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A study identified in 10 awake instrumented rats the influence of intraneous N (G)-monomethyl-L-arginine (L-NMMA), an endothelium-derived relaxing factor (EDRF) inhibitor, on mean circulatory filling pressure (MCFP) to establish whether nitirc oxide, a possible EDRF, modulates baseline venous tone. L-arginine reversed the influence of L-NMMA on MCFP. An almost similar rise in MCFP was observed in the control unblocked state and the ganglionic blocked state, and the baseline venous tone is lowered by nitric oxide.

The estimation of venous compliance (VC) as a function of aging is carried out by employing an awake instrumented rat model, including 10 month old young rats and 30 month-old rats. This involves measurement of mean Fischer 344/Brown Norway hybrid rats. An increase in mean circulation filling pressure (MCFP) is negligible in case of transient volume expansion, and a decline in MCFP is almost independent of transient volume depletion. The computed value of VC in older rats is 25% greater than VC pertaining to younger rats.

Lay persons might think physicians spend all their time in hospitals or clinics or that physicians fly their private jets to exclusive resorts for long weekends. But physicians are regular people just like their patients, and, when not on the job, they do many of the same things for the same reasons: playing with pets and doing sports, music, and art. Physicians might not have a blue-ribbon dog, might not have played varsity basketball in college, might not have gone to Julliard before medical school, might not have had one-person exhibits at the Metropolitan Museum of Art, but what they do when they are not wearing their white coats can make them better physicians when they put the coats back on again. [ABSTRACT FROM AUTHOR]

Poetry and Medicine Eight days after they had cut into my chest, put me on a bypass pump, excised a valve consumed by Staph, stitched a new one in I read what they had said about the scan of my head two weeks before. Footnotes 1 Article InformationCorresponding Author: Joseph Gascho, MD ().Conflict of Interest Disclosures: None reported. "Innumerable" I read, "Septic emboli" I read, "to both cerebral hemispheres.". [Extracted from the article]

Study objective — The aim was to determine if myocardial systolic thickening increases when coronary flow is augmented by infusing intracoronary vasodilators (adenosine and papaverine).Design — Systolic thickening fraction was measured with pulsed Doppler crystals and sonomicrometer crystals before and during the intracoronary infusion of adenosine and papaverine.Subjects — Sixteen anaethetised mongrel dogs were studied.Measurements and main results — Intracoronary adenosine did not alter systemic haemodynamics, but did induce a three- to fourfold increase in myocardial blood flow. Intracoronary papaverine caused a slight decrease in systemic arterial pressure and rise in heart rate. Neither intracoronary adenosine nor intracoronary papaverine increased systolic thickening: control thickening fraction (TF%) = 20 (SEM 1)%, adenosine TF% = 18(1)%; control TF% = 22(2)%, papaverine TF% = 20(2)%.Conclusions — These experiments do not support the hypothesis that an increase in myocardial blood flow induced by intracoronary vasodilators causes an increase in myocardial systolic function. [ABSTRACT FROM PUBLISHER]

Study objective – The aim was to determine the relation between systolic function and depth below the epicardial surface, using pulsed Doppler crystals.Design – Systolic excursion in mm was measured at multiple depths below the epicardial surface. Measurements were made during control conditions.Subjects – Thirty four anaesthetised mongrel dogs were studied.Measurements and main results – A total of 333 measurements of systolic excursion were made during control conditions at 1 to 3 crystal sites per dog. Two models were constructed; the model which assumed a quadratic relation between depth (d) and systolic excursion (EX) (EX = 0.498 + 0.176d + 0.006d2) fit the data better than did a model which assumed a linear relation (EX = −0.0716 + 0.254d).Conclusions – These data support the prediction from geometric models that systolic excursion increases in a non-linear fashion from subepicardium to subendocardium. [ABSTRACT FROM PUBLISHER]

Study abjective – Previous experiments from our group have shown that left anterior descending coronary occlusion in the presence of hypotension caused by intravenous glyceryl trinitrate in an open chest canine model caused endocardial flow to fall in myocardium supplied by a stenosed circumflex coronary artery. The aim of the present study was to assess the effects of hypotension in a similar open chest model but without the vasodilating effect of glyceryl trinitrate on coronary vessels.Design – Blood flow to and function of remote myocardium supplied by a stenosed circumflex coronary artery [gradient 27(SEM 3) mm Hg] was determined in anaesthetised dogs after haemorrhage induced hypotension [mean aortic pressure 70(3) mm Hg] and after left anterior descending coronary occlusion. Transmural blood flow was measured using microspheres and myocardial wall thickness with sonomicrometer crystals.Subjects – 11 healthy mongrel dogs were used, weight 25 kg (range 19-33).Measurements and main results – Haemorrhage induced hypotension in the setting of a circumflex stenosis reduced endocardial blood flow to the posterior myocardial bed from 0.84(0.14) to 0.57(0.07) ml·min−1·g−1 but did not alter percent myocardial thickening. When the left anterior descending coronary artery was occluded in the presence of the circumflex stenosis and haemorrhage induced hypotension, there was no further decrease in endocardial blood flow to or thickening of the posterior myocardial bed, despite a reduction in mean coronary artery pressure from 54(3) to 43(3) mm Hg.Conclusions – These findings are in contrast to our previous findings where hypotension was induced by glyceryl trinitrate. Remote myocardial ischaemia appears to be attenuated in this two vessel stenosis-occlusion model in which hypotension is produced by haemorrhage. [ABSTRACT FROM PUBLISHER]

To determine whether or not the fall in coronary perfusion pressure after coronary occlusion is the cause of remote myocardial ischaemia, regional myocardial blood flow was measured using radiolabelled microspheres before and after left anterior descending (LAD) occlusion in the presence of a left circumflex artery stenosis in 22 anaesthetised dogs. Aortic pressure was maintained constant at the time of left anterior descending artery occlusion in 13 dogs (group 1) and proximal left circumflex artery pressure was held constant by a servocontrolled pump in nine dogs with a carotid artery-left circumflex artery shunt (group 2). Despite the maintenance of constant mean aortic pressure in group 1, remote posterior bed mean(SEM) endocardial flow fell from 0.69(0.05) to 0.43(0.07) ml·min−1·g−1 (p<0.05). In the dogs in which left atrial pressure rose to ≤9 mmHg after left anterior descending artery occlusion, remote bed endocardial flow did not fall significantly (0.66(0.07) to 0.56(0.11) ml·min−1·g−1; NS). In contrast, remote bed endocardial flow fell from 0.73(0.07) to 0.28(0.06) ml·min−1·g−1 (p<0.0001) after left anterior descending artery occlusion in the dogs in which left atrial pressure rose to >9 mmHg. The fall in remote bed endocardial flow was prevented in group 2 dogs by maintaining proximal left circumflex artery pressure constant (0.95(0.08) to 0.86(0.09) ml·min−1·g−1; NS).An important mechanism for the development of remote myocardial ischaemia appears to be the fall in proximal coronary perfusion pressure at the time of coronary occlusion. [ABSTRACT FROM PUBLISHER]

Inadequate coronary reserve is present in left ventricular hypertrophy secondary to hypertension. Since this abnormality might be due in part to vascular hypertrophy of coronary resistance vessels in response to chronic hypertension, we studied a model of ventricular hypertrophy without hypertension. Volume-overload hypertrophy was produced by creating complete heart block in mongrel dogs; 6 to 7 weeks later the dogs were studied in the awake state. The thirteen dogs with chronic heart block had a 49% increase (P<0.05) in left ventricular mass compared with eight control dogs. The major findings in this study were: 1) at rest, coronary blood flow (microsphere technique) per unit weight of left ventricle was not increased in dogs with hypertrophy; and 2) the minimal coronary vascular resistance per unit weight of left ventricle calculated during iv adenosine infusion at a rate that produced maximal vasodilatation was not significantly higher in dogs with left ventricular hypertrophy than in controls (16.4±1.0 vs 14.7±1.5 kPa·litre−1·min·100 g, respectively). Minimal coronary vascular resistance of the entire left ventricle was significantly less in dogs with hypertrophy than controls (13.0±0.8 vs 17.3±1.7 kPa·litre−1·min, respectively). This data suggests that vascular hypertrophy of coronary resistance vessels related to chronic hypertension may be the cause of the increased minimal coronary vascular resistance seen in dogs with pressure-overload left ventricular hypertrophy. [ABSTRACT FROM PUBLISHER]