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Biomedical subjects

S A Barman

Publications and source records attributed to S A Barman.

32 records · Page 2Linked to original sources
PubMed1995

Mechanism of action of endothelin-1 in the canine pulmonary circulation.

Possible mechanisms of action by which endothelin (ET)-1 has an effect on pulmonary vascular resistance and compliance in the canine pulmonary circulation were investigated in the isolated blood-perfused dog lung by use of vascular occlusion techniques. In the present study, ET-1 (10(-8) M) increased pulmonary vascular resistance and pulmonary capillary pressure by postcapillary vasoconstriction. In addition, ET-1 decreased total vascular compliance and middle-compartment compliance. Pretreatment with the ETA receptor antagonist BQ-610 (10(-7) M) or the protein kinase C inhibitors staurosporine (10(-6) M) and calphostin C (10(-6) M) completely blocked the pressor effect of ET-1. Elimination of extracellular calcium mobilization through voltage-dependent calcium channels by verapamil (10(-5) M) or modulation of G protein signal transduction by pertussis toxin challenge (15 micrograms/kg) had no significant effect on the ET-1-induced pulmonary vascular response. The results of the present study indicate that ET-1 causes pulmonary vasoconstriction in the canine pulmonary circulation through ETA receptor mediation and protein kinase C activation, possibly leading to intracellular calcium release. In contrast, the ET-1-induced pulmonary vascular response does not appear to involve extracellular calcium entry through voltage-dependent calcium-channel activation or pertussis toxin-sensitive G protein-signaling mechanisms.

Animals↗
PubMed1993

Effects of left atrial and airway pressures on airway blood flow.

The blood flow contributions of the pulmonary and systemic circulations to airway blood flow from the trachea down to the 5th generation airways when either 15 cmH2O positive end expiratory pressure (PEEP) or 20 mmHg left atrial pressure was applied were assessed in anesthetized dogs by injecting 15-microns radiolabeled microspheres into the right and left heart, respectively. After the microsphere injections, the animals were killed, and the tracheal cartilage, tracheal muscle-mucosa, main bronchi and the 2nd generation bronchi down to the 5th generation airways were excised and collected for radioactive counting. The results of this study showed that under normal conditions, tracheal blood flow was primarily systemic (> 95% of total tracheal blood flow) averaging 15-26 ml.min-1 x (100 g)-1, while both the pulmonary [10 ml.min-1 x (100 g)-1] and systemic circulations [15 ml.min-1 x (100 g)-1] contributed substantially to main bronchi blood flow. The systemic blood flow contribution to the lower airway generations (2nd to the 5th generation airways) stayed relatively constant, averaging 13-31 ml.min.(100 g)-1 while the pulmonary blood flow contribution increased significantly in these airway segments to a maximum of over 100 ml.min-1 x (100 g)-1 at the 5th generation. At 15 cmH2O PEEP, the systemic contribution to all of the airway segments (except the 5th generation, P < 0.09) and the pulmonary component to the main bronchi, significantly decreased (P < 0.05). In contrast, elevated left atrial pressure had little effect on the pulmonary and systemic contributions to airway blood flow. The results of this study suggest that elevated PEEP has a greater effect than elevated left atrial pressure on the systemic blood flow contribution to the airways, while the pulmonary blood flow contribution to the airways is affected very little by either of these perturbations.

Animals↗
PubMed1993

Effect of endothelin-1 on canine airway blood flow.

The effect of endothelin-1 (ET-1) on the blood flow contributions of the pulmonary and systemic circulations to the trachea and main bronchi were measured in anesthetized dogs by injecting 15-microns radiolabeled microspheres into the right and left heart, respectively. After the microsphere injections the animals were killed, and the tracheal cartilage, tracheal muscle mucosa, and main bronchi were excised and collected for radioactive counting. The results of this study showed that under normal conditions tracheal blood flow was primarily systemic (> 95% of total tracheal blood flow) averaging 25-50 ml/min/100 g, whereas both the pulmonary (9-10 ml/min/100 g) and systemic circulations (19-20 ml/min/100 g) contributed substantially to main bronchi blood flow. Administration of ET-1 i.v. decreased systemic tracheal cartilage blood flow from 25.3 +/- 3.8 to 14.5 +/- 2.8 ml/min/100 g, systemic tracheal mucosal blood flow from 50.0 +/- 7.0 to 25.0 +/- 7.0 ml/min/100 g, and systemic main bronchi blood flow from 19.4 +/- 4.6 to 11.6 +/- 3.4 ml/min/100 g (p < 0.05). These results indicate that ET-1 is a potent constrictor of the airway circulation and may contribute to airway ischemia seen in different airway disease states.

Animals↗
PubMed1991

Sustained effects of endothelin-1 on rabbit, dog, and rat pulmonary circulations.

Effects of endothelin-1 (10(-8) M) on the pulmonary vascular resistance-compliance profile were examined in isolated blood-perfused rabbit, dog, and rat lungs using occlusion techniques. Capillary permeability was assessed by filtration coefficient (Kfc). Cyclooxygenase products were assessed by radioimmunoassay. In rabbit lungs, endothelin-1 increased all resistances except large vein; ibuprofen reversed the constriction. Endothelin-1 decreased total vascular compliance (CT), which was reversed by ibuprofen. Cyclooxygenase products were unchanged by endothelin-1 or endothelin-1 plus ibuprofen. In dog lungs, large vein resistance increased after endothelin-1; ibuprofen increased large arterial resistance. Endothelin-1 decreased CT and middle compartment compliance, and endothelin-1 plus ibuprofen decreased large vessel compliance (CLV). Ibuprofen reversed the endothelin-1 increase in plasma 6-oxo-prostaglandin F1 alpha. In rat lungs, ibuprofen reversed the endothelin-1 increase in small arterial resistance. Endothelin-1 decreased CLV, and endothelin-1 plus ibuprofen returned the compliance to baseline values. Ibuprofen potentiated the endothelin-1 increase in plasma prostanoids. Endothelin-1 plus indomethacin increased vascular resistance and blocked prostaglandin production. Kfc was increased only in rat lung after endothelin-1 plus ibuprofen. In summary, endothelin-1 increased pulmonary vascular resistance, which was attenuated by prostacyclin in dogs and rats. In rabbits, the resistance increase was reversed by ibuprofen.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Pulmonary embolism: emboli and fibrinolysis inhibition in isolated canine lungs.

The effect of fibrinolysis inhibition with tranexamic acid on pulmonary microvascular permeability during glass bead embolization was investigated in the isolated lung. Lung lobes from nonheparinized dogs were treated in vivo with the equivalent of 0.6 g/kg 100 microns glass bead emboli alone, emboli after tranexamic acid, tranexamic acid alone, or the bead vehicle alone. After 40-50 min, the lobes were isolated for ex vivo perfusion with heparinized autologous blood. There were no changes in any parameter over the 120-min perfusion period. Blood flow at 120 min was decreased after both emboli alone and emboli with tranexamic acid, reflecting an increase in vascular resistance compared with the Tween or tranexamic acid controls. Furthermore, tranexamic acid increased the ratio of pre- to postcapillary resistance in embolized lobes compared with that after emboli alone or in the Tween or tranexamic acid controls. The isogravimetric capillary pressure and the osmotic reflection coefficient were not significantly decreased by tranexamic acid compared with those after emboli alone; however, it did result in an increase in the capillary filtration coefficient compared with that after emboli alone or in the control groups. We conclude that although fibrinolysis inhibition does not clearly exacerbate the lung injury seen after emboli, the tranexamic acid-induced changes in hemodynamics would tend to accelerate edema formation.

Animals↗
PubMed1990

Effect of pulmonary venous pressure elevation on vascular resistance and compliance.

The effect of pulmonary venous pressure elevation on the longitudinal distribution of resistance and compliance in the canine pulmonary circulation was determined at control vascular tone and after vascular tone was increased with histamine. The arterial, venous, and double-occlusion techniques were used in isolated dog lungs blood perfused at constant flow. The large and small blood vessel resistances and compliances were studied under both vascular tone conditions when pulmonary venous pressure was elevated above isogravimetric venous pressure conditions in successive 5 cmH2O increments up to 30 cmH2O. The results of this study indicate that pulmonary venous pressure elevations to 20 cmH2O above isogravimetric venous pressure significantly decrease total vascular resistance by reducing both the small and large vein resistances, an effect which is more pronounced in the histamine-treated lungs. Also, under control vascular tone, both the middle compartment compliance and total compliance were greatly decreased over this pressure range. Histamine treatment significantly reduced both the large vessel and middle compartment compliances before and during low venous pressure elevation. When venous pressure was then raised to at least 25 cmH2O above control outflow pressure with histamine present, the middle compartment compliance was again significantly decreased.

Animals↗
PubMed1989

Histamine's effect on pulmonary vascular resistance and compliance at elevated tone.

Histamine's effect on the longitudinal resistance and compliance distribution in the canine pulmonary circulation was determined under control and elevated vascular tone using the thromboxane analogue U46619. The arterial-, venous-, and double-occlusion techniques were used in isolated blood-perfused dog lungs at both constant flow and constant pressure. Large and small blood vessel resistances and compliances were studied in lungs given the following treatments: 1) histamine; 2) histamine in lungs pretreated with the H1-receptor antagonist diphenhydramine, and 3) histamine in lungs pretreated with the H2-receptor antagonist cimetidine. The results of this study indicate that histamine constricts small and large veins through H1-receptor mediation at both normal and elevated vascular tone. When vascular tone was elevated, H2-receptor vasodilatation was also apparent in all blood vessel segments. Histamine decreased total, middle compartment, and large vessel vascular compliances by an H1-receptor effect. When vascular tone was elevated, histamine's H1-receptor-mediated vasoconstrictor effect on compliance vessels was less due to the presence of an H2-receptor-mediated vasodilatory system.

Animals↗
PubMed1989

Acetylcholine's effect on vascular resistance and compliance in the pulmonary circulation.

Acetylcholine's effect on the distribution of vascular resistance and compliance in the canine pulmonary circulation was determined under control and elevated vascular tone by the arterial, venous, and double occlusion techniques in isolated blood-perfused dog lungs at both constant flow and constant pressure. Large and small blood vessel resistances and compliances were studied in lungs given concentrations of acetylcholine ranging from 2.0 ng/ml to 200 micrograms/ml. The results of this study indicate that acetylcholine dilates large arteries at low concentrations (less than or equal to 20 ng/ml) and constricts small and large veins at concentrations of at least 2 micrograms/ml. Characterization of acetylcholine's effects at constant pulmonary blood flow indicates that 1) large artery vasodilation may be endothelial-derived relaxing factor-mediated because the dilation is blocked with methylene blue; 2) a vasodilator of the arachidonic acid cascade (blocked by ibuprofen), probably prostacyclin, lessens acetylcholine's pressor effects; 3) when vascular tone was increased, acetylcholine's hemodynamic effects were attenuated; and 4) acetylcholine decreased middle compartment and large vessle compliance under control but not elevated vascular tone. Under constant pressure at control vascular tone acetylcholine increases resistance in all segments except the large artery, and at elevated vascular tone the pressor effects were enhanced, and large artery resistance was increased.

Acetylcholine↗
PubMed1989

Nerve-sparing dissection as alternative to anesthesia of carotid sinus nerve in preparation for carotid endarterectomy.

This prospective randomized study was undertaken to determine intraoperatively the hemodynamic effects of local anesthesia of the carotid sinus nerve during carotid dissection in preparation for endarterectomy. Twenty carotid endarterectomy patients were divided into 2 groups: a control group of 10 patients, in whom ordinary saline solution was infiltrated into the carotid bifurcation; and a study group of 10 patients, in whom 5 mL of 2% lidocaine hydrochloride was infiltrated. To determine whether a nerve-sparing dissection might in itself be adequate to prevent the perioperative hemodynamic instability associated with carotid endarterectomy, we took scrupulous care in all patients to avoid injuring the carotid sinus nerve. After we had established baseline values for heart rate and blood pressure in each patient, we recorded heart rate and blood pressure again intraoperatively, every 2 minutes during a 10-minute period. Because the series was small, an analysis of variance showed no statistically significant changes in these values during carotid dissection in either group. However, intraoperative increases in systolic pressure (p < 0.0064) and mean pressure (p < 0.0028) were greater in the lidocaine group. Neither group experienced any deaths, or any neurologic or hemodynamic sequelae during 48 hours of postoperative observation. We conclude that local anesthetic injection of the carotid sinus nerve before carotid dissection and endarterectomy is unnecessary when nerve-sparing dissection is performed; and we conclude further that such injection might actually be deleterious to intraoperative systolic and mean blood pressures.

Journal Article↗
PubMed1988

Pulmonary and systemic blood flow contributions to upper airways in canine lung.

The blood flow contributions and drainage patterns of the pulmonary and systemic circulations in the upper airways (trachea and main bronchi) were assessed in anesthetized dogs by injecting 15-micron radiolabeled microspheres into the right and left heart, respectively. After the animals were killed, the tracheal cartilage, tracheal muscle-mucosa, and main bronchi were excised. The tracheal cartilage and tracheal muscle-mucosa were divided into lower, middle, and upper segments for blood flow determinations. The pulmonary contribution to tracheal blood flow was very small, averaging only 0.6 +/- 0.3 ml.min-1.100 g-1 (means +/- SE), being higher in the lower segments. The systemic contribution to these same tracheal regions was significantly (P less than 0.05) higher, averaging 20.9 +/- 5.5 ml.min-1.100 g-1 (means +/- SE) and higher in the upper segments. The pulmonary and systemic circulations each contributed approximately 50% to the main bronchi blood flow, which averaged 11.2 +/- 4.2 ml.min-1.100 g-1 (means +/- SE). The pulmonary blood flow contribution alone to the trachea and main bronchi was also determined in subsequent experiments that utilized the isolated lung, and these blood flows were not significantly different from the pulmonary contribution measured in the intact lungs. The present results indicate that the systemic (bronchial) circulation is the primary source of tracheal blood flow and that both the pulmonary and systemic circulations may contribute approximately 50% of the blood flow to the main bronchi in dog lungs.

Animals↗
PubMed1987

Effect of histamine on cardiac sarcolemmal calcium binding as indicated by use of ionic lanthanum.

To determine whether the inotropic effect of histamine might be associated with enhanced calcium binding to the sarcolemmal-glycocalyx complex, the effect of histamine on lanthanum binding to the cell membrane in the presence of verapamil was assessed. Rabbit hearts were perfused firstly with histamine, secondly with histamine and verapamil, and subsequently with histamine in the presence of lanthanum and verapamil. Subsequent transmission electron microscopy showed the presence of bound lanthanum on both the cellular surface and cytoplasmic vesicles of most cardiac myocytes, which is in contrast to the absence of lanthanum binding that occurs in the presence of verapamil alone. Furthermore, this histamine mediated enhancement of lanthanum binding is not affected by the H1 antagonist diphenhydramine but is reduced by the H2 antagonist cimetidine. This visual evidence of an apparent enhancement of lanthanum binding under histamine and subsequent attenuation with cimetidine supports the hypothesis that histamine may exert its positive inotropic effect by causing increased calcium binding to the sarcolemmal-glycocalyx complex of cardiac muscle and that the effect is mediated at least in part by H2 receptors.

Animals↗
PubMed1987

Histamine induced alteration of calcium binding to microvascular endothelium as indicated by use of ionic lanthanum.

To determine whether histamine's effect on microvascular permeability might be associated with altered calcium binding, the influence of histamine on lanthanum binding to vascular endothelium was assessed in the presence of verapamil. Isolated rabbit hearts were perfused firstly with histamine, secondly with histamine and verapamil, and subsequently with histamine in the presence of lanthanum and verapamil. Examination by transmission electron microscopy showed that 92% of microvessels examined contained bound lanthanum on plasma membranes, plasmalemmal vesicles, or endothelial clefts of vascular endothelium, or all three, in both atria and ventricles, which is in contrast to the low proportion (4%) of microvessels containing bound lanthanum found in the presence of verapamil alone. The enhancement of lanthanum binding was reduced by both H1 and H2 receptor antagonists. This evidence supports the hypothesis that the increase in vascular permeability with histamine may be associated with increased calcium binding to vascular endothelial membranes and that both H1 and H2 receptors play a part in this activity.

Animals↗
PubMedDate not supplied

Fenfluramine potentiates canine pulmonary vasoreactivity to endothelin-1.

The appetite suppressant fenfluramine, a serotonin uptake inhibitor, has been implicated in the development of primary pulmonary hypertension (PPH). The effect of fenfluramine on the pressor response to endothelin-1 (ET-1) in the canine pulmonary circulation was determined using the isolated perfused dog lung. Pulmonary vascular resistance was measured using vascular occlusion techniques. Group 1 (n=4) consisted of isolated lung lobes treated with 10(-8)M ET-1 alone. For group 2 (n=4) and group 3 (n=4), dogs were given 15 mg fenfluramine daily for 14 days prior to sacrifice for isolated lung perfusion. In group 2, lobes were treated with 10(-7)M fenfluramine after lung isolation. In group 3, the isolated lobes were treated with 10(-8)M ET-1 similar to group 1. Acute treatment of the isolated lobes in group 2 with 10(-7)M fenfluramine increased pulmonary arterial pressure. In group 3, administration of 10(-8)M ET-1 potentiated the effect of ET-1 on post-capillary resistance relative to group 1, and elicited an increase in precapillary resistance, an effect not present in group 1. These results indicate that chronic fenfluramine exposure potentiates the pulmonary vasoconstrictor response to ET-1, and suggests that elevated levels of serotonin may < > the pulmonary circulation to become hyperreactive to other vasoactive substances possibly leading to the development of disease states such as primary pulmonary hypertension.

Animals↗