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Biomedical subjects

S A Magder

Publications and source records attributed to S A Magder.

11 recordsLinked to original sources
PubMed1993

Role of endothelium-derived relaxing factor in reactive hyperemia in canine diaphragm.

We studied the effect of NG-nitro-L-arginine (L-NA) on reactive hyperemia in the vascularly isolated hemidiaphragm of anesthetized dogs pretreated with indomethacin. In nine animals, the diaphragm was autoperfused from the left femoral artery. Phrenic arterial flow was interrupted for 10-120 s during a control period and after 20 min of L-NA infusion (6 x 10(-4) M). Postocclusive flow and duration of hyperemia during the control period increased progressively with increasing occlusion duration. After L-NA infusion, baseline and postocclusive flow in response to all occlusions declined significantly compared with control values. However, when normalized as percentage of baseline flow, postocclusive flow remained similar to that during the control period. By comparison, the duration of reactive hyperemia was significantly shortened by L-NA infusion. In five animals, we repeated the same protocol during pump perfusion of the diaphragm at a fixed flow rate. L-NA infusion increased baseline and postocclusive phrenic resistance in response to all occlusion durations; however, postocclusive phrenic resistance as percentage of baseline remained similar to control values. In addition, hyperemia durations in response to 60- and 120-s occlusions were shortened significantly by L-NA infusion. We conclude that 1) endothelium-derived relaxing factor plays an important role in the regulation of baseline vasomotor tone in the diaphragm and 2) modulation of endothelium-derived relaxing factor release contributes to the reactive vasodilatory response to transient vascular occlusion in the diaphragm.

Animals↗
PubMed1993

Diaphragmatic function before and after laparoscopic cholecystectomy.

BACKGROUND: Diaphragm dysfunction is a primary cause of ventilatory impairment after upper abdominal surgery. Laparoscopic procedures may result in less dysfunction. To test this, diaphragmatic function was studied in ten healthy adult patients undergoing elective laparoscopic cholecystectomy and in five undergoing laparoscopic hernia repair. METHODS: Respiratory gas exchange, ventilation, and breathing pattern were measured before and 3 h after surgery. Respiratory drive was evaluated from the relationship of P0.1 to end-tidal carbon dioxide (PETCO2) during tidal breathing. Diaphragm contractile function was assessed from maximal transdiaphragmatic pressure (Pdimax), and Pdi during a maximal sniff maneuver (Pdisniff). RESULTS: Oxygen consumption and carbon dioxide production did not change after surgery. Pdimax decreased by more than 50% in the laparoscopic cholecystectomy group, but Pdisniff did not change. Tidal volume and the ratio of inspiratory time over total cycle time decreased by 30% and 13%, respectively, PETCO2 increased by 9%, and minute ventilation did not change. In contrast, there was no variation in ventilatory function in patients undergoing laparoscopic hernia repair. In both groups, P0.1 did not change, which excludes depressed respiratory drive as an explanation for the decreased Pdimax in laparoscopic cholecystectomy. Contractile failure of the diaphragm was discounted as well, because Pdisniff did not change, even in the laparoscopic cholecystectomy group. CONCLUSIONS: Although laparoscopic cholecystectomy does not increase metabolic demands in the early postoperative period, it impairs diaphragm function. The internal site of surgical intervention appears to be the critical variable determining diaphragmatic inhibition after laparoscopic abdominal surgery.

Adult↗
PubMed1992

Effects of diaphragmatic ischemia on the inspiratory motor drive.

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.

Afferent Pathways↗
PubMed1992

Oxygen delivery-independent effect of blood flow on diaphragm fatigue.

To determine the effect of blood flow on diaphragm fatigue independent of oxygen delivery, the left hemidiaphragm was vascularly isolated in 14 pentobarbital-anesthetized, mechanically ventilated dogs. Fatigue (decline in tension generation) of the left diaphragm was induced by phrenic nerve stimulation at 10 Hz, 12/min, duty cycle of 0.5 for 8 min. Two stimulation periods separated by 30 min of rest were performed in each animal. Diaphragmatic O2 delivery during the two periods was the same. In Group 1 (n = 8), the diaphragm was autoperfused from the femoral artery (high O2-low flow) during the first stimulation period. The tension generated by the diaphragm during this period declined progressively to 47.7% of initial values. In the second period in this group, the diaphragm was pump perfused with arterial blood, diluted with an equal volume of 6% dextran at a flow rate twice that of the first period (low O2-high flow). Tension in this period declined to 76% of initial tension (p less than 0.05 compared with high O2-low flow). In Group 2 (n = 6), stimulation performed while perfusing the diaphragm in the first period with diluted arterial blood at a flow rate twice that recorded during autoperfusion (low O2-high flow) produced a decline in tension to 70% of the initial values. In the second period, the diaphragm was perfused with undiluted arterial blood at a flow rate equal to 50% of that of the first period (high O2-low flow). Tension during this period declined to 56% of initial values (p less than 0.05 compared with low O2-high flow).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Intravenous bicarbonate and sodium chloride both prolong endurance during intense cycle ergometer exercise.

To determine the effects of neutralizing exercise systemic acidosis via the intravenous route upon endurance and metabolic responses, eight lean, normal, postabsorptive men exercised to exhaustion at about 80% of their VO2 max (69 +/- 3%, mean +/- SEM, of maximum power output) on a cycle ergometer. Exercise studies were performed either with no infusion (control) or with a total infusion volume of about 1.5 L, mainly as 1.3% sodium bicarbonate or as 0.9% sodium chloride (NaCl), infused (double-blind) throughout exercise. The sodium bicarbonate was to prevent acid-base change, the sodium chloride was as a control for the volume infused. Arterialized venous blood and breath-by-breath analysis of expired gases were obtained. [H+] (nmol.L-1) and [HCO3-] (mmol.L-1) at exhaustion were similar in control and NaCl (46.5 +/- 1.8, 19.9 +/- 0.9), but remained unchanged from rest values with bicarbonate (38.4 +/- 0.9, 24.8 +/- 1.5, p less than 0.005 vs control and NaCl). At exhaustion, VO2, VCO2, RER, heart rate, and systolic BP as well as FFA, glycerol, alanine, insulin, norepinephrine, and epinephrine did not differ among protocols. Endurance was markedly prolonged (p less than 0.01) with bicarbonate (31.9 +/- 5.8 min) and NaCl (31.8 +/- 4.1 min) compared with the control (19.0 +/- 2.9 min) condition. Plasma glucose at exhaustion was higher (p less than 0.025) in the control compared to bicarbonate and NaCl experiments, while lactate was higher (p less than 0.025) in the bicarbonate than in the control and NaCl experiments. Thus, the prolonged endurance with sodium bicarbonate infusion could not be explained either by its effect of maintaining blood acid-base equilibrium or concomitant metabolic changes.

Acid-Base Equilibrium↗
PubMed1987

Adaptation of human left ventricular volumes to the onset of supine exercise.

UNLABELLED: The purpose of this study was to measure the changes and rates of adaptation of left ventricular volumes at the onset of exercise. Eight asymptomatic subjects, in whom intramyocardial markers had been implanted 3-6 years previously during aortocoronary bypass surgery, exercised in the supine position at a constant workload of 73.6 W for 5 min. Six also exercised first at 16.4 W, and then against a workload which progressively increased by 8.2 W every 15 s. Cardiac volumes were measured by computer assisted analysis of the motion of the implanted markers. In the constant workload test, cardiac output increased rapidly from 5.7 +/- 1 min-1 to 10.3 +/- 1.9 1 min-1 by 2 min and then increased more slowly to 10.8 +/- 2.0 1 min-1 by 5 min. The cardiac output increase was mainly due to an increase in heart rate from 68 +/- 12 beats min-1 to 120 +/- 16 beats min-1 with minimal changes in stroke volume. The time constant for the early increase in cardiac output was 45s and for heart rate, 35s. With progressively increasing workloads, there was an almost linear increase of heart rate and cardiac output, but these increased at a slower rate than during the early phase of the constant load exercise test. IN CONCLUSION: rapid changes in cardiac output during supine exercise were produced by changes in heart rate; changes in stroke volume provided minor adjustments to cardiac output; the end-diastolic volume was almost constant.

Adaptation, Physiological↗
PubMed1983

Effect of negative pleural pressure on left ventricular hemodynamics.

Negative pleural pressure alters left ventricular (LV) function. LV volume changes have been studied in human subjects, but little is known of the hemodynamic effects. The effect of changes of pleural pressure on LV hemodynamics during a Mueller maneuver (inspiration against an obstruction) was studied in 11 subjects and during quiet, unobstructed inspiration in 3. During the Mueller maneuver, there was an initial decrease in pulmonary wedge pressure and aortic systolic pressure, almost as great as the decrease in pleural pressure. Thereafter, these pressures increased despite a sustained reduction in pleural pressure. Toward the end of the Mueller maneuver, pulmonary wedge transmural pressure averaged 31 +/- 12 mm Hg and in 6 patients large v waves developed. The increase in aortic transmural pressure averaged 30 +/- 16 mm Hg. Aortic pulse pressure decreased on the first beat from control levels of 59 +/- 21 to 47 +/- 21 (p less than 0.001) and then returned to control levels. During normal breathing in 3 subjects, studied with intraesophageal balloons, there was a similar increase in both transmural aortic and transmural pulmonary wedge pressures with a decrease in pleural pressure 6 mm Hg during inspiration. Thus, increased negative pleural pressure was associated with a marked increase in pulmonary wedge transmural pressure; the increase was approximately proportionate to the decrease in pleural pressure. It is suggested that this increase was due to increased impedance to LV ejection and to right ventricular expansion interfering with LV diastolic filling.

Adult↗
PubMed1981

Experience with ergonovine provocative testing for coronary arterial spasm.

We reviewed our experience with the ergonovine provocative test for coronary arterial spasm in 40 patients with pain in the chest believed to be angina pectoris and in one patient with a myocardial infarction and normal coronary arteries. Twenty-nine patients had normal coronary arteries, while 12 had mild to moderate lesions. Ergonovine maleate was administered incrementally in total cumulative doses of 0.25 mg to 1.2 mg. The effect of ergonovine on coronary arterial caliber was determined by comparing the arterial diameter from the angiogram obtained after administration of ergonovine with that from the control. Measurements were made at the same preselected points in both films and also at points of greatest response. Excluding the three cases with complete occlusion, the mean reduction in coronary arterial diameter at preselected points was 12 +/- 15 percent. When the points of greatest response were examined, the maximum reduction in coronary arterial diameter was less than 25 percent in 13 patients, 25 to 50 percent in 20 patients, and more than 50 percent in eight patients. The patterns of response included complete occlusion of a vessel in the three patients with variant angina, diffuse narrowing in 16, diffuse and focal narrowing in six, and spasm at the catheter tip in three patients. All patients with maximum reductions of more than 50 percent in coronary arterial diameter and six of those with maximum reductions of 25 to 50 percent had pain in the chest, but only the three with complete occlusion had associated changes in the S-T segment. Thus, the response in patients with variant angina represents one end of a spectrum of responses to administration of ergonovine. In addition, a large number of patients may have ergonovine-induced pain in the chest without electrocardiographic changes and only an intermediate degree of coronary arterial spasm.

Adult↗