Eleven patients with borderline hypertension and high cardiac output were compared to 16 paid healthy volunteers. Cardiac output, heart rate, and intraarterial blood pressure were determined at rest, after administration of 0.2 mg/kg of propranolol i.v., and after administration of an additional 0.04 mg/kg of atropine. In four additional patients, response to infusion of isoproterenol before and after administration of 0.2 mg/kg of propranolol i.v. was evaluated. Resting heart rate and cardiac output in patients with borderline hypertension were elevated. After propranolol infusion, the values decreased more in the patients with borderline hypertension, but remained significantly elevated. After atropine administration, the difference in cardiac output and heart rate between the two groups disappeared. Consequently, patients with borderline hypertension and hyperkinetic circulation simultaneously exhibit an increase of sympathetic and a decrease of parasympathetic tone. HemodynamicsIT IS NOW well documented that many young patients with borderline hypertension have an increased resting cardiac output.1-6 Heart rate in patients with borderline hypertension also tends to be elevated,4-6 but the reports on that topic are not unanimous.2'3 Recently, a condition of concurrent elevation of heart rate and cardiac output but normal, labile or established high blood pressure has been described under the name of hyperdynamic beta-adrenergic circulatory state.7The mechanism by which the heart rate and blood pressure are elevated in borderhne
Eighty-eight observations on 77 patients with borderline hypertension and 82 single observations in healthy control subjects are reported. Hemodynamic effects of assumption of the sitting position, mild exercise, infusion of dextran, blockade with propranolol and with a combination of propranolol and atropine are evaluated. In the recumbent position, patients with borderline hypertension have increased cardiac output and "normal" peripheral resistance. Under all other experimental conditions, the peripheral resistance in patients with borderline hypertension was elevated. Increased resistance was accompanied by a decrease of the cardiac output. After administration of the atropine and propranolol combination, cardiac output in patients with borderline hypertension was significantly below the normal. Nevertheless, whether cardiac output was high or low and resistance normal or elevated, patients with borderline hypertension maintained mild elevations of the blood pressure. Consequently, borderline hypertension is not caused solely by elevations of cardiac output.
The main objective was to evaluate the viability of the SARS-CoV-2 viral particles excreted in stools. In addition, we aimed to identify clinical factors associated with the detection of SARS-CoV-2 RNA in feces, and to determine if its presence is associated with an unfavorable clinical outcome, defined as intensive care unit (ICU) admission and/or death. A prospective multicenter cohort study of COVID-19 adult patients, with confirmed SARS-CoV-2 infection by RT-PCR assay in nasopharyngeal (NP) swabs admitted to four hospitals in Spain, from March 2020 to February 2021. Sixty-two adult COVID-19 patients had stool samples collected at admission and/or during the follow up, with a total of 79 stool samples. SARS-CoV-2 RNA was detected in stool samples from 27 (43.5%) out of the 62 patients. Replicative virus, measured by the generation of cytopathic effect in cell culture and subsequent RT-PCR confirmation of a decrease in the Ct values, was not found in any of these stool samples. Fecal virus excretion was not associated with the presence of gastrointestinal symptoms, or with differences in the evolution of COVID-19 patients. Our results suggest that SARS-CoV-2 replicative capacity is null or very limited in stool samples, and thus, the fecal–oral transmission of SARS-CoV-2 as an alternative infection route is highly unlikely. In our study, the detection of SARS-CoV-2 RNA in feces at the beginning of the disease is not associated with any clinical factor nor with an unfavorable clinical outcome.
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