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Biomedical subjects

M B Maron

Publications and source records attributed to M B Maron.

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

Effect of hemolysis on reflection coefficient determined by endogenous blood indicators.

The osmotic reflection coefficient (sigma) can be estimated from the increases in hematocrit and plasma protein concentration that result from fluid filtration occurring in an isolated perfused organ. We determined what effect perfusion pump-induced hemolysis has on the value of sigma determined by this technique in both the isolated canine left lower lung lobe (LLL) and forelimb by comparing estimates of sigma obtained before and after correction for hemolysis. Hemolysis was corrected by using the slopes of the relationships between hematocrit and plasma hemoglobin concentration and between the plasma protein and hemoglobin concentrations to correct hematocrit and protein concentration to a state of zero hemolysis. Uncorrected estimates of sigma in the LLL were 1.19 +/- 0.14 (SE) at a venous pressure (Pv) of 12 Torr (n = 7) and 0.90 +/- 0.02 at a Pv of 19 Torr (n = 6). Both sets of LLL's yielded sigma values of 0.77 +/- 0.03 after hemolysis correction. In the forelimb (n = 5), uncorrected and corrected estimates of sigma of 0.99 +/- 0.03 and 0.85 +/- 0.01, respectively, were obtained. The latter values were similar to sigma's (0.88 +/- 0.01) determined by lymph analysis in five additional forelimbs. We conclude that hemolysis results in overestimates of sigma. After hemolysis correction, this technique yields similar results to those obtained from lymph analysis for the forelimb and from published values for the LLL.

Animals↗
PubMed1985

Effect of high doses of aspirin on pulmonary hemodynamics and lung water.

The purpose of this study was to determine if aspirin, in doses that elevate plasma salicylate concentrations to values reported in patients with salicylate-induced pulmonary edema, produce pulmonary vasoconstriction in a canine, isolated perfused left lower lung lobe (LLL) preparation. In 10 LLL's, aspirin (avg 97.8 mg/dl plasma) caused LLL arterial pressure to rise from 9.1 +/- 0.3 to 23.0 +/- 1.8 (SE) Torr. In contrast, no vascular pressure changes were observed in placebo-treated control LLL's. Sodium meclofenamate and indomethacin, structurally dissimilar cyclooxygenase inhibitors, elicited similar responses to aspirin, suggesting that a mechanism involving products of prostaglandin cyclooxygenase was involved in producing the vasoconstriction. The double-occlusion technique was used to localize the sites of the vasoconstriction. The results suggested that all three drugs caused both lobar arterial and venous tone to increase. Although high doses of aspirin produced pulmonary vasoconstriction in the isolated, perfused LLL, the aspirin-treated LLL's gained less weight and extravascular water than the control lobes.

Animals↗
PubMed1985

Pulmonary hemodynamics and lung water content during splanchnic ischemic shock.

Pulmonary hemodynamics and lung water content were evaluated in open-chest dogs during splanchnic arterial occlusion (SAO) shock. Mean pulmonary arterial pressure [Ppa = 13.0 +/- 0.6 (SE) mmHg] and pulmonary venous pressure (4.1 +/- 0.2 mmHg) were measured by direct cannulation and the capillary pressure (Ppc = 9.0 +/- 0.6 mmHg) estimated by the double-occlusion technique. SAO shock did not produce a significant change in Ppa or Ppc despite a 90% decrease in cardiac output. An 18-fold increase in pulmonary vascular resistance occurred, and most of this increase (70%) was on the venous side of the circulation. No differences in lung water content between shocked and sham-operated dogs were observed. The effect of SAO shock was further evaluated in the isolated canine left lower lobe (LLL) perfused at constant flow and outflow pressure. The addition of venous blood from shock dogs to the LLL perfusion circuit caused a transient (10-15 min) increase in LLL arterial pressure (51%) that could be reversed rapidly with papaverine. In this preparation, shock blood produced either a predominantly arterioconstriction or a predominantly venoconstriction. These results indicate that both arterial and venous vasoactive agents are released during SAO shock. The consistently observed venoconstriction in the intact shocked lung suggests that other factors, in addition to circulating vasoactive agents, contribute to the pulmonary hemodynamic response of the open-chest shocked dog.

Animals↗
PubMed1985

A canine model of neurogenic pulmonary edema.

The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40-60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.

Animals↗
PubMed1984

Effect of histamine on coronary microvascular permeability.

The effect of histamine on coronary vascular permeability was assessed under conditions of elevated venous pressure in the spontaneously beating, isolated canine heart perfused with autologous blood. The apparent volume of fluid filtered from the vasculature to the interstitium (VF) was calculated from the increase in plasma protein concentration and also from the increase in hematocrit. The ratio of the protein-filtered volume to the hematocrit-filtered volume (VF,Pr/VF,Hct) was used to evaluate changes in permeability. In the absence of histamine, the VF,Pr/VF,Hct was near unity (1.05 +/- 0.11), which indicated that the blood proteins and the red blood cells had concentrated equally. Thus the transudate was essentially protein free. On exposure to histamine (3.8 +/- 0.3 microgram base/ml blood), VF,Pr/VF,Hct decreased to 0.37 +/- 0.06 (P less than 0.001), which indicated that coronary vascular permeability had increased. This value remained constant throughout the 60 min of histamine exposure. Aortic perfusion pressure decreased significantly (P less than 0.05) from 111 +/- 11 to 84 +/- 5 mmHg during the 1st min of histamine exposure and rose slowly thereafter. In four of the seven hearts, concomitant increases in left ventricular isovolumic pressure development (13-31 mmHg) and heart rate (4-29 beats/min) were observed. In the remaining hearts, neither variable was affected by histamine. We conclude that histamine causes an increase in the permeability of the canine coronary microvasculature but fails to increase heart rate or left ventricular performance consistently.

Animals↗
PubMed1984

Cigarette smoke causes acute fluctuations in the cyclic GMP content of the isolated intact lung.

The injection of a single bolus of the gas phase of cigarette smoke into the airway of an isolated, perfused and ventilated, canine lung preparation resulted in a sevenfold increase in lung cyclic GMP content by 2 s after exposure. Recovery of control levels occurred by 2 min after injection. Repeated smoke exposures of the same lung resulted in similar increases. These results indicate that cigarette smoke may activate lung guanylate cyclase when delivered through the airway and suggest that lung cyclic GMP levels may fluctuate acutely during smoking.

Animals↗
PubMed1983

Modification of lymph during passage through the lymph node: effect of histamine.

The possibility that histamine may cause the fluid and protein content of lymph to be altered during passage through the lymph node was evaluated using the canine perfused popliteal lymph node preparation. This preparation enables nodal perfusion via an afferent lymphatic (all other afferents are ligated) with artificial lymph of known composition and collection of the total efferent effluent for analysis of potential changes in volume and composition. In 11 dogs, the node was perfused at an average flow rate of 0.229 ml/min with artificial lymph containing 3.71 g/100 ml albumin. Under base-line conditions, there was no significant modification of the lymph as it passed through the node. The addition of histamine to the infusate (2-4 micrograms base/ml) caused the efferent lymph flow to increase to 0.295 ml/min (35.3% increases, P less than 0.05), the efferent protein concentration to increase to 4.32 g/100 ml (15.2% increases, P less than 0.05), and the efferent protein flux to increase from 8.40 to 12.86 mg/min (58.0% increases, P less than 0.05). The appearance of Evans blue dye-tagged protein and plasma protein fractions, not originally present in the lymph, in the efferent lymph at this time further indicated that the source of the added fluid and protein was the nodal vasculature. Mass balance calculations indicated that the addition of a fluid with a protein concentration of approximately 90% that of plasma to the lymph could account for the observed increases in efferent lymph flow and protein concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Time course of lung volume changes during prolonged treadmill exercise.

It has been known since the 1920s that runners completing marathon races have reduced forced vital capacity (FVC) values. To investigate the time course of these lung volume alterations, we measured FVC and residual volume (RV) in 11 runners before, after, and at 30-min intervals during a 2.5-h treadmill run at just under their marathon pace (70% VO2max). Mean distance run was 21.5 +/- 1.5 (SD) miles in the 2.5-h period. During the first 60 min, both RV and total lung capacity (TLC) decreased by 110 ml, however, this change was not significant (P greater than 0.05). A high correlation (r = 0.93) was observed between delta RV and delta TLC during the first 5 min, while FVC remained unchanged. From 60-90 min, all lung volumes remained constant. From 90-150 min, lung volumes changed in a direction similar to that observed after a marathon, i.e., FVC decreased significantly (5.51 to 5.37 liter between 90 and 150 min, P less than 0.05), TLC remained unchanged (7.41 vs 7.42 liter, P greater than 0.05), and RV showed a nonsignificant increase from 1.90 to 2.05 liter (P greater than 0.05). The data are consistent with multiple mechanisms playing a role in pulmonary function changes during prolonged exercise. The smaller mean decrease in FVC observed in this study, as compared to that found during a marathon, suggested that the marathon imposes a greater demand on the lungs than did treadmill exercise of the duration and relative intensity used in this study.

Adult↗
PubMed1983

Pulmonary hemodynamic responses during superior mesenteric artery occlusion.

We investigated the possibility that the reestablishment of blood flow to the intestine after a 2-h occlusion of the superior mesenteric artery (SMA) may liberate vasoactive substances in quantities sufficient to cause pulmonary vasoconstriction. Experiments were conducted in dogs in which we compared the hemodynamic responses of the animal's left lower lung lobe (LLL), which was perfused at constant flow with blood pumped from the animal's pulmonary artery, with those of its intact right lung. Changes in systemic hemodynamics were similar to those reported by others for this stress. By 1 h after the release of the occlusion, cardiac output and stroke volume had fallen by 41.1 and 50.0%, respectively. Comparable changes were not observed in sham-operated control animals. Following the release of the occlusion, we observed an average 0.9 torr (P less than 0.10) increase in LLL arterial pressure, no significant changes in left atrial pressure, and a 11.9% increase (P less than 0.025) in LLL vascular resistance. In the intact right lung, no significant changes in pulmonary arterial pressure were observed at this time. Although the responses of the LLL suggested that some very small increase in vasomotor tone may have occurred, the small magnitude of the response indicated that the lung vasculature is only minimally affected during the early phases of this stress.

Animals↗
PubMed1982

An isolated perfused dog lung preparation for the study of cyclic GMP metabolism: effects of sodium nitroprusside and oxygen.

The intact, isolated perfused dog lung was evaluated as a model for studies directed at defining the role of oxidative modulation of lung cyclic GMP metabolism in pulmonary function. Sodium nitroprusside added to the perfusion blood increased the cyclic GMP content of lung over 4-fold in a dose-dependent manner. Although sodium nitroprusside administration caused changes in lung vascular resistance, these occurred independently of the changes in cyclic GMP. Ventilation of lungs with a high oxygen gas mixture containing 95% O2. 5% CO2 acutely increased the cyclic GMP content of lungs after 15 min from 1.3 +/- 0.06 (mean +/- SE) to 3.4 +/- 0.12 pmol cyclic GMP/mg protein. Cyclic GMP levels returned toward control during continued ventilation with the high oxygen concentration. The oxygen-induced elevation of lung cyclic GMP content was not accompanied by changes in lung vascular resistance. The results indicate that the isolated perfused lung may be useful in studies of cyclic GMP, tissue oxidation and pulmonary function.

Animals↗
PubMed1982

Differential effects of histamine on protein permeability in dog lung and forelimb.

In this study, the effects of histamine on the microvascular permeability of a canine, isolated perfused left lower lung lobe (LLL) and a forelimb preparation were evaluated by comparing the apparent filtered volumes (VF) calculated from the increases in hematocrit (Hct) and plasma protein concentration (Pr) observed during filtration. In the LLL and forelimb, the elevation of venous pressure (Pv) to 15.5 Torr resulted in a ratio of filtered volumes (VF,Pr/VF,Hct) of 0.97 and 0.99, respectively. In the LLL, histamine administration did not significantly change this ratio, whereas the addition of methylene blue decreased it to 0.62. In the forelimb, histamine transiently decreased VF,Pr/VF,Hct to 0.23. After recovery, the elevation of Pv to cause further filtration resulted in a ratio of 0.94. These data suggest that intrinsic differences in the regulation of microvascular permeability exist between blood vessels of the lung and forelimb, in that a histamine dose that significantly increased the protein permeability of the forelimb had no measurable effect on the LLL.

Animals↗
PubMed1980

Pulmonary inactivation of serotonin and site of serotonin pulmonary vasoconstriction.

To determine whether the site of serotonin-induced pulmonary vasoconstriction is influenced by serotonin uptake and inactivation within the lung, we utilized an isolated perfused left lower lobe of the dog lung, which could be perfused with flow in the normal direction (i.e., blood flowing into the lobar artery) or in the retrograde direction (i.e., blood flowing into the lobar vein). To localize the site of vasoconstriction, we utilized an outflow occlusion technique in which the changes in lobar vascular resistance were divided into changes in arterial and venous resistances. Serotonin infusion constricted vessels on the arterial side of the site of serotonin uptake during both forward and retrograde perfusion while having much less influence on the venous side. However, during retrograde perfusion the serotonin infusion rate required to produce a given increase in arterial resistance was approximately 85 micrograms/min greater than during forward perfusion. Thus, it would appear that serotonin was primarily an arterial constrictor in this preparation and that, although the lung removed a substantial quantity of serotonin, the uptake and inactivation within the lung had relatively little influence on the site of serotonin vasoconstriction.

Animals↗
PubMed1980

Adrenal component to pulmonary hypertension caused by nicotine administration in the dog.

In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.

Adrenal Glands↗
PubMed1980

Pulmonary venoconstriction caused by elevated cerebrospinal fluid pressure in the dog.

Previously we found that raising cerebrospinal fluid pressure (PCSF) caused pulmonary vasoconstriction mediated by adrenal catecholamines. To localize the site of this vasoconstriction we used the outflow occlusion technique to divide changes in the pulmonary arteriovenous pressure gradient (Pa-v) into upstream and downstream pressure drops. Experiments were conducted in 10 dogs in which the animal's left lower lung lobe was denervated and perfused at constant flow and outflow pressure with blood pumped from the dog's pulmonary artery. Raising PCSF to 218 Torr caused Pa-v to rise from 9.0 to 12.5 Torr. Most (83%) of this increase resulted from an increase in the downstream pressure drop. Previous studies have indicated that changes in the upstream and downstream pressure drops, as measured by this technique, are highly correlated with changes in the resistance of the arterial and venous sides of the vascular bed. Thus, it appears that elevated PCSF caused primarily pulmonary venoconstriction. Similar results were obtained with norepinephrine and epinephrine infusion. This is consistent with previous studies, indicating that adrenal catecholamines are responsible for the increase in Pa-v in response to PCSF in this preparation.

Animals↗
PubMed1979

Pulmonary hemodynamic responses to elevated cerebral spinal fluid pressure in the dog.

To investigate the possibility that a pulmonary vasomotor reflex contributes to the pulmonary hemodynamic response to elevated cerebral spinal fluid pressure (PCSF), we studied 10 chloralose-anesthetized dogs in which the left lower lobe (LLL) perfusion was isolated to eliminate the influence of passive factors and of circulating vasoactive agents. Left lower lobe neural integrity was tested by electrically stimulating the stellate ganglion. This resulted in a 35.5% increase in lobar vascular resistance and a 29.1% increase in systemic vascular resistance. Elevating the PCSF to 137 Torr caused the systemic vascular resistance to increase 33.0%, but resulted in no change in LLL vascular resistance. In the intact right lung, this PCSF elevation resulted in increases in pulmonary artery and left atrial pressures, but no change in right lung vascular resistance. Because the neurally intact LLL did not respond to PCSF elevation and the responses of the right lung could be accounted for by passive mechanisms, we conclude that no pulmonary vascular reflex was elicited by PCSF elevation in this preparation.

Animals↗
PubMed1979

Adrenal component to pulmonary hypertension induced by elevated cerebrospinal fluid pressure.

In this study we investigated the possibility that a circulating vasoactive agent contributes to the pulmonary hypertension elicited by elevated cerebrospinal fluid pressure (PCSF) using a denervated canine left lower lung lobe (LLL) preparation that was pump perfused with mixed venous blood at constant flow and venous pressure. Raising the PCSF to an average 190 Torr resulted in a 34.3% increase in LLL inflow pressure. This response was eliminated by adrenal venous occlusion and also by alpha-blockade of the LLL. The results indicated that adrenal catecholamines were responsible for the LLL response. The passively induced elevation of left atrial pressure (Pla) that occurs in the intact animal during elevated PCSF was stimulated in the LLL by raising the outflow pressure. This maneuver attenuated the increase in LLL vascular resistance and suggested that the elevation in Pla seen in the intact animal could mask humorally mediated responses of the magnitude we observed.

Adrenal Glands↗
PubMed1979

Pulmonary function in rabbits with BCG-induced lung disease.

This study was performed to determine whether the lung histological changes which occur in rabbits following intravenous injection of killed Bacilli Calmette-Guérin (BCG) are accompanied by measurable changes in pulmonary function. We measured pulmonary function in New Zealand white rabbits 3 weeks after intravenous injection of BCG and in normal rabbits. After a tracheostomy and carotid artery catheterization was performed, each anesthetized rabbit was placed in a body plethysmograph for pulmonary function testing. Following the measurements, the lungs were removed for weighing and histological evaluation. In the BCG-treated rabbits, the lung weight/body weight ratios were 152% greater, the pulmonary resistance was 104% higher, dynamic compliance was 45% lower, minute ventilation was 28% greater, and the delta AaPO2 gradient was 13 torr higher than in the normal control rabbits. Histological evaluation of the BCG-treated animals revealed diffuse pulmonary involvement with non-caseating granulomas.

Airway Resistance↗