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Biomedical subjects

R Zelis

Publications and source records attributed to R Zelis.

At least 217 records · Page 12Linked to original sources
PubMed1969

Comparison of the reflex reactivity of skin and muscle veins in the human forearm.

To determine the relative participation of skin and muscle capacitance beds of the forearm in venomotor reflexes, epinephrine iontophoresis was combined with forearm plethysmography so that the volume of muscle veins could be estimated simultaneously with the volume of cutaneous veins, at a constant venous pressure. With this technique not only are the cutaneous veins markedly constricted but they also are prevented from filling since skin blood flow is abolished. In 10 normal subjects, the venous volume in the elevated control forearm at a congesting pressure of 30 mm Hg (VV[30]) was 3.16 +/-0.30 SEM cc/100 cc, while in the iontophoresed arm it was 2.54 +/-0.31 cc/100 cc. Thus the forearm cutaneous VV[30] was 1.62 cc/100 cc. With a deep breath, ice to the forehead, and leg exercise, and cutaneous VV[30] decreased 19.8% (P < 0.01), 36.6% (P < 0.01), and 32.6% (P < 0.02), respectively, whereas the muscle VV[30] was not altered significantly. Similar results were observed using the isolated forearm technique and a deep muscle vein. The infusion of epinephrine intra-arterially did not decrease reflex venomotor reactivity until cutaneous blood flow was completely suppressed, indicating that the inability of the veins to react in the iontophoresed arm was not the result of epinephrine diffusion into the muscle bed. Thus, these results indicate that, in the forearm, only cutaneous veins participate in venomotor reflexes. Further, since the forearm is principally composed of skeletal muscle and the hand skin, an explanation is provided for the observation that veins of the forearm, studied as a whole, appear less reactive to stimuli than veins of the hand. An explanation also is provided for fainting which occurs during motionless standing despite intense venoconstriction, thereby emphasizing the importance of the skeletal muscle pump in the legs in preventing postural syncope.

Adult↗
PubMed1969

New trends in the treatment of angina pectoris.

Traditionally when considering the pharmacologic basis of therapy in angina pectoris, attention is focussed on alterations of coronary blood flow. Yet the diseased coronary arteries in these patients often do not appear to be capable of responding to vasodilatory drugs. Since the pain of myocardial ischemia is relieved by a number of interventions without an increase in coronary blood flow, the concept herein considered is that angina pector is best viewed as an unfavorable relation between myocardial oxygen requirements and availability. Thus, the clinical value of the major antianginal agents is thought to be based importantly upon their actions to reduce myocardial oxygen consumption rather than to increase coronary blood flow. Sublingual nitroglycerin possesses a powerful dilator effect on veins which reduces venous return and thereby the size of the heart and intra-myocardial tension; thus myocardial oxygen requirements are diminished. The beta-adrenergic receptor blocking drug, propranolol (Inderal(R)), inhibits sympathetic stimulation of the heart at rest and during exercise. Thus, myocardial oxygen requirements are diminished by the reduction in heart rate and diminished contractility. As a result of this latter action, cardiac output is reduced and thereby arterial pressure and intramyocardial tension is lowered. In patients with advanced heart disease and borderline cardiac compensation, propranolol is hazardous because it removes the availability of one of the important reserve mechanisms for maintaining cardiac compensation-the sympathetic support of the failing heart. The introduction of electrical stimulation of the carotid sinus nerves as a means of therapy in patients with angina pectoris has provided a powerful tool for the treatment of patients with refractory ischemic pain.

Angina Pectoris↗
PubMed1968

A comparison of the effects of vasodilator stimuli on peripheral resistance vessels in normal subjects and in patients with congestive heart failure.

The objective of this investigation was to characterize the mechanism of peripheral vasoconstriction observed in heart failure and to determine whether it can be attributed to the augmented sympathetic nervous activity, characteristic of this state. The response of the resistance bed in the forearm after release of inflow occlusion (reactive hyperemia), to hand exercise, and to local heating and the response of the calf resistance vessels to arterial occlusion and intra-arterial sodium nitrite and phentolamine were studied in 23 patients with congestive heart failure and 21 normal subjects. In the normal subjects, reactive hyperemia blood flow after varying periods of arterial occlusion greatly exceeded the values observed in patients with heart failure. Local anesthetic blockade and intra-arterial phentolamine did not significantly alter the reactive hyperemia response in heart failure patients, militating against the possibility that increased sympathetic vasoconstrictor activity is responsible for the reduction of this response. Following compensation, the reactive hyperemia response returned toward normal. The striking elevations of the forearm blood flow observed after hand exercise and heating of the forearm in normal subjects were also markedly attenuated in patients with heart failure. Following intra-arterial phentolamine and/or sodium nitrite, peak calf blood flow was still significantly reduced in heart failure. These observations indicate that (1) heart failure is characterized by a striking reduction in the response to a variety of endogenous and exogenous vasodilator stimuli; (2) circulating catecholamines and sympathetic vasoconstrictor activity are not solely responsible for the elevation of peripheral vascular resistance and the reduced response to vasodilator stimuli in heart failure; and (3) heart failure may increase systemic vascular resistance directly by altering the mechanical properties and reducing the dilating ability of the resistance vessels.

Adult↗
PubMedDate not supplied

The pharmacologic effect of aerosolized terbutaline sulfate in exercise-induced bronchospasm.

Bronchospasm can be induced in asthmatics when exercised according to a multistage branching treadmill protocol that allows them to achieve 80 per cent of maximal age-predicted heart rate. This degree of exercise is usually achievable and allows inducible bronchospasm to occur. This present study was undertaken to investigate the effect of terbutaline sulfate aerosol in exercise-induced broncho-spasm. Asthmatics were exercised to 80 per cent of their maximal heart rate, and FEV1.0 and MMEFR were assessed while standing using a Jones Pulmonar II waterless spirometer at 5, 15, and 30 minutes after exercise. After a standard rest period defined by a return to baseline of FEV1.0, MMEFR, and heart rate for 30 minutes, the subjects were administered either 0.50 mg aerosolized terbutaline sulfate or placebo and then exercised again. The pulmonary function parameters were again recorded after this exercise. Preterbutaline and postplacebo exercise resulted in a significant reduction in FEV1.0 and MMEFR, while after treatment with terbutaline not only did bronchospasm not occur but bronchodilation occurred (P less than 0.01). Inhaled terbutaline appeared to normalize the exercise tolerance of the asthmatics and restore physiologic pulmonary airway conductance according to the parameters of FEV1.0 and MMEFR.

Adult↗
PubMedDate not supplied

The pharmacokinetics and pharmacology of oral diltiazem in normal volunteers.

Oral diltiazem is being used increasingly in the treatment of Prinzmetal's angina. This study investigated the pharmacokinetics, electrocardiographic effects, and blood pressure responses of normal male volunteers to various single oral doses of diltiazem. Doses selected were 30, 60, 90, and 120 mg. Thirteen subjects received 30 mg. 12 subjects received 60 mg, 10 subjects received 90 mg diltiazem, and four subjects received 120 mg diltiazem AUCs for the 60, 90, and 120 mg doses were 565, 984, and 1258 ng/ml . hr, respectively. The values for t1/2, beta, and tmax were similar after each dosing.

Adult↗
PubMedDate not supplied

Cardiocirculatory adjustments to exercise following myocardial infarction in rats.

The sequential changes of the cardiocirculatory response to exercise over time in rats with myocardial infarction and failure were studied. Hemodynamics and regional blood flow (RBF, radioactive microspheres) were determined at rest and during exercise either at 1, 10 or 42 days after infarction (MI, infarct size 41.4 +/- 2.6% of LV) or sham procedures (SH). Whereas the response to exercise was attenuated one day after surgery in MI and SH, cardiocirculatory recovery was present in SH at 10 days and LV systolic and end-diastolic pressures separated SH and MI groups. Renal vasoconstriction during exercise occurred 10 days after MI and BF to working muscle during exercise was significantly lower in MI as compared to SH. At 42 days after MI manifest heart failure was present and despite significant blood flow redistribution (p less than 0.05 MI vs SH in renal and cutaneous beds) impaired skeletal muscle flow was observed along with increased vascular resistance in working muscle during exercise. We conclude that the cardiocirculatory response to exercise following large MI follows a distinctive time-dependent pattern, which differs from that observed at rest. Besides exaggerated sympathetically mediated vasoconstriction during exercise, impaired vasodilatation in skeletal muscle at exercise emerged.

Animals↗
PubMedDate not supplied

Skeletal muscle glycogen depletion during submaximal exercise in rats with chronic heart failure.

The purpose of the present study was to determine whether or not abnormalities in glycogen utilization occur in the working skeletal muscles of rats with a myocardial infarction (MI) and chronic heart failure (CHF). Accordingly, glycogen concentrations were measured at rest and following 45 min of submaximal swimming in noninfarcted (SHAM) and MI rats. The tissues examined included the liver and the vastus intermedius, plantaris, soleus and the white portions of the gastrocnemius and tibialis anterior muscles of the rat's hindlimb. Results were analyzed by a two-way analysis of variance and demonstrated that the exercise protocol produced a significant amount of glycogen depletion in the liver and the vastus intermedius and plantaris muscles of the SHAM and MI groups of rats. Although the amount of glycogen utilized in the liver was similar between the SHAM and MI groups of rats, the amount of glycogen utilized in the vastus intermedius and plantaris muscle was significantly greater for the MI group of rats when compared to their SHAM counterparts. The results suggest that the glycogen depletion abnormalities found in the working muscles of the MI rat with CHF are related to accelerated rates of glycogen breakdown and utilization. Furthermore, the results also support the contention that these glycogen depletion abnormalities are primarily located in muscles that are primarily oxidative in nature. The mechanisms responsible for these abnormalities in skeletal muscle glycogen utilization during exercise in the MI rat with CHF have yet to be determined.

Animals↗
PubMedDate not supplied

Abnormalities in the regional circulations accompanying congestive heart failure.

In congestive heart failure, patients appear to have alimited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur...

Basement Membrane↗