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In teaching hospitals, bedside case presentation is a commonly used form of instruction. A group of students and physicians gather around a hospitalized patient's bed and discuss the case. It is used because it allows the student to inspect the patient's condition and see physician-patient interaction at work. However, for some patients, this interaction has been thought to be very stressful, and it has been suggested that this stress can itself be harmful to the patients, particularly those having critical heart diseases. An anxiety- rating instrument and blood tests were used to evaluate a group of 20 heart patients during bedside case presentations. There were no increases in heart rate or blood concentrations of norepinephrine, a hormone which increases blood pressure. There were slight increases in the average blood pressure during bedside presentations. Subjective findings revealed that patients actually felt "reassured" during the presentations. The patients also felt the physicians "cared more about them" as they discussed their disease. Patients found that they, too, learned more about their illness during the case presentations. The bedside case presentation in teaching hospitals was perceived by the patient as a positive event and did not induce stress using this model for evaluation.

Objective: The aim of this study was to investigate whether the role of nitric oxide (NO) in regulating blood flow (BF) to working skeletal muscle is impaired in chronic heart failure (CHF). Methods: The effect of NG-nitro-l-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, was studied in conscious rats with and without CHF due to myocardial infarction (MI). BF to the hindquarter musculature was measured with radiolabelled microspheres during exercise after 4 min of treadmill running (10% grade, 20 m/min) before and after L-NAME (20 mg/kg i.a.) administration. Results: Before L-NAME administration, BF measured in the total hindquarter musculature was less (P < 0.05) during exercise in rats with a large MI (MI size; 44 ± 2% of the left ventricular endocardial circumference; n = 8) when compared with sham-operated rats (SHAM; n = 10) and rats with a small MI (MI size; 25 ± 4%; n = 5). The BF measured during exercise following L-NAME administration was similar between the 3 groups. Of the 28 individual hindquarter muscles, BF was reduced in 23 and 19 muscles following the administration of L-NAME for the SHAM rats and rats with a small MI, respectively. In comparison, BF was reduced to only 4 of 28 muscles in rats with a large MI. Conclusions: These results suggest that the contribution of the NO pathway to the hyperaemic BF responses found in the hindquarter muscles during exercise could be attenuated in rats with CHF. This attenuation of the NO pathway may be associated with the impairment of skeletal muscle BF distribution during exercise in CHF. [ABSTRACT FROM PUBLISHER]

The aim was to evaluate mechanisms regulating tissue noradrenaline in congestive heart failure. Methods: Tissue noradrenaline was measured in the conscious post myocardial infarction rat model of congestive heart failure and in sham operated rats (1) under control conditions, (2) 6 h after inhibition of tyrosine hydroxylase by the intraperitoneal administration of α-methyl-paratyrosine (AMPT) (100 mg·kg−1 every 2 h), (3) 6 h after AMPT with desipramine pretreatment (0.3 mg·kg−), and (4) following exhaustive exercise after AMPT. Tissue noradrenaline was extracted with perchloric acid and measured by high performance liquid chromatography with electrochemical detection. Results: In control animals without drug, tissue noradrenaline concentration was lower in the following tissues in the rats with myocardial infarction compared with the sham operated group: left and right ventricles, spleen, soleus and white gastrocnemius muscles, kidney cortex, and tail artery. After AMPT, tissue noradrenaline concentration in the sham operated group was significantly lower than control; in the myocardial infarction group the fall in noradrenaline was only significant in the kidney, and group differences were no longer present. In the sham operated animals, coadministration of desipramine with AMPT attenuated the fall in tissue noradrenaline caused by AMPT in the heart and spleen. With exercise to exhaustion, cardiac noradrenaline was lower in rats with myocardial infarction than in sham operated rats, but higher in the soleus muscle. Conclusions: These data suggest that tissue noradrenaline depletion in congestive heart failure is not isolated to the heart, and it occurs despite activation of mechanisms that might be operating to conserve neuronal noradrenaline. One mechanism may be reduced organ blood flow to retard diffusion of noradrenaline into the circulation. If this increases interstitial noradrenaline concentration, it would facilitate prejunctional α2 receptor restraint on noradrenaline release. Metabolic coronary vasdilatation during exercise reverses this process, and makes the heart most susceptible to noradrenaline depletion in congestive heart failure.Cardiovascular Research 1992;26:933–938 [ABSTRACT FROM PUBLISHER]

The purpose of the present study was to determine if pretreatment with dexamethasone 6 mg·kg−1 would preserve coronary artery blood flow during reperfusion, thus preventing the no reflow phenomenon. Blood flow to small segments of the left ventricle was measured by the use of 15 μm tracer microspheres in intact dog hearts. During 2 hours of occlusion of the anterior descending coronary artery by balloon catheter, dexamethasone produced a small increase of the blood flow to perfused myocardium, when compared with untreated animals; this effect was not seen in underperfused segments of the myocardium. In nontreated animals, reperfusion of the underperfused portion of the left ventricle did not lead to a restoration of flow to normal when measured 1 hour later. In fact, the “no reflow ” phenomenon resulted in a post reperfusion left ventricular segment which was similar to that measured during coronary arterial occlusion. However in the dexamethasone treated animals there was a decrease in the extent of left ventricular underperfusion from 19 to 6%. It is concluded that dexamethasone protects the border zone of canine myocardium during occlusion, and prevents the no reflow phenomenon in underperfused regions during reperfusion. [ABSTRACT FROM PUBLISHER]

In order to evaluate right and left ventricular stretch receptors without concomitantly stimulating those of the contralateral ventricle, 12 dogs were placed on total cardiopulmonary bypass. Balloons connected to compliant reservoirs were introduced into the right and left ventricles. Changes in systemic, gracilis muscle, and paw perfusion pressure at a constant flow were used as indices of systemic, muscle, and cutaneous vascular resistance. To induce left ventricular stretch, the balloon in that chanber was rapidly inflated from a mean pressure of 1.33 kPa (10 mmHg) to a mean pressure of 7.32 kPa (55 mmHg) for 15 s (6.00 kPa [45 mmHg] increment). For right ventricular stretch, the pressure was increased from 0.67 to 4.00 kPa (5 to 30 mmHg) for 30 s (3.34 kPa [25 mmHg] increment). Both left and right ventricular stretch produced a significant fall in systemic (-4.92 kPa [-37 mmHg], -36%) and gracilis muscle (-5.59 kPa [-42 mmHg],-30%) perfusion pressure, with only minimal changes in cutaneous vascular resistance (-0.80 kPa [-6 mmHg], -4%). This reflex was found to be vagally mediated, to have a low threshold for stimulation (left ventricle, 0.67 kPa [5 mmHg] increment; right ventricle, 1.33 kPa [10 mmHg] increment), and to have a neurogenic sympathetic alpha-adrenergic efferent limb. The low threshold for stimulation suggests that these reflexes may play a physiological role with changes in body position and may be important in such pathological conditions as semilunar valvular stenosis and myocardial infarction. [ABSTRACT FROM PUBLISHER]