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Biomedical subjects

R M Raymond

Publications and source records attributed to R M Raymond.

61 records · Page 4Linked to original sources
PubMed1980

Effects of intravenously infused histamine on canine forelimb transvascular protein efflux following adrenergic receptor blockade.

The intravenous infusion of high doses of histamine (400 micrograms base/min) produced only small increases in weight (approximately equal to +30 g) and lymph total protein concentration (+ 0.9 g/100 ml) in canine forelimbs perfused at constant inflow. The weight gain was associated with profound decreases in aortic pressure (112 to 30 mm Hg) and in forelimb perfusion pressure (105 to 75 mm Hg) and marked increases in forelimb skin small-vein pressure (from 12 to 25 mm Hg). After treatment with phentolamine, the intravenous infusion of these doses of histamine under the same conditions produced marked decreases in forelimb perfusion pressure (120 to 60 mm Hg) and failed to increase forelimb skin small-vein pressure, yet still produced only minimal increases in weight (+ 12 g) and lymph total protein concentration (+ 0.8 g/100 ml). Following treatment with both phentolamine and propranolol, the intravenous infusion of histamine caused very marked increases in forelimb weight (approximately equal to +75 g) and lymph total protein concentration (+ 2.9 g/100 ml). These marked increases in forelimb weight and lymph formation were associated with profound decreases in perfusion pressure (112 to 60 mm Hg) but no change in skin small-vein pressure relative to control. These same increases in weight and lymph total protein concentration were observed after treatment with propranolol alone. Thus, treatment with propranolol markedly increased net fluid filtration and protein efflux during intravenous infusions of massive doses of histamine, idicating that this edemogenic agent causes an endogenous release of catecholamines which tend to antagonize the direct actions of histamine on the microvascular membrane via stimulation of beta-adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1979

Morphological and physiological correlation of bradykinin-induced macromolecular efflux.

Bradykinin applied topically for 4 min produced marked dose-related increases in the number of fluorescent dextran (mol wt 145,000) vascular leakage sites exclusively from small postcapillary venules--evidence for an increase in macromolecular permeability. The increase in macromolecular permeability was short-lived, making repeated applications possible. The number of bradykinin-induced venular fluorescent dextran leakage sites could be greatly reduced by the simultaneous topical application of isoproterenol, and this antagonism of the increase in macromolecular permeability could be prevented by pretreatment with propranolol. The topical application of papaverine failed to antagonize the increase in the number of venular leakage sites of fluorescent dextran by bradykinin. A continuous 90-min superfusion of bradykinin elicited an initial marked increase in the number of fluorescent dextran venular leakage sites, which then waned after 20-30 min, returning to near control despite the continued superfusion with bradykinin. In canine forelimbs the bradykinin-induced increase in protein efflux, total protein transport, and lymph flow also peaked in approximately 30 min and then waned markedly despite continued local intra-arterial infusions of this agent for prolonged periods. The morphological data from the cheek pouch agrees well with the physiological data from the forelimb, suggesting that an increase in protein efflux in the canine forelimb could be readily explained by an increase in the number of large pores.

Animals↗
PubMed1979

Methylprednisolone in the prevention of cerebral hemodynamic and metabolic disorders during endotoxin shock in the dog.

These results provide evidence that steroid pretreatment and subsequent post-treatment prevent cerebral hemodynamic and metabolic alterations during four hours of Escherichia coli endotoxin shock in the dog. However, in this study, no data are provided on how the steroid prevents an increase in cerebral vascular resistance, and no clear answer is available in the literature. While active vasodilation or alpha-adrenergic blocking properties, or both, have been attributed to glucocorticoids, recent evidence does not support these findings during normal conditions or circulatory shock. If the increase in cerebral vascular resistance is passive, steroids may help by preventing platelet aggregation, cell disruption and subsequent microvascular plugging. Intravenously administered fluids, dextran-saline solution, while in themselves are probably not important to survival, may augment cerebral blood flow during shock through a blood dilutional effect. Finally, it is possible that steroids act to permit normal, long term cerebral auto-regulation, which is apparently impaired during endotoxin shock in the dog.

Animals↗
PubMed1979

Cerebrospinal fluid composition during endotoxin shock in the dog.

Cerebrospinal fluid (CSF) electrolytes, lactate, pyruvate, total proteins, and osmolality, together with arterial plasma electrolytes, total proteins, osmolarity, and systemic arterial blood pressure were monitored during 2 mg/kg and 5 mg/kg E coli endotoxin shock in spontaneously breathing dogs. During four hours of shock, Na+, K+ osmolarity, and total proteins did not change in either plasma or CSF. CSF lactate and lactate/pyruvate ratio were significantly elevated, whereas pyruvate was decreased throughout the four hours of shock. Systemic arterial blood pressure was below control during the entire shock period. Saline control experiments yielded no significant changes in all parameters monitored. These data show that during four hours of shock the brain has shifted form aerobic to anaerobic metabolism the degree of which is not sufficient to cause any detectable changes in membrane permeability or alterations in Na+/K+ active processes.

Animals↗