis, cardiac function will also improve.

Ferricyanides↗
PubMed1980

Afterload reduction and preload augmentation improve the anesthetic management of patients with cardiac failure and valvular regurgitation.

Data were collected from 17 patients with valvular regurgitation and ventricular failure who were about to undergo prosthetic replacement of an insufficient cardiac valve. Awake control hemodynamic measurements revealed that these patients came to the operating room with a high systemic vascular resistance of 38 units and low cardiac and stroke volume indices of 2.2 L/min/m2 and 30 ml/beat/m2, respectively. A preanesthetic infusion of nitroprusside together with almost 2 L of lactated Ringer's solution caused vascular resistance to decrease to 19 units (normal) while filling pressure remained high. As a result, while the combined therapy continued, neither the induction of anesthesia nor surgical stimulation produced cardiovascular deterioration; in fact, cardiac index measured above 3.1 L/min/m2 and stroke volume index above 40 ml/beat/m2 throughout anesthesia and surgery. We conclude, therefore, that the combination of afterload reduction and preload augmentation provides the best possible environment within which to conduct the anesthetic management of patients with valvular regurgitation and ventricular failure.

Adult↗
PubMed1979

Hypertension during anesthesia on discontinuation of sodium nitroprusside-induced hypotension.

The authors had observed that on intraoperative discontinuation of sodium nitroprusside being administered to induce hypotension, mean arterial pressure increased to above the pre-hypotension level. Twelve patients who recieved hypotensive anesthesia for surgical correction of cerebral aneurysms were studied to evaluate the role of the renin-angiotensin system in this phenomenon. In the awake state, mean arterial pressure was 100 +/- 2 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the establishment of stable halothane-nitrous oxide anesthesia, mean arterial pressure decreased to 85 +/- 1 torr and plasma renin activity increased to 4.4 +/- 0.1 ng/ml/hr. No appreciable change in either occurred over the next two hours of operation. During sodium nitroprusside-induced hypotension, mean arterial pressure decreased to 49 +/- 2 torr and plasma renin activity increased to 15.2 +/- 0.2 ng/ml/hr. Thirty minutes after discontinuation of sodium nitroprusside administration, mean arterial pressure increased to 112 +/- 2 torr, which was not only higher than the prehypotension level, but also significantly higher than that recorded in the awake state. Plasma renin activity at that time was 10.9 +/- 0.1 ng/ml/hr. As the half-life of plasma renin is 15 min, the data suggest that the persistently increased plasma renin activity is probably responsible for the increase of arterial pressure following sodium nitroprusside-induced hypotension.

Adolescent↗
PubMed1979

Comparison of intraoperative nitroprusside unloading in mitral and aortic regurgitation.

To compare the hemodynamic effect of vasodilator therapy on different regurgitant lesions, we infused sodium nitroprusside intraooperatively in 12 patients with mitral regurgitation and 15 with aortic regurgitation. During the critical period preceding establishment of cardiopulmonary bypass, both groups had developed intense vasoconstriction and cardiac decompensation. All demonstrated improved cardiac function with vasodilator therapy; however, the degree of improvement with nitroprusside differed in the two groups. Stroke volume increased 10 ml. per beat per meter squared in those patients with aortic regurgitation and only 6 ml. per beat per meter squared in those with mitral regurgitation (p less than 0.05). The percent increase in stoke volume induced by nitroprusside was inversely correlated to the preoperative left ventricular ejection fraction (r = 0.44, p less than 0.02). Patients with aortic regurgitation had lower preoperative left ventricular ejection fractions than those with mitral regurgitation (0.53 versus 0.63, p less than 0.02). Therefore, we conclude that patients with aortic regurgitation derived greater intraoperative hemodynamic benefit from unloading with nitroprusside, because they came to surgery with greater impairment of left ventricular contractility. Although nitroprusside improved cardiac function in both groups, only the patients with aortic regurgitation achieved normal pulmonary artery pressure (17 torr) and pulmonary vascular resistance (2.1 units) as a result of unloading. Those with mitral regurgitation continued to have pulmonary hypertension (28 torr) and increased pulmonary vascular resistance (3.9 units) despite vasodilator therapy. Thus the data suggest that patients with mitral regurgitation derived less hemodynamic benefit from intraoperative nitroprusside therapy because they were also limited by right ventricular dysfunction and a less responsive pulmonary vasculature.

Adult↗