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G D Giraud

Publications and source records attributed to G D Giraud.

36 records · Page 2Linked to original sources
PubMed1996

Myocardial imaging with a new transpulmonary lipid-fluorocarbon echo contrast agent: experimental studies in pigs.

The development of echo contrast agents that can provide reliable opacification of the myocardium after intravenous injection is an important advancement for the clinical application of contrast echocardiography. In this study, the hemodynamic effects and echocardiographic characteristics of a new lipid-fluorocarbon echo contrast agent, Aerosomes MRX 115 (ImaRx Pharmaceutical Corp., Tucson, Ariz.) were studied in six anesthetized ventilated pigs. Intravenous injection of this new agent in doses ranging from 0.0005 to 0.01 ml/kg produced significant measurable and visible myocardial opacification without any effect on heart rate, systemic pressure, partial pressure of oxygen, or left ventricular systolic function. The two largest doses (0.005 and 0.01 ml/kg), however, resulted in mild reversible increases in mean pulmonary artery pressure of 12 and 16 mm Hg, respectively. In four animals, epicardial images were obtained before and during coronary artery occlusion. Intravenous contrast injection during coronary occlusion permitted delineation of the hypoperfused myocardial segment. This capability may further expand the utility of contrast echocardiography.

Animals↗
PubMed1996

Effects of estrogen and progestin on aortic size and compliance in postmenopausal women.

OBJECTIVE: Our purpose was to determine whether sex steroids alter aortic size and compliance in postmenopausal women. STUDY DESIGN: Twenty-six postmenopausal women were randomized to receive either conjugated estrogens 0.625 mg per day (group 1) or conjugated estrogens 0.625 mg per day and medroxyprogesterone 2.5 mg per day (group 2). Aortic cross-sectional area was measured by magnetic resonance imaging before and after 3 months of hormone therapy. RESULTS: Estradiol levels increased in both group 1 and group 2 (p < 0.0001). Ascending aortic cross-sectional area increased from 439 +/- 7 mm2 to 466 +/- 7 mm2 in group 1 (p < 0.008) but was unchanged in group 2. Within the range of aortic pressures studied, no change in aortic compliance could be detected. CONCLUSION: Estrogen therapy in postmenopausal women was associated with an increase in aortic size; but this effect was not detectable with the addition of progestin. The potential antagonistic effect of progestin on estrogen-induced aortic enlargement suggests that the favorable cardiovascular effects of postmenopausal estrogen therapy cannot be automatically extended to the combination estrogen-progestin.

Aorta, Thoracic↗
PubMed1996

Right ventricular function in chronically anemic fetal lambs.

OBJECTIVE: Our purpose was to determine whether the increase in extravascular fluid in chronic fetal anemia occurs either because of heart failure or despite successful cardiac adaptation. STUDY DESIGN: Right ventricular function curves were obtained in five ovine fetuses at the start, midpoint, and end of 5 to 8 days of anemia induced by isovolemic daily hemorrhage. Least-squares fit of the ascending and plateau lines of stroke volume versus right atrial pressure were used to establish breakpoints (intersection of the ascending and plateau lines), which were compared by analysis of variance for repeated measures. Myocardial blood flow was measured by microspheres. RESULTS: Carotid arterial oxygen content was reduced from 7.0 +/- 0.3 to 2.1 +/- 0.1 ml/dl and the hematocrit from 29% +/- 1.8% to 13% +/- 0.6%. Breakpoint analysis of function curves showed that although right atrial pressure remained unchanged (3.4 +/- 0.7 and 3.6 +/- 0.6 mm Hg) stroke volume increased from 1.03 +/- 0.14 to 1.62 +/- 0.25 ml/kg. Both right and left ventricular coronary blood flow were increased, 1351 +/- 313 and 1166 +/- 264 ml/min per 100 gm. Excess fluid was present in abdomen and chest of most animals at autopsy. CONCLUSION: Tissue edema during severe anemia occurs despite normal right atrial pressure, increased stroke volume, and markedly increased coronary blood flow, markers of successful cardiac adaptation.

Anemia↗
PubMed1996

Exhaled nitric oxide during exercise: site of release and modulation by ventilation and blood flow.

To define the site of release and factors modulating exhaled nitric oxide (NO) during exercise in humans, we measured exhaled NO output during exercise, during exercise after balloon occlusion of the nasopharynx (to exclude nasal NO), and at rest with isocapneic hyperventilation or dobutamine infusion. Exhaled NO output increased from rest to exercise (57 +/- 10 to 171 +/- 30 nl.min-1.m-2; P < 0.003; n = 8). Exclusion of nasal NO reduced exhaled NO at rest and during exercise. Calculated nasal contribution at rest (53 +/- 5%) decreased during exercise (29 +/- 6%; P < 0.05), whereas nonnasal contribution increased (47 +/- 5 to 71 +/- 6%; P < 0.05). Isocapneic hyperventilation at rest increased exhaled NO output (51 +/- 8 to 94 +/- 22 nl.min-1.m-2; P = 0.05). Dobutamine infusion did not increase exhaled NO output. We conclude that nasal exhaled NO decreases (and nonnasal exhaled NO increases) with exercise. We also conclude that, under the conditions of this study, increased exhaled NO output during exercise is more closely related to increased ventilation than to increased blood flow.

Adult↗
PubMed1996

Nasal contribution to exhaled nitric oxide at rest and during breathholding in humans.

We characterized the nasal contribution to exhaled nitric oxide (NO) at rest and during breathholding in humans. Exhaled NO was greater during nose breathing (141 +/- 17 nl/min/M2, mean +/- SEM) compared with mouth breathing (68 +/- 6 nl/min/M2, n = 8, p < 0.001). After voluntary closure of the soft palate (VCSP) to eliminate nasal NO, exhaled NO from the mouth decreased further (30 +/- 4 nl/min/M2, p < 0.001). Release of NO into nasal passages during VCSP (217 +/- 19 nl/min/M2) was greater than exhaled NO during nasal breathing (141 +/- 17 nl/min/m2, p < 0.001), suggesting that nasal NO is taken up by the respiratory tract. During mouth breathing or nose breathing, NO concentrations sampled with a bronchoscope were higher in the nasopharynx than at the epiglottis or in the trachea in five subjects. Increased peak exhaled NO after a breathhold (33 +/- 7 ppb) was reduced (10 +/- 4 ppb, p < 0.001) after balloon occlusion of the nasopharynx. NO concentration during breathholding increased to a greater extent in the nasopharynx than in the pharynx or trachea. We conclude that the majority of exhaled NO at rest and during a breathhold originates in the nasopharynx.

Adult↗
PubMed1995

Effects of ductus arteriosus occlusion on pulmonary artery pressure during in utero ventilation in fetal sheep.

Seven fetal sheep were prepared to study the short-term effects of in utero ventilation and ductus arteriosus occlusion on pulmonary artery pressure and on fetal right ventricular function assessed using the right atrial pressure-right ventricular stroke volume relationship. Nine days post-surgery (140 days gestation), blood gas and haemodynamic values were obtained before and during in utero ventilation with 100% O2, and during ventilation with the ductus arteriosus occluded. Oxygen content increased significantly from 7.2 to 14.5 ml dl-1 with ventilation and remained elevated at 14.4 ml dl-1 with ventilation with the ductus arteriosus occluded. In utero ventilation produced a left to right atrial pressure gradient and depression of the right atrial pressure-right ventricular stroke volume relationship. Ductus arteriosus occlusion during in utero ventilation reduced the left to right atrial pressure gradient, and along with a decrease in pulmonary artery pressure, resulted in an upward shift of the right atrial pressure-right ventricular stroke volume relationship, but only to the preventilation level. This study indicates that the fetal right atrial pressure-right ventricular stroke volume relationship is significantly altered, both by changes in the left to right atrial pressure gradient and by changes in pulmonary artery pressure seen with in utero ventilation and subsequent ductus arteriosus occlusion.

Animals↗
PubMed1994

Spontaneous echo contrast and hemorheologic abnormalities in cerebrovascular disease.

BACKGROUND AND PURPOSE: Spontaneous echo contrast (SEC) is thought to represent a risk factor for cardioembolic stroke. In vitro studies suggest that SEC results from interaction between red cells and fibrinogen. To better understand the relation between SEC and stroke and to investigate the in vivo genesis of SEC, we examined the relation between SEC, the constituents of the blood, and plasma and serum viscosity in patients with acute stroke or chronic cerebrovascular disease. METHODS: Fifty patients with acute stroke or chronic cerebrovascular disease referred for transesophageal echocardiogram (TEE) were studied by transthoracic echocardiography and TEE. Complete blood count, fibrinogen, albumin, gamma-globulin, and plasma and serum viscosity determinations were made. Left atrial SEC was graded as absent, mild, or marked by means of TEE. RESULTS: SEC was absent in 31 patients, mild in 10 patients, and marked in 9 patients. Higher grade of SEC was associated with a significantly greater percentage of patients with atrial fibrillation and larger left atrial dimension. Atrial fibrillation was present in 23% of the patients in the SEC absent group, 50% of the patients in the mild SEC group, and 78% of the patients in the marked SEC group (P < .01). Left atrial diameter averaged 3.8 +/- 0.6 cm in the SEC absent group, 4.3 +/- 1.1 in the mild SEC group, and 4.9 +/- 0.7 in the marked SEC group (P < .001). Hematocrit, white blood cell count, and platelet count did not differ among the three groups. Fibrinogen, gamma-globulin, plasma viscosity, and serum viscosity values were all significantly higher in the presence of SEC (P < .05). Fibrinogen values were 361 +/- 97 mg/dL in the SEC absent group and 427 +/- 135 mg/dL in the marked SEC group. gamma-Globulin levels were 0.75 +/- 0.23 g/dL in the SEC absent group and 1.06 +/- 0.48 g/dL in the marked SEC group. Both plasma viscosity (1.97 cp) and serum viscosity (1.64 cp) were higher in the marked SEC group than in the SEC absent group (1.77 and 1.50 cp, respectively). CONCLUSIONS: In patients with acute stroke or chronic cerebrovascular disease, the severity of SEC was not related to albumin, hematocrit, white cell count, or platelet count but rather to elevated fibrinogen levels and concomitant increases in both plasma and serum viscosity. Moreover, increasing grade of SEC was associated with significantly increased left atrial diameter and a higher percentage of patients in atrial fibrillation.

Aged↗
PubMed1993

Estrogen-induced left ventricular chamber enlargement in ewes.

We studied the chronic effect of administration of a single large intramuscular dose of 17 beta-estradiol on left ventricular chamber size and output in the ewe. Fourteen oophorectomized ewes were successfully instrumented and studied, with measurements made of left ventricular, aortic, right and left atrial pressures, left ventricular stroke volume, and left ventricular minor axis dimension. Unanesthetized ewes were studied before and 1, 2, and 3 wk after intramuscular administration of 0.6 mg/kg 17 beta-estradiol (7 ewes) or 1.5 ml sesame oil placebo (7 ewes). Left ventricular end-diastolic pressure-end-diastolic dimension (LVEDP-EDD) and left ventricular end-diastolic pressure-stroke volume (LVEDP-SV) relationships were quantified during graded inferior vena caval occlusion and volume infusion. Left ventricular end-diastolic diameter was larger after estrogen but not after placebo administration. The LVEDP-EDD relationship shifted progressively rightward, indicating left ventricular chamber enlargement in the estrogen group but was unchanged in the placebo group. The plateau limb of the LVEDP-SV relationship in the estrogen group shifted up from a mean stroke volume of 77.1-89.5 ml/beat and did not change in the placebo group. We conclude that administration of a single large intramuscular dose of 17 beta-estradiol resulted in left ventricular chamber enlargement and increased stroke volume in the ewe.

Animals↗
PubMed1992

Maximal myocardial blood flow is enhanced by chronic hypoxemia in late gestation fetal sheep.

The measurement of maximal myocardial blood flow gives information about the total cross-sectional area of the coronary resistance vessels. During a continuous left atrial infusion of adenosine (60 micrograms.kg-1.min-1), maximal myocardial blood flow was measured in 4 fetuses hypoxemic for a minimum of 5-8 days (pH = 7.33 +/- 0.01, arterial PCO2 = 49.8 +/- 4.2 Torr, arterial PO2 = 16.1 +/- 1.3 Torr, and arterial concentration of O2 = 5.3 +/- 1.2 ml/dl). These data were compared with an identically instrumented group of normoxemic fetuses (n = 7) following the same study protocol (pH = 7.38 +/- 0.02, arterial PCO2 = 43.1 +/- 3.8 Torr, arterial PO2 = 19.8 +/- 2.0 Torr, and arterial concentration of O2 = 7.9 +/- 1.0 ml/dl) (P < 0.05). At comparable arterial pressures, the maximal myocardial flow (ml.min-1.100 g tissue-1) for hypoxemic vs. normoxemic fetuses was 974 +/- 273 and 630 +/- 181 for the total myocardium, 986 +/- 367 and 602 +/- 192 for the left ventricular free wall, 1,025 +/- 346 and 614 +/- 178 for the septum, and 1,231 +/- 274 and 757 +/- 269 for the right ventricular free wall, respectively (P < 0.01). These data suggest that hypoxemia in the fetus can significantly alter the coronary vascular bed, which, if confirmed, would represent an important adaptation in the developing fetus.

Animals↗
PubMed1992

Severe right ventricular pressure loading in fetal sheep augments global myocardial blood flow to submaximal levels.

BACKGROUND: It has previously been shown that the fetal right ventricle (RV) is sensitive to changes in arterial pressure and that its stroke volume is significantly reduced with acute increases in pulmonary arterial pressure. However, the myocardial blood flow (MBF) response to increases in pulmonary arterial pressure have not been investigated in the fetus. METHODS AND RESULTS: To assess whether the RV afterload sensitivity to arterial pressure is associated with limitation in MBF, seven fetal lambs were instrumented at 130 days of gestation with a pulmonary arterial occluder and intravascular catheters. RV stroke volume was measured by an electromagnetic flow probe and MBF by 15-microns labeled microspheres. MBF was determined at baseline and during incremental increases in pulmonary arterial pressure. Maximal MBF was determined in seven additional fetuses during adenosine infusion. The highest tolerated pressure was associated with a 50% reduction in RV stroke volume. The highest pulmonary arterial occlusion pressure resulted in a doubling of MBF to all regions of the heart (266 +/- 99 to 504 +/- 158, 193 +/- 69 to 387 +/- 100, and 171 +/- 66 to 338 +/- 134 ml/min/100 g for the RV, septum, and left ventricle, respectively). The best correlation for increases in both RV and global MBF was the RV heart rate-systolic pulmonary pressure product. Adenosine infusion was associated with a threefold increase in global MBF that was significantly greater than the MBF achieved during pulmonary arterial occlusion. CONCLUSIONS: The fetal RV sensitivity to acute pressure loading is not associated with limitation of MBF. The fetal myocardium has a remarkable flow reserve that allows for preservation of function during acute increases in arterial pressure.

Adenosine↗
PubMed1989

Vascular pressure-volume relationships in pregnant and estrogen-treated guinea pigs.

We investigated the relationship between mean circulatory filling pressure (MCFP) and blood volume in nonpregnant (NP), estrogen-treated (E), and pregnant (P) guinea pigs. Reversible circulatory arrest was produced by rapid ventricular pacing or acetylcholine in unanesthetized animals remote from surgery. MCFP (mmHg) was higher for E (7.1 +/- 0.3) than for NP (5.8 +/- 0.5) or P (5.3 +/- 0.4). The gradient for venous return, the difference between MCFP and right atrial pressure (mmHg), did not differ in NP- (6.0 +/- 0.5), P- (5.8 +/- 0.5), or E- (5.8 +/- 0.4) treated animals. Capacitance, the blood volume (ml/kg) at an MCFP of 6 mmHg, was increased in P (84 +/- 6) and E (89 +/- 7), compared with NP (64 +/- 5) animals. Compliance, the ratio of the change in volume to change in pressure in the range of 6-12 mmHg (ml.kg-1.mmHg-1), was greater in P (4.4 +/- 0.3) than NP (3.5 +/- 0.3) animals. Hexamethonium blockade did not affect MCFP, capacitance, or compliance. We conclude that the effect of blood volume expansion on the circulation in pregnancy cannot be predicted from knowledge of MCFP-blood volume relationships in the nonpregnant animal, because capacitance and compliance are altered. Estrogen administration to nonpregnant animals reproduces some of these effects.

Animals↗
PubMed1989

The effect of acute hypoxaemia on ventricular function during beta-adrenergic and cholinergic blockade in the fetal sheep.

The effect of acute hypoxaemia on right and left ventricular function was investigated in 8 fetal sheep (137-140 days gestation). Fetuses were instrumented with electromagnetic flow sensors on the ascending aorta and the main pulmonary artery. After 8 days recovery, hypoxaemia was achieved by reducing the maternal ewe's inspired O2 concentration to 13.1 +/- 1.5%. Control and hypoxaemic arterial blood values were pH 7.37 +/- 0.04 (SD) and 7.35 +/- 0.06, PCO2 48.0 +/- 2.8 and 47.6 +/- 5.1 mmHg, PO2 19.9 +/- 2.2 and 11.4 +/- 1.5 mmHg, haematocrit 37.5 +/- 1.2 and 39.5 +/- 2.2, respectively. Arterial pressure increased insignificantly with acute hypoxaemia (50.2 +/- 3.9 to 53.6 +/- 8.1 mmHg). Left and right ventricular performance was assessed by generating biventricular function curves relating stroke volume to mean atrial pressure. All function curves were composed of steep ascending and plateau limbs that intersected at a breakpoint. Comparing control and hypoxaemia function curves, the left ventricular stroke volume breakpoints were 0.79 +/- 0.20 and 0.78 +/- 0.21 ml/kg, respectively, while the right ventricular stroke volume breakpoints were 0.99 +/- 0.11 and 0.88 +/- 0.21 ml/kg (n.s.). In 4 fetuses, acute hypoxaemia was associated with significant increases in arterial blood pressure (P less than 0.05). In these fetuses, the right ventricular function curve was shifted significantly downward compared to the control right ventricular curve. When nitroprusside was given to these hypertensive fetuses to return blood pressure to control levels, the right ventricular function curve returned to baseline. We conclude that even under conditions of extreme hypoxaemia, ventricular function is well preserved in the normotensive fetal sheep. However, when increases in arterial pressure also accompany hypoxaemia, detectable changes in right ventricular function can be accounted for by changes in arterial pressure.

Animals↗
PubMed1984

Decreased nutrient blood flow during dopamine- and epinephrine-induced intestinal vasodilation.

Mesenteric blood flow returned to control values promptly upon termination of i.a. infusions of vasodilator doses of acetylcholine (ACh) and isoproterenol (Iso) into the canine superior mesenteric artery (SMA). However, termination of vasodilator infusions of dopamine (DA) and epinephrine (Epi) into the SMA resulted in an additional increase in flow resembling the reactive hyperemic response observed upon termination of norepinephrine infusion into the SMA. In experiments that measured the effect of these agents on intestinal oxygen kinetics, i.a. ACh and Iso increased oxygen uptake but did not affect percent oxygen extraction. Equivasodilator i.a. infusions of DA and Epi decreased percent oxygen extraction. DA decreased oxygen uptake whereas Epi did not alter oxygen uptake. After administration of phenoxybenzamine, the effects of i.a. DA and Epi on oxygen kinetics became identical to those produced by equivasodilator infusions of ACh or Iso. Moreover, the reactive hyperemia-like response on cessation of DA and Epi infusions was abolished. In experiments that utilized 125I absorption from the jejunum as a measure of intestinal mucosal blood flow, i.a. ACh and Iso were found to increase mucosal blood flow in proportion to the increase in total SMA flow. In contrast, i.a. doses of DA and Epi that increased SMA flow nevertheless decreased mucosal flow. It was concluded that vasodilator doses of dopamine and Epi decrease oxygen delivery to the intestine at least in part due to a decrease in mucosal blood flow; this probably involves action on alpha adrenoreceptors.

Absorption↗
PubMed1983

Haemodynamic responses to dopamine and dobutamine infusions as a function of duration of infusion.

In normal animals, dopamine and dobutamine produce similar haemodynamic effects. However, clinical observations on patients in heart failure suggest that dobutamine produces a more favourable and stable haemodynamic effect. One explanation is that the inotropic action of dopamine is largely an indirect one mediated through noradrenaline release, while that of dobutamine is direct. If this were true, one would predict that the haemodynamic effects of dopamine and dobutamine would be similar over short-term infusions, but that the response to dopamine would be attenuated with time as a result of noradrenaline depletion. Experiments are reported which are consistent with this explanation. 15-min infusions of graded doses of dopamine and dobutamine produced indistinguishable haemodynamic effects in a dog model in which the haemodynamic characteristics of heart failure were produced by a chronic aorta-left atrial shunt: dopamine also produced the expected increase in mesenteric and renal flows with this short-term exposure. With long-term infusions of dopamine (5 h), the specific mesenteric/renal vasodilatation was lost with time, and indices of myocardial contractility also were attenuated with time. In contrast, the haemodynamic actions of dobutamine were well maintained. Both amines lowered total peripheral resistance and ventricular filling pressures over the entire period. These results suggest that the haemodynamic responses to dopamine change with time, and that some of the discrepancies between animal observations (short term) and those in patients (invariably long term) can be explained on this basis rather than on the basis of species differences or underlying pathology. They also suggest that dopamine is a less suitable 'inotropic' drug than dobutamine.

Animals↗
PubMed1982

Effect of a specific and a nonspecific vasodilator on regional blood flows in experimental heart failure.

Urotensin I, a vasoactive peptide isolated from fish urophyses, has previously been demonstrated to cause specific mesenteric dilation in the dog. This mechanism of action should limit its maximal cardiovascular actions: no additional cardiovascular effects should ensure once maximal mesenteric vasodilation is achieved. Provided that the mesenteric vasodilatation does not result in decreased flow to other organs, the agent may, therefore, offer a theoretical advantage as an afterload reducing agent. In pentobarbital anesthetized dogs which were in heart failure as a result of chronic aortico -- left atrial shunt, the effects of urotensin I on cardiovascular hemodynamics were compared with the effects of a nonspecific vasodilator, sodium nitroprusside. At equidepressor doses (approximately 15% decrease in mean arterial pressure; sodium nitroprusside, 2 micrograms . kg-1 . min-1 i.v.; urotensin I, 10 mU . kg-1 . min-1 i.v.), both agents produced comparable falls in total peripheral resistance, left ventricular end diastolic pressure, and pulmonary capillary wedge pressure. Forward cardiac output was increased by both substances, although the increases were not statistically significant. Shunt flow, estimated by echocardiography, was reduced by both. In spite of the marked similarity in hemodynamic effects in this model, the two agents affected regional blood flows differently. Sodium nitroprusside did not significantly alter regional flows measured by radioactive microspheres, although calculated splanchnic, skin, and myocardial vascular resistances were reduced. In contrast, urotensin I, as in the normal dog, greatly increased mesenteric blood flow; this redistribution of cardiac output did not, however, result in underperfusion of other vital organs. These data suggest that urotensin I may be a useful agent in the reduction of afterload in heart failure, particularly since the unique mechanism of action appears to minimize the potential for adverse effects due to excessive dosage.

Animals↗
PubMed1981

Measurement of mucosal blood flow by assay of absorption of 125I from the intestinal lumen.

A method which utilized the absorption of 125I as a measure of intestinal mucosal blood flow was developed. In the pentobarbital anesthetized dog a segment of mid-jejunum was isolated from adjacent vasculature and perfused with 125I solution. Superior mesenteric artery flow, blood flow to the isolated segment of intestine and 125I absorption were measured. Changes in 125I absorption were found to correlated closely with changes in blood flow (r = 0.95). Using an autoradiographic technique 125I absorption was found to be localized to the intestinal mucosa.

Animals↗
PubMedDate not supplied

Toxic methemoglobinemia after topical anesthesia for transesophageal echocardiography.

Topical benzocaine spray is an anesthetic agent that is commonly used during transesophageal echocardiography (TEE). This agent is believed to be relatively safe because of very low systemic absorption. We report a case of toxic methemoglobinemia induced by benzocaine use for pharyngeal anesthesia during TEE. Physicians who perform TEE and use benzocaine or other topical anesthetics need to be familiar with this potential complication and have the necessary treatment readily available.

Aged↗